Systemic Pharm Flashcards

1
Q

What are three targets of natimicrobials

A

Cell wall
DNA
Proteins

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2
Q

What parts of the cell wall in microbes do we target

A

Peptidoglyan (brick)

Transpeptidase (glue)

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3
Q

Cell wall synthesis blockers

A

Bacitracin
PNC
Cephalosporins

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4
Q

PCNs

A

Amoxicillin

Dicloxicilin

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5
Q

Cephalosporins

A

Cephalexin

Ceftriaxone

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6
Q

Protein synthesis inhibitors target

A

30s and 50s ribosomal subunits

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7
Q

30s protein synthesis inhibitors

A
buy AT 30
Aminoglycosides
-gentamicin
-tobramycin
Tetracyclines 
-tetracycline 
-doxycline 
-minocycline
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8
Q

50s protein synthesis inhibitors

A

Collect Money at 50

  • macrolides: erythromycin, azithromycin, alrithromycin
  • Clindamycin (lincomycin)
  • Chloramphenacol
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9
Q

How do we inhibit DNA for microbes

A

Folic acid synthesis (synthase and reductase)

DNA gyrase and topopolymerase 4 (FQs)

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10
Q

Inhibitors of folate synthase

A

Sulfonamide
Trimethoprim
Pyrimethamine

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11
Q

DNA gyrase and topoisomerase inhibitors

A

FQs

  • 2nd G=ciprofloxain, ofloxacin
  • 3rd G=levofloxacin
  • 4th G=gatifloxacin, moxifloxicin, besifloxacin
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12
Q

Peptidoglycan

A

The structural building block of bacterial cell walls; it contains polysaccharide chains that are cross linked via the enzyme transpeptidase. Bacitracin inhibits the transfer of peptidoglycan into the growing bacterial cell wall. All PCNs and cephalopods inhibit cell wall synthesis by inhibiting transpeptidase

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13
Q

MOA of bacitracin

A

Prevents bacterial cell wall synthesis by inhibiting the transfer of peptidoglycans

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14
Q

Clinical indications of bacitracin

A

Bacterial agent that is only effectsi against gram +; only available in ointment form and is often RXed for the treatment of blepharitis (staph)

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15
Q

Polysporin

A

Broads spectrum topical ophthalmic antibiotic ointment that contains the gram + coverage of bacitracin with the gram - coverage of polymyxin B

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16
Q

Neosporin

A

Neomycin + polysporin

Polysporin=bacitracin + polymyxinB

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17
Q

MOA of PCN (amoxicillin and dicloxacillin)

A

Inhibits transpeptidase

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18
Q

Which has better gram - coverage, amoxicillin or dicloxacillin

A

Amoxicillin

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19
Q

Penicillinase

A

Amoxicillin is not resistance to this but dicloxacillin is

Amoxicillin + calvulonic acid=Augmentin and this IS resistant to penicillinase

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20
Q

Dicloxacillin and augmentin are RXed for

A

Combat bacterial infections of the eyelid (hordeolum, preseptal cellulitis) caused by S aureus

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21
Q

DOC for MSS

A

Dicloxacillin

Not effective against MRSA though

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22
Q

Adverse effects of PCN

A

Hypersensitivity reaction

  • type 1=anaphylactic shock and urticaria
  • type 4=contact dermatitis

Render oral BC ineffective
Can cause SJS

Generally PCNs are very safe in all trimesters of pregnancy

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23
Q

MOA of cephalosporins (cephalexin, Ceftriaxone)

A

Inhibit transpeptidase

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24
Q

Clinical indications of cephalosporins

A

Similar to PCNs, all have good gram + coverage. 3rd and 4th generation are more effective against gram negative

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25
Q

Cephalexin uses

A

1st generation cephalosporin
Skin infections (that are primarily caused by gram + bacteria)
Dacryoadenitis, dacryocystitis, and preseptal cellulitis

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26
Q

Ceftriaxone

A

3rd generation cephalosporin
Gonorrhea
IV is treatment of choice for gonococcal conjunctivitis and orbital cellulitis

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27
Q

Treatment of choice for gonococcal conjunctivitis and orbital cellulitis

A

IV ceftriaxone

Gram negative

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28
Q

Adverse effects of cephalosporins

A

Hypersensitivity reactions
Alters vit K absorption, thinning of hte blood
Contraindicated in warfarin

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29
Q

Coverage cephalosporin

A

1st generation=gram +

3rd and 4th generation gram + and -

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30
Q

Which has better gram negative coverage, aminoglycosides or tetracyclines

A

Aminoglycosides

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31
Q

Aminoglycosides

A

Gentamicin

Tobramycin

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32
Q

MOA of aminoglycosides (tobramycin/gentamicin)

A

Bind to the 30s subunit of the bacterial ribosome to inhibit bacterial protein synthesis; effective against gram negative and gram + bacteria, with better coverage of the gram negative spectrum

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33
Q

Ocular indications of aminoglycosides (tobramycin/gentamicin)

A

Tobramycin is available in topical ophthalmic form and ointment form. Gentamicin and tobramycin topical ophthalmic solutions are available in fortified concentration, and are RXed with fortified cefazolin for the treatment of sight threatening ulcers

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34
Q

Tobradex

A

Tobramycin + dexamethasone

Inflammatory ocular conditions with an associated bacterial infection (staph marginal keratitis, corneal infiltrates)

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35
Q

AmiNOglycOSides

A

Nephtotoxicity
Ototoxicity
Ocular surface disease

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36
Q

Drugs taken on an empty stomach

A

PAT
PCNs, azithromycin, tetras

*doxy is the exception

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37
Q

Adverse effects of aminoglycosides

A

Topical ophthalmic aminoglycosides cause SPK and delayed healing

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38
Q

Tetracyclines

A

30s
Tetracycline
Doxycycline
Minocycline

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39
Q

MOA of tetracycline

A

Inhibit bacterial protein synthesis by binding to the 30s ribosomal subunit and preventing access to aminoacyl tRNA; they are bacteriostatic ABx

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40
Q

Clinical inidincations of doxycycline

A

Meibomianitis
Acne rosacea
Chlamydia ocular infections
Post RCE

TAKEN WITH FOOD

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41
Q

Minocyline indications

A

Low doses for long term managment of acne vulgaris

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42
Q

Pharmacokinetics of tetracyclines

A

The absorption in the GI tract is impaired by cations in dairy products, antacids, and iron-containing compounds. The primary route of excretion of through the kidney; thus tetras are contraindicated in pateitns with renal failure. Doxy is th excretion, it can be taken with food and is eliminated in fecal matter, and can therefore be RXed in patients with renal failure

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43
Q

Adverse affects of tetras

A

Contraindicated in pregnancy and in children. Side effects include pseudotumor cerebri, bone growth retardation, and discoloring of teeth. Minocyline may cause blue sclera and pigmented cysts on the conjunctiva

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44
Q

Blockers of the 50s ribosomal subunit

A

CM

Chloramphenicol, clindamycin,lincomycin, marolides (erythromycin, azithromycin, clarithromycin)

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45
Q

Chloramphenicol MOA

A

Inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit; it is effective against gram + and gram - bacteria. It can be formulated as an ointment for topical ophthalmic solution

Dinosaur
We dont use it that much anymore

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46
Q

Drugs contraindicated in pregnancy

A

FAT
FQs
Aminoglycosides
Tetras

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47
Q

Drugs that are safe in pregnancy

A

PAC
Pens
Azithromycin
Cephalosporin

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48
Q

P cerebri drugs

A
CATS
Contraceptive 
Acutane 
Tetra 
Synthroid/steroid
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49
Q

Drugs that can cause a blue scleral

A

Steroids

Minocycline

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50
Q

Adver effects of chloramphenicol

A

TOPICAL ophthalmic use has caused fatal aplastic anemia

Extended therapy may result in optic neuritis

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51
Q

What is the only topical drug that can cause fatal aplastic anemia

A

Chloramphenicol

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52
Q

MOA of macrolides (erythromycin, azithromycin, clarithromycin)

A

Inhibit the bacterial protein synthesis by binding to the 50S subunit of the bacterial ribosome

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53
Q

What can treat chlamydia

A

Doxy

Azithromycin

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54
Q

Uses of oral azithromycin

A
Chlamydia infections (trachoma and AIC)
Single gram dose 
Taken on an empty stomach
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55
Q

Topical ophthalmic azithromycin uses

A

Bacterial conjunctivitis and blepharitis

BID x 2 days, then QD x 5 days

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56
Q

Topical ophthalmic erythromycin ointment uses

A

Uncommonly RXed for active bacterial infections due to its poor resistance profile; it is more commonly RXed for prophylaxis and is dosed at night. It is also RXed for prophylaxis of gonococcal ophthalmia neonatorum

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57
Q

Oral clarithromycin uses

A

Respiratory infections

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58
Q

Azasite

A

Contains the preservative BAK. Patients who wear CL are advised against CL wear during the treatment with azasite

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59
Q

MOA of lincomycin/clindamycin

A

Inhibit the bacterial protein synthesis by REVERSIBLY binding to the 50s subunit of the bacterial ribosome

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60
Q

Clinical indications of clindamycin/lincomycin

A

MRSA

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61
Q

Drugs for MRSA

A

Bacteria Can’t Decide
Bactrim (TMP-sulf)
Clindamycin
Doxycycline

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62
Q

Sulfonamide MOA

A

Inhibit dihydropteroate synthase, an enzyme that converts PABA to dihydrofolic acid as the first step of folic acid synthesis; these drugs are bacteriostatic agents that are RXed to treat gram + and gram - infections

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63
Q

Ophthalmic indications of sulfonamide

A

Rarely used topically

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64
Q

Side effects of topical sulfonamide

A

Burning, stinging, contact dermatitis, and local photosensitization

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65
Q

Systemic indications of sulfonamide

A

Sulfadiazine + pyrimethamine=toxo treatment

Sulfamethoxazole + trimethorpim=bactrim

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66
Q

Adverse effects of sulfonamides

A

Can cause kernicterus in infants due to bilirubin accumulation within the brain (they are contraindicated during pregnancy); they may also have a myopic shift in the patients refractive error. Topical and oral sulfonamides may also cause SJS

