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p2 year > acne, drug induced derm, atopic derm, glaucoma > Flashcards

acne, drug induced derm, atopic derm, glaucoma Flashcards

1
Q

acne formation

A
  • cells produce too much keratin, dead cells build up; OR; makeup/external factors
  • blockage of follicle shaft
  • sebum (oil) builds up behind blockage
  • bacteria grows
  • infection, WBC move to area
  • inflammation –> acne!
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2
Q

what are the four mechanisms of acne we are trying to prevent with therapy?

A
  • follicular hyperproliferation/hyperkeratinization
  • inc sebum production (androgens)
  • inflammation
  • bacteria growth
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3
Q

what is the oil of hair follicles called

A

sebum

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4
Q

what bacteria grows in acne?

A

Cutibacterium acnes (Propionibacterium acnes)
aka C. acnes

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5
Q

what is acne vulgaris?

A

common acne
- lesions most common on face, also back, chest, arms, neck
- onset following puberty, could be younger
- males more affected

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6
Q

what factors inc acne vulgaris?

A
  • emotional stress –> CRH
  • repetitive stress –> harsh soaps
  • occlusions and pressure –> clothing, makeup
  • heat, humidity –> topical acne, more oil
  • occupational acne –> fryer grease, …
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7
Q

what is the pH of healthy skin? how does this impact drugs?

A

4.7-5.7

we want soaps/cleansers around this pH, if not could trap more and worsen acne!!

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8
Q

does food affect acne?

A

very individual –> what impacts one person may not impact another
- chocolate
- fatty food
- milk
- soda
- high sugar foods

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9
Q

acne course

A

stages:
1. micrcomedone – not visible, pores with sebum and dead skin
2. whitehead (closed comedone)
2. blackhead (open comedone)
3. papules/pustules – raised
4. cysts
5. nodules (pseudocysts) – infection
6. pustule/pimple – lots of pus
7. scarring

  • worse in fall and winter
  • could last weeks to months if untreated
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10
Q

drugs that cause acneiform lesison

A
  • glucocorticoids
  • oral contraceptives
  • androgens
  • lithium
  • phenytoin
  • valproic acid
  • cyclosporine
  • isoniazid
  • azathioprine
  • disulfiram
  • phentermine
  • iodides
  • bromides
  • danazol
  • high dose vitamin B
  • high dose vitamin D
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11
Q

goals of acne treatment

A
  • remove keratin plug
  • dec sebum production
  • dec bacterial inflammation
  • reduce scarring

**consider psychological aspects on acne always!!

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12
Q

acne treatment self-care

A
  • gentle cleanser (CeraVe) twice a day
  • don’t pick
  • stop offending agents (food, harsh cleaners/makeup)
  • avoid facial scrubs
  • water-based lotions/cosmetics
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13
Q

CI to acne self care

A
  • pregnant, IBD/colitis
  • self care fail after 3 months
  • moderate-severe acne
  • comedogenic drugs (drug causing)
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14
Q

what type of medication (self-care, OTC, Rx) should be used based on skin type/location?

A

dry: lotion, cream
oily: gels, foams –> allow evaporation
hairy: foam
large area: solutions (are drying tho), pledgets (round applicator)

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15
Q

what do all acne treatments cause?

A

drying!!!

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16
Q

mild acne

A
  • few-several (<10) papules/pustules
  • no nodules
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17
Q

moderate acne

A
  • several-many (10-40) papules/pustules with comedomes
  • few-several nodules
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18
Q

severe acne

A
  • numerous-extensive (>40) papules/pustules
  • many nodules
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19
Q

what patho does isotretinoin (oral retinoid) target?

A
  • follicular hyperproliferation
  • increased sebum production
  • inflammation

NOT
- bacterial proliferation
- androgen receptor inhibition

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20
Q

what patho does benzoyl peroxide target?

A
  • bacterial proliferation (C. acnes) –> bc oxidizing, therefore kills
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21
Q

what treatments target follicular hyperproliferation?