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67
Q

Trimethoprim and pyrimethamine MOA

A

Inhibit dihycrofolate reductase, an enzyme that converts dihydrofolic acid to tetrahydrofolic acid in the second step of folic acid synthesis

Trim reduces

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68
Q

Clinical indications of trimethoprim

A

Gram +/-, not as effective against pseudomonas

Combo with polymyxin B as polytrim

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69
Q

Indications of pyrimethamine

A

Given orally with sulfadi for toxoplasmosis

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70
Q

What is the best to use for bacterial conjunctivits in kids

A

Polytrim

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71
Q

Most potent ophthalmic ABX against MRSA

A

Trimethoprim and tobramycin

Besifoxacin and vancomycin also

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72
Q

Adverse effects of trimethoprim/pyrimethamine

A

Oral trimethoprim can cause bone marrow suppression, resulting in aplastic anemia, leukopenia, and granulocytopenia, pyrmethamine can have similar toxicity

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73
Q

MOA of FQs

A

Rapidly inhibit bacterial DNA synthesis by inhibiting DNA gyrase and topoisomerase 4

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74
Q

2nd generation FQ

A

Cirpofloxacin

Ofloxacin

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75
Q

3rd generation FQs

A

Levofloxacin

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76
Q

4th generation FQs

A

Gatifloxacin
Moxifloxacin
Besifloxacin

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77
Q

Topical ophthalmic indications of FQs

A

Contact lens realted ulcers, corneal abrasions, and bacterial conjunctivitis

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78
Q

Systemic indications of FQs

A

Ciprofloxacin is RXed for gram - urinary and GI infections. Moxifloxacin is approved for the treatment of pneumonia, sinusitis, and intracranial-abdominal and skin infections

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79
Q

Adverse effects of FQs

A

ORAL fluroquinoLONES can hurt the attachment to your BONEs; causing tendinitis. Oral FQs are contraindicated in pregnancy, chidlren, and adolescents below the age of 18 due to damage in cartilage formation and inhibition of bone growth

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80
Q

Effectiveness of the differnt generations of FQs

A

There are 4 generations, 3 and 4 have been formulated with improved effectiveness against gram + infections, however these drugs continue to be potent against gram - bac as well

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81
Q

Topical FQs and kids

A

All of the TOPICAL (NEVER ORAL) FQs are approved for kids 1 year and older EXCEPT LEVOFLOXACIN

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82
Q

Bacteriostatic agents

A

Tetracyclines, trimethoprim, sulfacetamde, and to some degree, erythromycin

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83
Q

Bacteriocidal agents

A

PNS, Cephs, bacitracin, aminoglycosides, FQs

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84
Q

Number one symptom of TB

A

Night sweats

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85
Q

TB is caused by

A

Mycobacterium TB

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86
Q

Active TB

A

Treated with a combo therapy

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87
Q

Latent TB

A

Treated with isoniazid or rifampin monotherapy

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88
Q

Active TB treatment is

A

RIPE

  • rifampin
  • isoniazid
  • ethambutol

Don’t need to know the P one

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89
Q

TB=RIPE Cheese

A

RIPE for the drugs

Cheese=caseous necrosis

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90
Q

MOA of rifampin

A

Prevents mRNA synthesis (transcription) by binding to the beta subunit of DNA dependent RNA POLYMERASE

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91
Q

Adverse effects of rifampin

A

Hepatotxicity (increased AST and ALT), orange/pink colored tears and urine

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92
Q

Isoniazid MOA

A

Prevents cell wall synthesis by inhibiting mycolic acid synthesis

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93
Q

Adverse effects of isoniazid

A

Hepatotoxicity, can also cause pyridoxine (vit B6) deficiency that may result in peripheral neuropathy. Rarely It can cause optic neuritis and optic atrophy, resulting in loss of vision

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94
Q

Ethambutol MOA

A

Inhibits synthesis of mycobacterium cell wall by inhibiting arabinosyl transferase

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95
Q

What are the two drugs that can be used in isolation for TB monotherapy (latent)

A

Rifampin

Isoniazid

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96
Q

Adverse effects of ethambutol

A
Optic neuritis (retrobulbar)
May be reversible vision loss
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97
Q

What TB drug is known to cause retrobulbar optic neuritis

A

Ethambutol

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98
Q

Antivirals for the flu

A

Oseltamivir (tamiflu)
-inhibits influenza A and B viral neuraminidase

Conjunctivitis due to influenza in 1% pts has been reported

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99
Q

MOA of HIV therapy (Zidovudine [Retrovir])

A

Reverse transcriptase inhibitor

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100
Q

AIDs occurs at what CD 4 count

A

<200

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101
Q

Clinical indications of zidovudine (Retrovir)

A

Major component of three-drug therapy for HIV. Also used during pregnancy to lower the risk of transmitting HIV to the fetus (vertical transmission)

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102
Q

Adverse effects of zidovudine (Retrovir)

A
  1. Bone marrow suppression
  2. Lactic acidosis
  3. Muscle breakdown
    Amblyopia and macular edema have also been reported
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103
Q

There is a vax for which Heps

A

A and B

None for C

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104
Q

Hepatitis C therapy

A

C=chronic

Ribavirin + interferon

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105
Q

MOA of ribivirin

A

Inhibits viral RNA polymerase

Always in combo with interferon for the treatment of hep C

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106
Q

Adverse effects of ribavirin

A

Conjunctivis
Retinopathy
Retinal vascular Occlusions

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107
Q

Ocular side effects of ribavirin

A
RIBAViriN
RD
Ischemia 
Bleeding
Arterial and Venous occlusions
Optic Neuritis 

VA normally OK

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108
Q

Why kind of virus is herpes

A

DNA

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109
Q

What do all herpes meds do

A

Inhibit DNA polymerase

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110
Q

Trifluridine MOA

A

Inhibits DNA polymerase for the treatment of herpes simplex keratitis
Not used often because 9x day dosing and thimerosol

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111
Q

Acyclovir, valacyclovir, famcyclovir MOA

A

DNA polymerase inhibitors

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112
Q

Indications of acyclovir, valacyclovir, and famcyclovir

A

Cold sores, genital sores, and shingles. They may also be RXed for HZO, HSV keratitis, and prophylaxis against recurrent HSV keratitis

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113
Q

Adverse effects of acyclovir, valacyclovir, and famcyclovir

A

Headaches and GI effects
Renal dysfunction
-be careful in those with renal dysfunction and the elderly. Monitor closely

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114
Q

Oral antivirals

A

Used to treat HSV epithelial keratitis, but topical ophthalmic treatment is considered the standard of care. Oral dosages should be decreased in patients with kidney disease

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115
Q

Gancylovir

A
  • DNA polymerase inhibitor
  • reduced corneal toxicity, 5x/day dosing (better than viroptic)
  • BAK instead of thimerosol
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116
Q

Clinical indications for gancyclovir

A

HSV keratitis

Intraocular sustained-release capsule for the treatment of CMV retinitis

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117
Q

CMV

A

Opportunistic infection
Vision threatening retinopathy in those with AIDS
-most common intraocualr infection in patients with AIDs
-treat with Zirgan (gancyclovir), if that doesnt work, use your safety “net” Foscarnet

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118
Q

Foscarnet

A
  • SAfety net for CMV if gancyclovir fails
  • DNA polymerase inhibitor, IV
  • nehprotoxicity and seizures
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119
Q

Fungal ucler

A

Feathery edges
Immunocompromised
Chronic beat up cornea
Tree branch

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120
Q

Fungus: ergosterol

A

Component of fungal cell membranes that is not found in human or animal cell walls.

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121
Q

Antifungal drugs

A

Natamycin, amphotericin B, nystatin
Ketoconazole, fluconazole, and miconozole
Griseofulvin

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122
Q

MOA of natamycin, amphotericin B, and nystatin

A

Bind to ergosterol and form pores

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123
Q

Clinical indictions for natamycin

A

Approved for the treatment of fungal blepharitis, conjunctivits, and keratitis caused by susceptible organisms of Candida, Aspergillus, and Fusarium

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124
Q

Clinical indications for Amphotericin B

A

Broad spectrum antifungal.
Fungal keratitis, and IV form to treat systemic and intraocular fungal infections.
Nephrotoxicity is common in IV form

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125
Q

Clinical indications of Nystatin

A
Candida oral (thrush) and vaginal (yeast) infections 
Not indicated for ophthalmic use
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126
Q

MOA of ketoconazole, fluconazole, and miconazole

A

Inhibit ergosterol synthesis

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127
Q

Clinical indications of ketoconazole

A

First oral azole antifungal drug and is indicated for the treatment of severe fungal corneal ulcers, systemic fungal infections, and acanthoemeba

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128
Q

Indications of fluconazole

A

Orally, topically, or through subconjunctival injections

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129
Q

Adverse effects of the azoles

A

Hepatotoxicity

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130
Q

MOA of griseofulvin

A

Inhibits fungal mitosis by interfering with microtubule formation

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131
Q

Clinical indictions of griseofulvin

A

Scalp and skin, fingernails and toenails

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132
Q

Treatment of toxoplasmosis

A

Sulfadi + pyrimethamine

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133
Q

Antiparasitic drugs

A

Chloroquine

Lindane

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134
Q

MOA of chloroquine

A
  1. Results in the build up of heme within the RBCs; this accumulation is toxic to the “intra-erythrocytic” plasmodium parasite responsible for malaria
  2. Inhibits phosphlipase A2 to decrease inflammation, not generally used for this
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135
Q

Adverse effects of chloroquine

A

Whorl K
Bulls eye maculopathy: granular hyperpigmentation surrounded by zone of depigmentation
Binds melanin=migration of RPE cells-permanent

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136
Q

What does a plaquenil screening consist of

A

10-2 VF

SD-OCT

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137
Q

Why does chloroquine cause bulls eye maculopathy

A

Binds to melanin of the RPE cells, causing localized RPE damage and subsequent migration of RPE cells to the outer nuclear and OPL. The initial sign of bulls eye maculopathy is RPE mottling within the macula

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138
Q

Risk of developing bulls eye maculopathy in chloroquine

A
  • > 2.3mg/kg body weight (Hydroxychloroquine is >5mg/kg)
  • treatment > 5 years
  • abnormal renal function
  • high body fat
  • > 60yo
  • liver disease
  • concomitant retinal disease
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139
Q

Scotomas of chloroquine

A

Central and paracentral most common

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140
Q

Lindane

A
Antiparacytic 
MOA: lipophlic structure absorbed through the exoskeleton of insects, resulting in seizures and death 
-lice, scabies 
-causes conjunctivits 
-not for the eyes
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141
Q

Peptidoglycan

A

The structural building block of bacterial cell walls; it contains polysaccharide chains that are cross linked via the enzyme transpeptidase. Bacitracin inhibits the transfer of peptidoglycan into the growing bacterial cell wall. All PCNs and cephalopods inhibit cell wall synthesis by inhibiting transpeptidase

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142
Q

MOA of bacitracin

A

Prevents bacterial cell wall synthesis by inhibiting the transfer of peptidoglycans

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143
Q

Clinical indications of bacitracin

A

Bacterial agent that is only effectsi against gram +; only available in ointment form and is often RXed for the treatment of blepharitis (staph)

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144
Q

Polysporin

A

Broads spectrum topical ophthalmic antibiotic ointment that contains the gram + coverage of bacitracin with the gram - coverage of polymyxin B

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145
Q

Neosporin

A

Neomycin + polysporin

Polysporin=bacitracin + polymyxinB

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146
Q

MOA of PCN (amoxicillin and dicloxacillin)

A

Inhibits transpeptidase

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147
Q

Which has better gram - coverage, amoxicillin or dicloxacillin

A

Amoxicillin

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148
Q

Penicillinase

A

Amoxicillin is not resistance to this but dicloxacillin is

Amoxicillin + calvulonic acid=Augmentin and this IS resistant to penicillinase

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149
Q

Dicloxacillin and augmentin are RXed for

A

Combat bacterial infections of the eyelid (hordeolum, preseptal cellulitis) caused by S aureus

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150
Q

DOC for MSS

A

Dicloxacillin

Not effective against MRSA though

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151
Q

Adverse effects of PCN

A

Hypersensitivity reaction

  • type 1=anaphylactic shock and urticaria
  • type 4=contact dermatitis

Render oral BC ineffective
Can cause SJS

Generally PCNs are very safe in all trimesters of pregnancy

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152
Q

MOA of cephalosporins (cephalexin, Ceftriaxone)

A

Inhibit transpeptidase

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153
Q

Clinical indications of cephalosporins

A

Similar to PCNs, all have good gram + coverage. 3rd and 4th generation are more effective against gram negative

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154
Q

Cephalexin uses

A

1st generation cephalosporin
Skin infections (that are primarily caused by gram + bacteria)
Dacryoadenitis, dacryocystitis, and preseptal cellulitis

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155
Q

Ceftriaxone

A

3rd generation cephalosporin
Gonorrhea
IV is treatment of choice for gonococcal conjunctivitis and orbital cellulitis

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156
Q

Treatment of choice for gonococcal conjunctivitis and orbital cellulitis

A

IV ceftriaxone

Gram negative

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157
Q

Adverse effects of cephalosporins

A

Hypersensitivity reactions
Alters vit K absorption, thinning of hte blood
Contraindicated in warfarin

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158
Q

Coverage cephalosporin

A

1st generation=gram +

3rd and 4th generation gram + and -

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159
Q

Which has better gram negative coverage, aminoglycosides or tetracyclines

A

Aminoglycosides

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160
Q

Aminoglycosides

A

Gentamicin

Tobramycin

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161
Q

MOA of aminoglycosides (tobramycin/gentamicin)

A

Bind to the 30s subunit of the bacterial ribosome to inhibit bacterial protein synthesis; effective against gram negative and gram + bacteria, with better coverage of the gram negative spectrum

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162
Q

Ocular indications of aminoglycosides (tobramycin/gentamicin)

A

Tobramycin is available in topical ophthalmic form and ointment form. Gentamicin and tobramycin topical ophthalmic solutions are available in fortified concentration, and are RXed with fortified cefazolin for the treatment of sight threatening ulcers

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163
Q

Tobradex

A

Tobramycin + dexamethasone

Inflammatory ocular conditions with an associated bacterial infection (staph marginal keratitis, corneal infiltrates)

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164
Q

AmiNOglycOSides

A

Nephtotoxicity
Ototoxicity
Ocular surface disease

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165
Q

Drugs taken on an empty stomach

A

PAT
PCNs, azithromycin, tetras

*doxy is the exception

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166
Q

Adverse effects of aminoglycosides

A

Topical ophthalmic aminoglycosides cause SPK and delayed healing

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167
Q

Tetracyclines

A

30s
Tetracycline
Doxycycline
Minocycline

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168
Q

MOA of tetracycline

A

Inhibit bacterial protein synthesis by binding to the 30s ribosomal subunit and preventing access to aminoacyl tRNA; they are bacteriostatic ABx

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169
Q

Clinical inidincations of doxycycline

A

Meibomianitis
Acne rosacea
Chlamydia ocular infections
Post RCE

TAKEN WITH FOOD

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170
Q

Minocyline indications

A

Low doses for long term managment of acne vulgaris

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171
Q

Pharmacokinetics of tetracyclines

A

The absorption in the GI tract is impaired by cations in dairy products, antacids, and iron-containing compounds. The primary route of excretion of through the kidney; thus tetras are contraindicated in pateitns with renal failure. Doxy is th excretion, it can be taken with food and is eliminated in fecal matter, and can therefore be RXed in patients with renal failure

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172
Q

Adverse affects of tetras

A

Contraindicated in pregnancy and in children. Side effects include pseudotumor cerebri, bone growth retardation, and discoloring of teeth. Minocyline may cause blue sclera and pigmented cysts on the conjunctiva

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173
Q

Blockers of the 50s ribosomal subunit

A

CM

Chloramphenicol, clindamycin,lincomycin, marolides (erythromycin, azithromycin, clarithromycin)

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174
Q

Chloramphenicol MOA

A

Inhibits bacterial protein synthesis by binding to the 50S ribosomal subunit; it is effective against gram + and gram - bacteria. It can be formulated as an ointment for topical ophthalmic solution

Dinosaur
We dont use it that much anymore

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175
Q

Drugs contraindicated in pregnancy

A

FAT
FQs
Aminoglycosides
Tetras

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176
Q

Drugs that are safe in pregnancy

A

PAC
Pens
Azithromycin
Cephalosporin

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177
Q

P cerebri drugs

A
CATS
Contraceptive 
Acutane 
Tetra 
Synthroid/steroid
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178
Q

Drugs that can cause a blue scleral

A

Steroids

Minocycline

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179
Q

Adver effects of chloramphenicol

A

TOPICAL ophthalmic use has caused fatal aplastic anemia

Extended therapy may result in optic neuritis

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180
Q

What is the only topical drug that can cause fatal aplastic anemia

A

Chloramphenicol

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181
Q

MOA of macrolides (erythromycin, azithromycin, clarithromycin)

A

Inhibit the bacterial protein synthesis by binding to the 50S subunit of the bacterial ribosome

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182
Q

What can treat chlamydia

A

Doxy

Azithromycin

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183
Q

Uses of oral azithromycin

A
Chlamydia infections (trachoma and AIC)
Single gram dose 
Taken on an empty stomach
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184
Q

Topical ophthalmic azithromycin uses

A

Bacterial conjunctivitis and blepharitis

BID x 2 days, then QD x 5 days

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185
Q

Topical ophthalmic erythromycin ointment uses

A

Uncommonly RXed for active bacterial infections due to its poor resistance profile; it is more commonly RXed for prophylaxis and is dosed at night. It is also RXed for prophylaxis of gonococcal ophthalmia neonatorum

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186
Q

Oral clarithromycin uses

A

Respiratory infections

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187
Q

Azasite

A

Contains the preservative BAK. Patients who wear CL are advised against CL wear during the treatment with azasite

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188
Q

MOA of lincomycin/clindamycin

A

Inhibit the bacterial protein synthesis by REVERSIBLY binding to the 50s subunit of the bacterial ribosome

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189
Q

Clinical indications of clindamycin/lincomycin

A

MRSA

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190
Q

Drugs for MRSA

A

Bacteria Can’t Decide
Bactrim (TMP-sulf)
Clindamycin
Doxycycline

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191
Q

Sulfonamide MOA

A

Inhibit dihydropteroate synthase, an enzyme that converts PABA to dihydrofolic acid as the first step of folic acid synthesis; these drugs are bacteriostatic agents that are RXed to treat gram + and gram - infections

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192
Q

Ophthalmic indications of sulfonamide

A

Rarely used topically

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193
Q

Side effects of topical sulfonamide

A

Burning, stinging, contact dermatitis, and local photosensitization

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194
Q

Systemic indications of sulfonamide

A

Sulfadiazine + pyrimethamine=toxo treatment

Sulfamethoxazole + trimethorpim=bactrim

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195
Q

Adverse effects of sulfonamides

A

Can cause kernicterus in infants due to bilirubin accumulation within the brain (they are contraindicated during pregnancy); they may also have a myopic shift in the patients refractive error. Topical and oral sulfonamides may also cause SJS

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196
Q

Trimethoprim and pyrimethamine MOA

A

Inhibit dihycrofolate reductase, an enzyme that converts dihydrofolic acid to tetrahydrofolic acid in the second step of folic acid synthesis

Trim reduces

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197
Q

Clinical indications of trimethoprim

A

Gram +/-, not as effective against pseudomonas

Combo with polymyxin B as polytrim

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198
Q

Indications of pyrimethamine

A

Given orally with sulfadi for toxoplasmosis

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199
Q

What is the best to use for bacterial conjunctivits in kids

A

Polytrim

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200
Q

Most potent ophthalmic ABX against MRSA

A

Trimethoprim and tobramycin

Besifoxacin and vancomycin also

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201
Q

Adverse effects of trimethoprim/pyrimethamine

A

Oral trimethoprim can cause bone marrow suppression, resulting in aplastic anemia, leukopenia, and granulocytopenia, pyrmethamine can have similar toxicity

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202
Q

MOA of FQs

A

Rapidly inhibit bacterial DNA synthesis by inhibiting DNA gyrase and topoisomerase 4

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203
Q

2nd generation FQ

A

Cirpofloxacin

Ofloxacin

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204
Q

3rd generation FQs

A

Levofloxacin

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205
Q

4th generation FQs

A

Gatifloxacin
Moxifloxacin
Besifloxacin

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206
Q

Topical ophthalmic indications of FQs

A

Contact lens realted ulcers, corneal abrasions, and bacterial conjunctivitis

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207
Q

Systemic indications of FQs

A

Ciprofloxacin is RXed for gram - urinary and GI infections. Moxifloxacin is approved for the treatment of pneumonia, sinusitis, and intracranial-abdominal and skin infections

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208
Q

Adverse effects of FQs

A

ORAL fluroquinoLONES can hurt the attachment to your BONEs; causing tendinitis. Oral FQs are contraindicated in pregnancy, chidlren, and adolescents below the age of 18 due to damage in cartilage formation and inhibition of bone growth

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209
Q

Effectiveness of the differnt generations of FQs

A

There are 4 generations, 3 and 4 have been formulated with improved effectiveness against gram + infections, however these drugs continue to be potent against gram - bac as well

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210
Q

Topical FQs and kids

A

All of the TOPICAL (NEVER ORAL) FQs are approved for kids 1 year and older EXCEPT LEVOFLOXACIN

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211
Q

Bacteriostatic agents

A

Tetracyclines, trimethoprim, sulfacetamde, and to some degree, erythromycin

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212
Q

Bacteriocidal agents

A

PNS, Cephs, bacitracin, aminoglycosides, FQs

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213
Q

Number one symptom of TB

A

Night sweats

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214
Q

TB is caused by

A

Mycobacterium TB

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215
Q

Active TB

A

Treated with a combo therapy

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216
Q

Latent TB

A

Treated with isoniazid or rifampin monotherapy

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217
Q

Active TB treatment is

A

RIPE

  • rifampin
  • isoniazid
  • ethambutol

Don’t need to know the P one

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218
Q

TB=RIPE Cheese

A

RIPE for the drugs

Cheese=caseous necrosis

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219
Q

MOA of rifampin

A

Prevents mRNA synthesis (transcription) by binding to the beta subunit of DNA dependent RNA POLYMERASE

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220
Q

Adverse effects of rifampin

A

Hepatotxicity (increased AST and ALT), orange/pink colored tears and urine

221
Q

Isoniazid MOA

A

Prevents cell wall synthesis by inhibiting mycolic acid synthesis

222
Q

Adverse effects of isoniazid

A

Hepatotoxicity, can also cause pyridoxine (vit B6) deficiency that may result in peripheral neuropathy. Rarely It can cause optic neuritis and optic atrophy, resulting in loss of vision

223
Q

Ethambutol MOA

A

Inhibits synthesis of mycobacterium cell wall by inhibiting arabinosyl transferase

224
Q

What are the two drugs that can be used in isolation for TB monotherapy (latent)

A

Rifampin

Isoniazid

225
Q

Adverse effects of ethambutol

A
Optic neuritis (retrobulbar)
May be reversible vision loss
226
Q

What TB drug is known to cause retrobulbar optic neuritis

A

Ethambutol

227
Q

Antivirals for the flu

A

Oseltamivir (tamiflu)
-inhibits influenza A and B viral neuraminidase

Conjunctivitis due to influenza in 1% pts has been reported

228
Q

MOA of HIV therapy (Zidovudine [Retrovir])

A

Reverse transcriptase inhibitor

229
Q

AIDs occurs at what CD 4 count

A

<200

230
Q

Clinical indications of zidovudine (Retrovir)

A

Major component of three-drug therapy for HIV. Also used during pregnancy to lower the risk of transmitting HIV to the fetus (vertical transmission)

231
Q

Adverse effects of zidovudine (Retrovir)

A
  1. Bone marrow suppression
  2. Lactic acidosis
  3. Muscle breakdown
    Amblyopia and macular edema have also been reported
232
Q

There is a vax for which Heps

A

A and B

None for C

233
Q

Hepatitis C therapy

A

C=chronic

Ribavirin + interferon

234
Q

MOA of ribivirin

A

Inhibits viral RNA polymerase

Always in combo with interferon for the treatment of hep C

235
Q

Adverse effects of ribavirin

A

Conjunctivis
Retinopathy
Retinal vascular Occlusions

236
Q

Ocular side effects of ribavirin

A
RIBAViriN
RD
Ischemia 
Bleeding
Arterial and Venous occlusions
Optic Neuritis 

VA normally OK

237
Q

Why kind of virus is herpes

A

DNA

238
Q

What do all herpes meds do

A

Inhibit DNA polymerase

239
Q

Trifluridine MOA

A

Inhibits DNA polymerase for the treatment of herpes simplex keratitis
Not used often because 9x day dosing and thimerosol

240
Q

Acyclovir, valacyclovir, famcyclovir MOA

A

DNA polymerase inhibitors

241
Q

Indications of acyclovir, valacyclovir, and famcyclovir

A

Cold sores, genital sores, and shingles. They may also be RXed for HZO, HSV keratitis, and prophylaxis against recurrent HSV keratitis

242
Q

Adverse effects of acyclovir, valacyclovir, and famcyclovir

A

Headaches and GI effects
Renal dysfunction
-be careful in those with renal dysfunction and the elderly. Monitor closely

243
Q

Oral antivirals

A

Used to treat HSV epithelial keratitis, but topical ophthalmic treatment is considered the standard of care. Oral dosages should be decreased in patients with kidney disease

244
Q

Gancylovir

A
  • DNA polymerase inhibitor
  • reduced corneal toxicity, 5x/day dosing (better than viroptic)
  • BAK instead of thimerosol
245
Q

Clinical indications for gancyclovir

A

HSV keratitis

Intraocular sustained-release capsule for the treatment of CMV retinitis

246
Q

CMV

A

Opportunistic infection
Vision threatening retinopathy in those with AIDS
-most common intraocualr infection in patients with AIDs
-treat with Zirgan (gancyclovir), if that doesnt work, use your safety “net” Foscarnet

247
Q

Foscarnet

A
  • SAfety net for CMV if gancyclovir fails
  • DNA polymerase inhibitor, IV
  • nehprotoxicity and seizures
248
Q

Fungal ucler

A

Feathery edges
Immunocompromised
Chronic beat up cornea
Tree branch

249
Q

Fungus: ergosterol

A

Component of fungal cell membranes that is not found in human or animal cell walls.

250
Q

Antifungal drugs

A

Natamycin, amphotericin B, nystatin
Ketoconazole, fluconazole, and miconozole
Griseofulvin

251
Q

MOA of natamycin, amphotericin B, and nystatin

A

Bind to ergosterol and form pores

252
Q

Clinical indictions for natamycin

A

Approved for the treatment of fungal blepharitis, conjunctivits, and keratitis caused by susceptible organisms of Candida, Aspergillus, and Fusarium

253
Q

Clinical indications for Amphotericin B

A

Broad spectrum antifungal.
Fungal keratitis, and IV form to treat systemic and intraocular fungal infections.
Nephrotoxicity is common in IV form

254
Q

Clinical indications of Nystatin

A
Candida oral (thrush) and vaginal (yeast) infections 
Not indicated for ophthalmic use
255
Q

MOA of ketoconazole, fluconazole, and miconazole

A

Inhibit ergosterol synthesis

256
Q

Clinical indications of ketoconazole

A

First oral azole antifungal drug and is indicated for the treatment of severe fungal corneal ulcers, systemic fungal infections, and acanthoemeba

257
Q

Indications of fluconazole

A

Orally, topically, or through subconjunctival injections

258
Q

Adverse effects of the azoles

A

Hepatotoxicity

259
Q

MOA of griseofulvin

A

Inhibits fungal mitosis by interfering with microtubule formation

260
Q

Clinical indictions of griseofulvin

A

Scalp and skin, fingernails and toenails

261
Q

Treatment of toxoplasmosis

A

Sulfadi + pyrimethamine

262
Q

Antiparasitic drugs

A

Chloroquine

Lindane

263
Q

MOA of chloroquine

A
  1. Results in the build up of heme within the RBCs; this accumulation is toxic to the “intra-erythrocytic” plasmodium parasite responsible for malaria
  2. Inhibits phosphlipase A2 to decrease inflammation, not generally used for this
264
Q

Adverse effects of chloroquine

A

Whorl K
Bulls eye maculopathy: granular hyperpigmentation surrounded by zone of depigmentation
Binds melanin=migration of RPE cells-permanent

265
Q

What does a plaquenil screening consist of

A

10-2 VF

SD-OCT

266
Q

Why does chloroquine cause bulls eye maculopathy

A

Binds to melanin of the RPE cells, causing localized RPE damage and subsequent migration of RPE cells to the outer nuclear and OPL. The initial sign of bulls eye maculopathy is RPE mottling within the macula

267
Q

Risk of developing bulls eye maculopathy in chloroquine

A
  • > 2.3mg/kg body weight (Hydroxychloroquine is >5mg/kg)
  • treatment > 5 years
  • abnormal renal function
  • high body fat
  • > 60yo
  • liver disease
  • concomitant retinal disease
268
Q

Scotomas of chloroquine

A

Central and paracentral most common

269
Q

Lindane

A
Antiparacytic 
MOA: lipophlic structure absorbed through the exoskeleton of insects, resulting in seizures and death 
-lice, scabies 
-causes conjunctivits 
-not for the eyes
270
Q

What is the first step in the arachidonic pathway

A

Phospholipase A2

271
Q

What are leukotrienes synthesized by

A

Lipoxygenase

272
Q

Thromboxanes

A

Induce platelet aggregation

273
Q

COX2

A

Synthesizes PGs that mediate inflammation

  • pain
  • fever
  • swelling
274
Q

COX1

A

Synthesizes PGs that inhibit gastric secretions and influence gastric motility
-protects our ONE stomach

275
Q

MOA of hydroxychloroquine (plaquenil)

A
  1. Inhibits phospholipase A2

2. Build up of heme

276
Q

Clinical indications for hydroxychloroquine

A

Lupus
RA
Malaria

277
Q

Adverse effects of hydroxychloroquine

A
Corneal deposition (whorl K)
Bulls eye maculopathy (greatest threat to vision)
278
Q

Ideal daily dose of hydroxychloroquine

A

toxic I’d >5mg/kg body weight

Do not exceed 400mg per day

279
Q

Toxic dose of chloroquine

A

> 2.3mg/kg body weight

280
Q

Risk factors for maculopathy in hydroxychloroquine include

A
Treatment duration > 5 years 
Abnornal renal function 
Liver disease
Age > 60
High body fat 
Concomitant retinal Disease
281
Q

Baseline exam for hydroxychloroquine

A
  • baseline dilated retinal exam within 1 year of beginning drug.
  • annual screenings initiated after 5 years
  • 10-2 HVF, SD-OCT
  • if patient is at a greater risk of development of bulls eye maculopathy, exams should occur every 6 months to 1 year after the baseline exam.
  • risk much higher with chloroquine than hydroxychloroquine
  • 2.3mg/kg chloroquine and 5mg/kg hydroxychloroquine
282
Q

Which is more toxic, chloroquine or hydroxychloroquine

A

Chloroquine

283
Q

Strong topical steroids

A

Pred acetate
Rimexolone
Difluprednate
Dexamethasone

284
Q

Weak topical steroids

A

Loteprednol

Fluorometholone (FML)

285
Q

What are the systemic steroids

A

Fluticasone
Triamcinolone
Hydrocortisone

286
Q

MOA of steroids

A

Inhibition of phospholipase A 2

287
Q

Steroids side effects

A
Increased blood sugar 
Insulin resistance 
Peptic ulcer (decreased PGs)
Decreased fibroblasts (decreased healing)
Osteoporosis
HTN
Psychiatric
288
Q

Ocular side effects of steroids

A

PSC cataracts (dose dependent, irreversible)
Glaucoma
Increased risk of secondary infections (HSV K)
Central serous chorioretinopathy

289
Q

What to inquire about before RXing oral steroids

A

Pregnancy
Peptic ulcers
Diabetes

290
Q

Hydrocortisone RXed for

A

Adrenal insufficiency

May also be used as a potent anti inflammatory medication

291
Q

What steroid should not be give to dark skinned patients

A

Triamcinolone

292
Q

Ophthalmic indications of triamcinolone via injection

A
  • DM mac edema
  • graves
  • intermediate or non resolving posterior uveitis
  • chalazia
  • recalcitrant Irvine gass CME
  • CME associated with noninfectious posteiror uveitis
  • mac edema secondary to CRVO
293
Q

Systemic indications for triamcinolone

A

Dermatoses
Asthma
exacerbations of MS
Arthritis

294
Q

Adverse effects of triamcinolone

A
Elevated IOP (decreased TM outflow) 
Endophthalmitis 
Depigmentation of the eyelid skin in darker skinned patients (permanent)
295
Q

Fluticasone

A
Steroid
Intrnasal corticosteroid (topical) indicated for treatment of allergic rhinitis
296
Q

Adverse effects of fluticasone

A

Cataract, increased IOP, conjunctivitis, and dry eye disease, CSCR

297
Q

Topical NSAIDs

A
Diclofenac 
Nepfenac 
Bromfenac 
Ketorolac
Flurbiprofen
298
Q

Oral NSAIDs

A

Aspirin
Indomethacin/ibuprofen/naproxen/naproxen sodium/piroxicam
Celecoxib

299
Q

What is the only irreversible COX 1 and 2 inhibitor

A

Aspirin

300
Q

MOA of apirin

A

Salicylate that inhibits the synthesis of PGs and thromboxanes by acting as an irreversible COX 1 and 2 inhibitor

301
Q

Clinical indications of Aspirin

A

Antipyresis (fever)
Anti-inflammtory effects
Analgesia
Reduces the risk of recurrent heart attacks in pts with heart disease

302
Q

Adverse effects of aspirin

A
GI effects (decreased COX1=increased acid)
Antiplatelet effects=bleeding complications in the eye (retinal and subconjunctival heme)
Reye’s syndrome in kids
303
Q

What are the reversible COX 1 and 2 inhibitors

A
Indomethacin 
Ibuprofen
Naproxen
Sodium naproxen
Piroxicam
304
Q
Clinical indications for Indomethacin 
Ibuprofen
Naproxen
Sodium naproxen
Piroxicam
A

Scleritis and episcleritis

305
Q
Indomethacin 
Ibuprofen
Naproxen
Sodium naproxen
Piroxicam 
Contraindicated in
A

Patients with heart disease

306
Q
Adverse effects of Indomethacin 
Ibuprofen
Naproxen
Sodium naproxen
Piroxicam
A

All increase the risk of bleeding complications in the eye
Risk if GI bleed
Fatal MI/stroke

307
Q

Which NSAIDs are safe for pateitns with cardiovascular disease

A

Aspirin ONLY

Indomethacin 
Ibuprofen
Naproxen
Sodium naproxen
Piroxicam 
ALL contraindicated in heart disease patients. Can increased BP
308
Q

Which NSAIDs can cause Reye’s syndrome

A

Aspirin ONLY

Indomethacin 
Ibuprofen
Naproxen
Sodium naproxen
Piroxicam 
DO NOT
309
Q

Which NSAID can be safely RXed in kids 6m and older

A

Ibuprofen

310
Q

What should NSAIDs be taken with in order to decrease effects on GI

A

Food

311
Q

Pigmentary retinopathy drugs

A

Chlorpazamine
Thioridazine
Indomethacin

312
Q

Ocular side effects of indomethacin

A

Increases the risk of bleeding in the eye
Whorl K
Retinary pigmentary changes (mottling)

313
Q

Misoprostol

A

Synthetic PG E1 that is chemically similar to PGE-2, the PG that protests the stomach lining. It is used for prevention and treatment of NSAID induced stomach ulcers. It’s main adverse effect is that is can cause miscarriages and premature labor

314
Q

MOA of celecoxib

A

Selective COX2 inhibitor

Spares the COX1 pathway and protects the stomach

315
Q

Adverse effects of celecoxib

A

SJS

316
Q

Contraindications of systemic NSAIDs

A

Patients with a history of an allergic reaction to other NSAIDs or to aspirin

317
Q

Parasympathetic acts on ___receptros

A

Cholinergic (muscarinic) receptors that target organs; promotes bronchoconstriction, miosis, rest and digest, and increase in secretions (SLUD: salivation, lacrimation, urination, defacation)

318
Q

Sympathetic acts on _____ receptors

A

Adrenergic (a and b) receptors on target organs; promotes bronchidilation, mydriasis, a decrease in secretions and fight or flight

319
Q

Direct cholinergic agonist (ocular)

A

Pilo

320
Q

Indirect cholinergic agonists (ocular)

A

Edrophonium
Echothiophate
Pyridostigmine
Neostigmine

ACHase blockers

321
Q

Donepizil

A

CNS ACHase inhibitor that is indicated for the treatment of Alzheimer’s (indirect cholinergic agonsit)

322
Q

Cholinergic antagonists

A
  • First generation H1 blockers: diphenhydramine, brompheniramine, chlorpheniramine, promethazine
  • antipsychotics: chlorpromazine, thioridazine
  • antidepressants: TCAs (amitriptyline, imipramine), MAOI (phenylzine)
  • muscle relaxant: cylcobenzaprine
  • anti-anxiety: diazepam
  • ipratropium
323
Q

Systemic A2 agonist

A

Clonidine

324
Q

Systemic B1/B2 agonist

A

Isoproteronol

325
Q

Systemic B2 agonist

A
Salmeterol
Albuterol
Levabuterol
Terbutaline 
Metaproterenol
326
Q

systemic B agonists and IOP

A

Increase aqueous humor production. Salmeterol is the only long acting B2 agonists and the only drug that does not carry a specific warning regarding use in patietns with glaucoma

327
Q

What is the only long acting B2 agonist that does not have a specific warning regarding use in glaucoma patients

A

Salmeterol

328
Q

Nonspecific alpha and beta agonist

A

Pseudoephedrine

329
Q

Dopamine agonsits

A

Bromocripitine
Methylphenidate
Dextroamphetamine

Increase adrenergic acitivtiy, do not give to narrow angle patients

330
Q

Parkinson’s drugs

A

Amantadine

Dopamine agonist
Adrenergic agonist, do not give to narrow angle patients

331
Q

Alpha 1 blockers

A

Prazosin
Tamsulosin
Terazosin

BPH drugs

332
Q

B-blockers

A

Propanolol
Labetolol
Atenolol
Metoprolol

333
Q

Nonselective B agonsits

A

Labetolol

Propranolol

334
Q

B1 specific antagonists

A

Atenolol, metoprolol

335
Q

Which BBlockers would have least affect on IOP

A

BEAM

  • betaxolol
  • atenolol
  • metoprolol

B1 selective

336
Q

Cold medication is targeted at

A

Ameliorating symptoms

337
Q

Pseudoephedrine

A

Cold medicine

MOA: nonspecific alpha and b agonist for nasal decongestion

338
Q

Adverse effects of pseudoephedrine

A

Tachycardia (b1), bronchodilator (b2), nervousness

Ocular: diplopia, and blurred vision, caution with increased IOP (B2)

339
Q

H1 receptors

A

In the smooth muscle of the bronchi, blood vessels, and intestines. Activating of H1 causes itching, vasodilation, increased vascular permeability, and contraction of smooth muscel in the GI tract

340
Q

H2 receptors

A

Located in the gastric parietal cells, the heart, pulmonary blood vessels, and cells of the immune system. Activation of H2 receptors causes itching, vasodilation, mucous discharge, and gastric secretions

341
Q

Which H receptor is found in the eye

A

Mostly H1

342
Q

Histamine release in the eye

A

H1 receptors

Itching, tearing, chemosis, dilation of conjunctival blood vessels and papillary reaction.

343
Q

First generation antihistamines

A

Diphenhydramine
Chlorpheniramine
Brompheniramine
Promethazine

344
Q

Which generation of anti histamine drugs causes anticholinergic type reactions in the eye and what are the reactions

A

First generation

Increased IOP, dry eye, mydriasis

345
Q

MOA of first generation H1 blockers

A

Block the interaction between histamine and H1 receptors

346
Q

Clinical indications of first generation H1 blockers

A

Allergic skin reactions

347
Q

Adverse reactions of first generstion H1 blockers

A

Sedation due to CNS penetration (BBB). All antihistamines especially first generation drugs, have anticholinergic effects including mydriasis, increased IOP, dry eye, dry mouth, and tachycardia

348
Q

What’s special about promethazine

A

First generation H1 blocker
Chemical structure similar to antipsychotic medications (phenothiazines)
Ocular side effects specific to this drug result from the phenothiazine structure and include corneal epithelial Keratopathy, corneal endothelial pigmentation, lenticular changes, and pigmentary retinopathy

349
Q

Second generation H1 blockers

A

Loratadine
Fexofenadine
Cetirizine

350
Q

Clinical indications of second generation H1 blockers

A

Allergic rhinitis, and chronic urticaria (hives)

351
Q

Adverse effects of secondary generation H1 blockers

A

Less CNS penetration and less CNS side effects. Cetirizine can cause abnormal EOM contractions (oculogyric crisis)

352
Q

Majority of peptic ulcer disease is caused by

A

Helicobacter pylori and/or NSAID use

353
Q

H2 blockers

A

Cimetidine
Ranitidine
Famotidine

354
Q

MOA of H2 blockers

A

Prevent histamine stimulation of gastric acid (HCl)secretion by blocking H2 receptors on gastric parietal cells

355
Q

Clinical indications of H2 blockers

A

Healing and preventing stomach ulcers and acid reflux

356
Q

Adverse effects of H2 blockers

A

Diarrhea; cimetidine has numerous drug interactions and can cause gynecomastia and loss of libido

357
Q

Proton pump inhibitors

A

Omeprazole

Esomeprazole

358
Q

MOA of PPIs

A

Inhibit H+/K+ ATPase (proton) pumps

359
Q

Clinical indications of PPIs

A

1st line therapy for peptic ulcer disease and GERD

360
Q

Sucralfate

A

Gastric lining protector

MOA: forms a paste like substance by binding to positively charged proteins and damaged ulcer tissue in the stomach.

361
Q

Adverse effects of sucralfate

A

Interfere with absorption of other oral medications, dont use within 2 hours of otherdrugs

362
Q

Bronchodilators stimulate ____ nervous system

A

Sympathetic

363
Q

Long acting B2 agonists

A

Salmeterol

364
Q

uses of salmeterol

A

Only long lasting B2 agonist we need to know

Maintenance therapy for COPD and asthma but NOT as a rescue inhaler

365
Q

Short acting B2 agonsits

A

Albuterol, levalbuterol, terbutaline
Metaproterenol
Isoproterenol

366
Q

Clinical indications of albuterol, levalbuterol, and terbutaline

A

Short acting B2 agonsits

Rescue inhaler for patients with asthma and COPD

367
Q

Clinical indications of metaproterenol

A

no longer recommended for asthma due to excessive cardiovascular effects from B1 stimulation

368
Q

Clinical indications of isoproterenol

A

No longer RXed for the treatment of asthma. Nonspecific B agonsits primarily indicated for the treatment of arrhythmias through B1 stimulation

369
Q

Adverse effects of short acting B2 agonsits

A

They have greater B2 than B1 activity, but the effects come from B1 activity on the heart
-tachycardia, heart palpitations, nervousness, tremors, nausea

370
Q

Short acting B2 agonsits and IOP

A

All have warnings about their use in glaucoma patients due to the risk of IOP increase

371
Q

Muscarinic antagonist for asthma

A

Ipratropium

  • blocks muscarinic receptors
  • inhibits bronchoconstricion
  • caution in narrow angle glaucoma due to pupil dilation
372
Q

Miscellaneous respiratory agents

A

Montelukast and Zafirlukast
Theophylline
Acetylcysteine

373
Q

Montelukast and Zafirlukast

A

Leukotriene receptor antagonists
Treat asthma and bronchoconstriction
Montelukast also used for allergic rhinitis

374
Q

Theophylline

A

Inhibits PDEs, leading to increase cAMP and increased release of epi.
Narrow TI
BBlockers, including topical ophthalmic agents such as timolol, have the potential to mitigate the bronchodilatory effects of theophylline

375
Q

Acetylcysteine

A

Mucolytic agent that breaks disulfide bonds in proteins of mucus in order to reduce its viscosity. The topical opthalmic form can be RXed as QID for filamentary keratitis, dry eye syndrome, and corneal burns

376
Q

Immunosuppressant medications

A

Methotrexate
Cyclosporine
Azathioprine

377
Q

Methotrexate MOA

A

Inhibits dihydrofolate reductase (like TMP and pyromethamine)which inhibits DNA synthesis
MOA in RA involves immunosuppressant and anti inflammatory mechanisms

378
Q

Adverse effects of methotrexate

A

Hepatotoxicty and myelosuppreison, increases the risk of opportunistic infections and lymphomas
Aplastic anemia
Optic neuritis

379
Q

Cyclosporine MOA

A

Prevents rejection of organ transplants by inhibiting the release of and production of interluelin-2 (IL-2), a chemical mediator responsible for T lymphocyte activation

380
Q

Restasis

A

RXed BID

Inhibits T cell activation by inhibiting production if IL-2

381
Q

Adverse effects of cyclosporine

A

Opportunistic infection

382
Q

Most common cause of reversible posteiror leukoencephalopathy syndrome (RPLS)

A

Oral cyclosporine
-HA, altered consciousness, seizures, and visual disturbances. DX based on MRI findings. Discontinue if this is diagnosed

383
Q

Azathioprine

A

Purine analong that inserts into DNA and RNA and stops replication
Used for RA and to prevent rejection of kidney transplant, ocular MG

384
Q

Tamoxifen

A
  • a competitive partial agonsit inhibitor of estradiol, which inhibits estrogen effects at the breast
  • treatment for breast cancer
385
Q

Adverse effects of tamoxifen

A

-crystalline retinopathy, whorl Keratopathy, thromboembolism (BRVO, CRVO)

386
Q

Cessation of tamoxifen and whorl K and crystalline maculopathy

A

Whorl K is generally reversible but maculoapthy can affect vision and is not always reversible

387
Q

Analgesics

A

OTC agents such as NSAIDS and acetaminophen. RX includes some NSAIDs, muscle relaxants, and tramadol

388
Q

Non opiate analgesics

A

Acetaminophen
Cyclobenzaprine
Tramadol

389
Q

MOA of acetaminophen

A

Not completely understood

DOES NOT HAVE ANTI INFLAMMATORY PROPERTIES

390
Q

What is the max amount of acetaminophen you can take in a day

A

4000mg

391
Q

Who can take acetaminophen

A

Anyone

Kids and pregs too

392
Q

Adverse effect of acetaminophen

A

Hepatotoxicity

TylenoL=liver metabolism

393
Q

Cyclobenzaprine MOA

A

Muscle relaxant

Inhibit alpha and gamma motor neurons

394
Q

Clinical indications for cyclobenzaprine

A

Muscle spasms

395
Q

Adverse effects of cyclobenzaprine

A

Drowsiness, loss of coordination, and anticholinergic effects; caution in pateitns with narrow angle glaucoma
Dry eye, mydriasis, increased IOP

396
Q

MOA of tramadol

A

Acts on Mu opiate receptors (although not considered a true opiate)
Inhibits serotonin and NE uptake within ascending pain pathways

397
Q

Adverse effects of tramadol

A

Dry mouth
Sedation
Dizziness
Nausea

398
Q

Opiate analgesics

A

Meperidine, oxycodone

399
Q

MOA of meperidine/oxycodone

A

Agonists of the Mu, Kappa, and Delta opiate receptors

400
Q

Adverse effects of opiate analgesics

A

Pin point miosis

Mydriasis with withdrawal

401
Q

Naloxone

A

Opioid antagonsit that is used to reverse the effects of opiates

402
Q

Migraine therapy

A

Sumatriptan

403
Q

MOA of sumatriptan

A

5-HT1B and 1D (serotonin subtype 1B and 1D) receptor agonists.
Vasoconstriction of cranial arteries
Reduces inflammation in the CNS

404
Q

Adverse effects of sumatriptan

A

NAION

Retinal artery occlusions and retinal venous thrombosis

405
Q

ANTIpsychotics

A

PHenothiazines

  • chlorpromazine
  • thioridazine
406
Q

MOA of antipsychotics (chlorpromazine, thioridazine)

A

Dopamine receptor antagonists

407
Q

Adverse effects of antipsychotics (chlorpromazine, thioridazine)

A

High doses can result in Parkinson’s like effects. Ocular side effects include

  • pigmentation effects: pigment on the corneal endothelium, anterior stellate catracts, and hyperpigmentation of the RPE (promethazine also, 1st gen H1 blocker)
  • anticholinergic effects: dry eye, mydriasis, and increased IOP
  • oculogyric crisis (also Zyrtec)
408
Q

Parkinson’s disease

A
Dopamine deficiency 
TRAP
-tremor at rest 
-rigidity 
-akinesia (hard time initiating movement)
-postural reflexes lost
409
Q

Antiparkinsons drugs

A

Amantadine

Bromocriptine

410
Q

Amantadine

A

Parkinson’s

-potentials dopamine effects by blocking its reuptake or augmenting it’s release in the brain

411
Q

Bromocriptine

A

Parkinson’s
-a dopamine agonsit that is most commonly used to treat prolactin secreting pituitary adenomas. But can also be used to treat parkinsons

412
Q

Bromocriptine can treat what conditions

A

Parkinson’s

Pituitary adenoma

413
Q

ADHD meds

A

Methylphenidate, dextroamphetamine

414
Q

MOA of methylphenidate and dextroamphetamine

A

Increase dopamine release

415
Q

Clinical indications for methylphenidate and dextroamphetamine

A

ADHD, narcolepsy, and depression

416
Q

Adverse effects of methylphenidate and dextroamphetamine

A

Mydriasis and dry eyes

Caution in acute angle glaucoma

417
Q

All medications that act as dopamine agonists in the CNS (ADHD and parkinsons drugs) and narrow angle glaucoma

A

Have adrenergic agonist side effects any may cause mydriasis that can precipitate angle closure in patients with narrow angles. For this reason, narrow angle glaucoma is a contraindication for these medications

418
Q

Donepizil

A
  • CNS ACHase inhibitor (like MG) that is RXed for alzheimers
  • will cause lower IOP due to muscarinic effects. Sudden discontinuation of the drug may lead to elevations in IOP
419
Q

What are the 4 main classes of antidepressants and what do they all ultimately do

A

TCAs
MAOIs
SNRI
SSRI

Increase serotonin
TCA, SNRI, and MAOIs also increase NE

420
Q

What are the side effects of all antidepressant drugs

A

Sedation, weight gain, and sexual dysfunction

421
Q

The primary method of treating depression involves

A

Increased serotonin levels in the CNS. Serotonin selective reuptake inhibitor are the first line treatment for depression

422
Q

What is the first lien treatment for depression

A

SSRIs

423
Q

Which antidepressants increase dopamine

A

NONE

424
Q

what are the SSRIs

A

Fluoxetine

Escitalopram

425
Q

MOA of SSRIs

A

Fluoxetine and escitalopram

-inhibits serotonin reuptake

426
Q

Adverse effects of SSRIs

A

Fluoxetine and escitalopram

  • fewer side effects compared to other anti depressants. They can cause mydriasis and should be used with caution in narrow angle glaucoma patients
  • serotonin syndrome may occur if Rxed with TCAs and especially MAOIs
427
Q

Serotonin syndrome

A

Due to excess serotonin activity in the CNS and is marked by a change in mental status (anxiety, confusion), autonomic hyperactivity (increased BP, pulse, temp), and neuromuscular problems (tremor, hyperreflexia)

428
Q

What are the SNRIs

A

Venlafaxine

Duloxetine

429
Q

MOA of SNRIs

A

Venlafaxine and duloxetine

Inhibits serotonin and NE reuptake

430
Q

Bupropion

A

Is an NDRI (inhibits the reuptake of dopamine and NE) and is RXed to treat depression and smoking cessation

431
Q

What are the TCAs

A

Amitriptyline

Imipramine

432
Q

MOA of TCAs

A

Amitriptyline and imipramine

Inhibitions NE and serotonin reuptake

433
Q

Adverse affected of TCAs

A

Amitriptyline and imipramine
Dry eye, increased IOP, blurred vision, and mydriasis. A TCA overdose is LIFE threatening. DO NOT RX FOR SUICIDAL PATIENTS

434
Q

What antidepressant should you never RX for a suicidal patient

A

TCAs, fatal overdose

435
Q

What is the MAOI

A

Phenelzine

436
Q

MOA of MAOI

A

Phenelzine

Inhibits MAO, the enzyme responsible for breaking down NE and serotonin

437
Q

Adverse effects of MAOI

A

Phenelzine
Glaucoma and nystagmus are reported ocular affects, caution in narrow angles
Foods with tyramine (wine, cheese, dried meats) cause lethal hypertensive crisis

438
Q

What drugs can exacerbate systemic effects of topical ophthalmic phenylephrine and other adrenergic agonists

A

MAOIs and TCAs

439
Q

ANTIanxiety medication

A

Diazepam

440
Q

MOA of diazepam

A

ANTIanxiety

Opens chloride channels by binding to GABA receptors

441
Q

GABA and anxiety

A

Increased GABA=decreased sympathetic activity

**increased sympathetic paradoxical effect in extreme populations

442
Q

Adverse effects of diazepam

A

Antianxiety drug

  • sedation, depression, confusion, bradycardia, and dyspnea; can be fatal if combined with alcohol or drugs. Occasionally cause mydriasis and nystagmus. Caution in narrow angle glaucoma
  • increased sympathetic paradoxical effect in extreme populations
443
Q

What are the anticonvulsants

A

Phenytoin
Phenobarbital
Topiramate

444
Q

Phenytoin MOA

A

Anticonvulsant

-acts on multiple NTs including NE, ACH, and GABA

445
Q

Adverse effects of phenytoin

A

Nystagmus, diplopia, EOM palsies, ataxia, and gingival hypoplasia

Funny-toin=funny looking eyes and gums

446
Q

Phenobarbital

A

Anticonvulsant

  • reduces glutamatergic excitatory transmission by blocking AMPA receptors
  • mydriasis, increased IOP, and cycloplegia
447
Q

Topiramate

A

Anticonvulsant

-MOA: multiple CNS effects that prevent seizures

448
Q

Adverse effects of topiramate

A

Blurred vision, diplopia, nystagmus, myopic shift (huge shift, not permanent)

May cause choroidal swelling, which moves the uvea forward and results in acute secondary angle closure glaucoma

449
Q

MOA of insulin

A

Binds to cell surface receptors, leading to activation of tyrosine kinase receptors and a phosphorylation cascade; it promotes the formation and storage of glycogen, proteins, and triglycerides within the liver, fat, and muscle tissue. The primary signal for insulin release is the presence of glucose in the blood

450
Q

Oral agents for diabetes

A

Biguanides: metformin
Sulfonylureas: glipizide, glyburide, chlorpropamide
Thiazolidinediones: pioglitazone, rosiglitazone

451
Q

MOA of Biguanides

A

Metformin
-decreases gluconeogensis in the liver and increases glucose uptake; it is usually the first oral medication RXed for DM because it DOES NOT CAUSE HYPOGLYCEMIA

452
Q

Which diabetes medication does not cause hypoglycemia

A

Metformin

453
Q

Adverse effects of metformin

A

Diarrhea, if patient has renal insufficiency or hepatic impairment they are greater risk of lactic acidosis

454
Q

MOA of sulfonylureas

A

Glipizide, glyburide, chlorpropamide
-increase the secretion of insulin by beta cells in the pancreases, decrease glucagon release, and increase the sensitivity of cells to insulin

455
Q

Adverse effects of sulfonyureas

A

Glipizide, glyburide, chlorpropamide

  • hypoglycemia
  • caution in those with sulfa allergies
456
Q

Beta blockers and DM

A

Increase the risk of hypoglycemia if taken with sulfonyureas. They may also mask the sympathetic response to hypoglycemia caused by any diabetic medication, as they prevent the usually symptoms associated with hypoglycemia such as tachycardia and tremors. The risk is lower, but still exists, with ocular beta blockers

457
Q

MOA of thiazolidinediones

A

Pioglitazone, rosiglitazone

  • Active peroxisome proliferator-activated receptor gamma
  • combat insulin resistance
458
Q

Adverse effects of thiazolidinediones

A

Pioglitazone and rosiglitazone

-new or worsening macular edema

459
Q

What does TSH do

A

Released from the anterior pituitary gland and binds to TSH receptors on the thyroid glandin the neck, stimulating the production of thyroid hormones (primarily T4). Hashimotots is an AI condition that is the most common cause of primary hypothyroidism, and requires a replacement of T4

460
Q

Levothyroxine

A

Synthetic T4 hormone
Can cause pseudotumor cerebri in kids
Used for hypothyroidism (hashimotos)

461
Q

Adverse ocular effects of estrogens

A
Dry eyes 
ON disease (optic neuritis, pseudotumor cerebri, papilledema)
Venous clotting (CRVO/BRVO)
462
Q

What is the class of drugs used to treat erectile dysfunction

A

PDE-5 inhibitors

463
Q

What are the PDE-5 inhibitors

A

Sildenafil and vardenafil

464
Q

MOA of PDE-5 inhibitors

A

Sildenafil and Vardenafil
-cGMP, which is broken down by PDE-5, relaxes vascular smooth muscle in the penis during an erection. These drugs inhibit PDE_5, thereby increased blood flow to the penis by prolonging the effects of cGMP=vasodilation

465
Q

Systemivside effects of PDE-6 inhibitors

A

Flushing and HA are common; priapism may occur and requires immediate medical attention

466
Q

Ocular adverse affects of PDE-5 inhibitors

A

Cyanopsia, blurred vision, and photosensitivity

-due to minor PDE-6 inhibition, which is found in rods and cones

467
Q

Link between ED meds and NAION

A

There is an increased incidence of NAION in men taking ED meds, but they already have reduced blood flow anyways, so not sure if its from the drug or their underlying problem

468
Q

BPH drugs

A

Alpha-1 blockers

-prazosin, terazosin, tamsulosin

469
Q

MOA of BPH drugs (zosins)

A

A1 blocker to relax smooth muscle in the bladder neck and prostate, thereby decreasing urinary outflow obstruction in men with BPH

470
Q

Adverse effects of BPH meds (zosins)

A

Interoperative floppy eyelid syndrome from tamsulosin (flomax)

471
Q

What are the classes of antihypertensive medications

A
ACE inhibitors
Angiotensin II receptor agonists (ARBS)
BBlockers 
Ca Channel blockers 
Diuretics 
Clonidine 
Hydralazine
472
Q

ACE inhibitor drugs

A

Lisinopril
Benazepril
Enalapril
Captopril

473
Q

MOA of ACE inhibitors

A
  1. Prevent the formation of angiotensin II by inhibiting angiotensin converting enzyme (ACE)
  2. Block the metabolism of bradykinins, resulting in vasodilation
474
Q

Adverse effects of ACE inhibitors

A

Cough

475
Q

Angiotensin II receptor agonist (ARBs)

A

Losartan

476
Q

MOA of losartan

A

Reduces BP by inhibiting angiotensin II directed contraction of vascular smooth muscle and stimulation of aldosterone secretion

477
Q

What’s better about ARBs than ACE inhibitors

A

No cough

478
Q

What are the BBlockers used for HTN

A

Propranolol, labetalol

metoprolol, atenolol

479
Q

Propranolol and labetalol MOA

A

Non selective beta 1 and beta 2 receptor antagonists; they also block the release of renin from the kidneys

480
Q

MOA of metoprolol and atenolol

A

Selective B1 receptors agonists
Less IOP effect here

“MA on the heart”

481
Q

CNS effects of BBlockers

A

Disorientation, depression, fatigue

482
Q

Cardiovascular effects of BBlockers

A

Bradycardia, arrhythmias, syncope

483
Q

Pulmonary affects of BBlockers

A

Dyspnea, wheezing, bronchospams

484
Q

GI effects of BBlockers

A

Nausea, vomiting, diarrhea, abdominal pain

485
Q

Reproductive effects of BBclokers

A

ED

486
Q

What are the calcium channel blockers

A

Nifedipine
Verapamil
Diltiazem

487
Q

MOA of Ca channel blockers for HTN

A

Verapamil, diltiazem, nifedipine

-block L type Ca channels, resulting in a marked decrease in intracellular free Ca2+

488
Q

Ca and smooth muscle

A

Decreased Ca and decreased smooth muscle contraction

489
Q

Cardio affects and Ca channel blockers

A

Verapamil and diltiazem more commonly have direct cardio effects

“VD-dipines”
Heart——>BV

490
Q

Ca Channel blockers and glaucoma

A

Some studies have suggested prescribing Ca channel blockers for the treatment of low tension glaucoma, as these drugs may increase perfusion to the optic nerve, how ever, this is not considered standard of care

491
Q

What part of the nephron do CAIs work

A

PCT

492
Q

What part of the nephron do HCTZ/CTZ work

A

DCT

493
Q

What part of the nephron does furosemide work in

A

Ascending loop of henle

494
Q

What part of the nephron does triamterene and spironolactone work

A

Collecting duct

495
Q

What is reabsorbed in the PCT

A

Bicarbonate, Na, H20

496
Q

What is reabsorbed in the descending loop of Henle

A

Last place H20 is reabsorbed without hormone help

497
Q

What reabsorbed in the DCT

A

Na, chloride

498
Q

What is reabsorbed in the ascending loop of henle

A

Na, Cl, K

499
Q

What is reabsorbed in the collecting duct

A

H20 with the help of aldosterone

500
Q

What part of the nephron does mannitol work

A

Works across the entire nephron

501
Q

What diuretic can cause hypokalemia

A

Furosemide

502
Q

Diuretics can treat

A

CHF, HTN, kidney disease

503
Q

What is the loop diuretic

A

Furosemide

504
Q

MOA of furosemide

A

Inhibits Na/2Cl-/K+ co-transporter in the thick ascending loop of henle. It also increased CA2+ secretion

505
Q

Adverse effects of furosemide

A

Hypokalmiea
Nephrotixicity
Ototoxicity

506
Q

MOA of the thiazides (HCTZ/CZ)

A

Inhibits NaCl reabsorption and decreased CA2+ excretion at the early DCT

507
Q

Adverse effects of thiazides

A

Acute transient myopia and acute angle closure glaucoma

508
Q

What are the potassium sparing diuretics

A

Spironolactone and triamterene

509
Q

Aldosterone stimulation

A

Aldosterone release is stimulated in response to decreased blood volume (angiotensin II) and increased K+ concentration. It increases Na+ reabsorption and K+ secretion in the collecting duct by opening epithelial sodium channels (ENaCs) and by activating the Na+/K+ ATPase pumps. The net effect is increased Na+ and Cl- reabsorption, and increased K+ and H+ secretion

510
Q

What the weak diuretics

A

Sprinolactone

Triameteren

511
Q

MOA of spironolactone

A

Blocks the action of aldosterone at the late DCT and collecting duct

512
Q

Adverse effects of spinrolactone

A

Hyperkalemia, gynecomastia, and antiandrogen effects

513
Q

MOA of triamterene

A

Directly blocks ENaCs in the late DCT and the late collecting ducts
Does not have antiandrogen effects like spironolactone

514
Q

Mannitol

A

Osmotic diuretics

-incapable of being absorbed

515
Q

What diuretics can cause dry eye

A

All of them

516
Q

Clonidine MOA

A

CNS a2 agonist that decreases sympathetic outflow and increases parasympathetic tone, resulting in decreased vascular resistance and decreased heart rate

517
Q

Adverse reaction of clonidine

A

Dry mouth, sedation, impotence, and severe rebound HTN

518
Q

What other drug is clonidine related to

A

Apraclonidine

It could decreased IOP

519
Q

MOA of hydralazine

A

Increases cGMP, resulting in smooth muscle relaxation; it also decreases afterload as it vasodilates arterioles more than veins

520
Q

Adverse effects of hydralazine

A

Compensatory tachycardia, fluid retention, and lupus like syndrome, conjunctivitis and increased lacrimation have also been reported

521
Q

Digoxin MOA

A

Inhibits the Na+/K+/ ATPase enzyme, which normally pumps Na+ out and K+ in; this leads to increased intracellular Ca2+

522
Q

Adverse effects of digoxin

A

Retrobulbar optic neuritis, BY color defects, and entropic phenomenon (snowy vision), blocks NAK channels in the PR

523
Q

Drugs to treat CHF

A

Digoxin
BBlockers
ACE inhibitors
Diuretics

524
Q

Amiodarone

A

Antiarrythmic drug

-primarily blocks K+ channels, but also blocks some Na+ and Ca2+ channels as well

525
Q

Clinical indications of amiodarone

A

Arrhythmias

526
Q

Adverse effects of amiodarone

A
  1. NAION
  2. Whorl K
  3. Anteiror supcasular lens deposits
527
Q

Anticoagulants

A

Warfarin
Clipidogrel
Dipyridamole

528
Q

Warfarin

A

Vitamin K antagonist

Interferes with clotting factors 2, 7, 9, 10

529
Q

What drug is contraindicated in patietns taking anticoagualtans

A

Cephs

530
Q

Adverse effects of warfarin

A

Should be stopped 96-115 hours prior to cataract surgery

Contraindicated in pregnancy and may also result in skin necrosis

531
Q

How can warfarins effects be reversed

A

Vit K

532
Q

Clopidogrel

A

Inhibits ADP receptor on platelet cell membranes that is needed for platelet aggregation and clot formation

533
Q

Adverse effects of clopidogrel

A

Irreversible effect on platelets (like aspirin)

534
Q

Dipyridamole

A

Inhibitions adenosine deaminase and PDE, resulting in the accumulation of cGMP and adenosine, which inhibits platelet aggregation and may cause vasodilation

535
Q

Adverse effect os dupyridamole

A

Aggrenox=this + aspirin

Risk of bleeding

536
Q

Meds that can cause bleeding problems in the eye

A
Warfarin
Clopidogrel
Dipyridamole 
NSAIDs
Aspirin
537
Q

Antihyperlipidemic agents

A
  • HMG CoA inhibitors
  • Fibric acid
  • bile acid binding resin
538
Q

Lovastatin, simvastatin, atorvastatin

A

HMG CoA reductase inihibitors
-Rate limiting step in cholesterol synthesis in liver
Lower LDL and trigs, and increase HDL

539
Q

Fibric acid for HDL

A

Gemfibrozil

540
Q

Gemfibrozil MOA

A

Binds to PPAR-a and increases the activity of lipoprotein lipase, which breaks down VLDL.
Lowers LDL and trigs (does not increase HDL)

541
Q

Cholestyramine

A

Bile acid binding resin

  • prevents bile acid reabsoprtion for HLD control
  • lowers LDL levels (does not increase HDL or lower trigs)
542
Q

MOA of isotretinoin

A

Reduces the size and degree of oil production from sebaceous glands
-affects meibomian glands

543
Q

Adverse effects of isotretinoin

A

Blepharoconjunctivitis
Dry eyes
pseudotumor cerebri

Also teratogenic and contraindicated in pregnancy

544
Q

Metronidazole

A

NOT FOR USE ON EYES
-topical agent RXed for acne rosacea, disrupts DNA and inhibits nuclei acid synthesis; also has anti-inflammtory properties

545
Q

Alcohol withdrawal

A

Can be life threatening

546
Q

Alcohol and vitamin deficiency

A

Chronic alcoholics can lead to thiamine deficiency (B1), resulting in an acute presentation of Wernickes encephalopathy, which is characterized by ophthalmoplegia, confusion, and ataxia. Untreated thiamine deficiency can lead to irreversible korsakoff syndrome, which is characterized by amnesia and confabulation

Give them B1 and this goes away (except korsakoff)

547
Q

Opioid withdrawal

A

Not life threatening

Pin point pupils when they are on it, mydriasis when they are going through withdrawal

548
Q

Cocaine addiction

A

Mydriasis

Withdrawal is not life threatening