A
  • oral retinoids
  • topical retinoids
  • azelaic acid
  • salicylic acid
  • hormonal therapy
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22
Q

what treatments target increased sebum production

A
  • oral retinoids
  • hormonal therapy
  • clascoterone cream
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23
Q

what treatments target bacterial (C. acnes) proliferation?

A
  • benzoyl peroxide
  • antibiotics (but HIGH RESISTANCE, need dual therapy)
  • azelaic acid
  • dapsone topical
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24
Q

what treatments target inflammation?

A
  • topical retinoids
  • oral retinoids
  • oral tetracyclines
  • azelaic acid
  • clascoterone cream
  • dapsone topical
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25
Q

what treatments target androgen receptor inhibition?

A
  • clascoterone cream
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26
Q

benzoyl peroxide MoA

A
  • antibacterial
  • comedolytic
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27
Q

benzoyl peroxide strength

A

2.5% (up to 10% but no extra benefit)
qd to tid as tolerable

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28
Q

benzoyl peroxide AE

A

bleaching –> hair, clothes!

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29
Q

benzoyl peroxide onset

A

3-12 weeks

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30
Q

topical retinoid MoA

A
  • normalize follicular hyperkeratosis (sloughing) / dec keratinocyte cohesiveness
  • dec inflammation
  • enhance penetration of other topical acne medications (adapalene + BP, tretinoin + clindamycin)
  • dec hyperpigmentation of scars
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31
Q

topical retinoid onsets

A

8-12 weeks

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32
Q

topical retinoid CI

A

pregnancy

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33
Q

topical retinoid administration

A

gently clean –> dry –> apply retinoid –> apply moisturizer

  • use thin layer
  • apply AT NIGHT to avoid sun
  • do NOT apply at same time as BP (bc BP will oxidize it)
  • apply to whole area (not spot treat)
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34
Q

topical retinoid AE

A
  • dryness
  • PHOTOSENSITIVITY
  • acute worsening of acne
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35
Q

topical retinoid allergy

A

Atralin (micronized tretinoin 0.05%) and soluble fish proteins

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36
Q

which drugs are photosensitive

A
  • topical retinoids
  • tetracycline oral antibiotics (tetracycline, minocycline, doxycycline, sarecycline)
  • isotretinoin
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37
Q

which drugs help with decreasing hyperpigmentation of scars

A
  • topical retinoids
  • azelaic acid
  • alpha hydroxy acids (glycolic acid, lactic acid)
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38
Q

topical retinoid order of strength/increasing irritation

A

adapalene
micro-encapsulated tretinoin
polyolperpolymer-2 tretinoin
tazarotene

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39
Q

types of retinoids

A
  • adapalene
  • tretinoin
  • tazarotene
  • trifarotene
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40
Q

which retinoid is OTC

A

adapalene 0.1% (differin)
- for 12+ yrs

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41
Q

azelaic acid MoA

A
  • inflammation
  • antibacterial
  • comedolytic
  • dec hyperpigmentation
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42
Q

azelaic acid dose

A

qd

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43
Q

how does azelaic acid dec hyperpigmentation

A

inhibit tyrosinase –> dec melanin

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44
Q

salicylic acid MoA

A

comedolytic, inflammation

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45
Q

topical antibiotic MoA

A
  • antibacterial (kill C. acnes)
  • inflammation
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46
Q

how to prevent topical antibiotic resistance

A

COMBO WITH BP

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47
Q

topical antibiotic options and AE/consideration

A

BP
clindamycin
erythromycin
dapsone
minocycline

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48
Q

topical BP AE

A

bleaches hair/clothes

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49
Q

topical clindamycin consideration/AE

A

add on BP
pseudomembraneous colitis

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50
Q

erythromycin consideration

A

add BP

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51
Q

topical dapsone AE

A

yellow-orange skin discolor IF SAME TIME AS BP –> separate!!

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52
Q

minocycline AE

A

HA

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53
Q

clascoterone cream MoA

A
  • androgen receptor inhibitor
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54
Q

clascoterone cream AE

A

HPA suppression (if occlusive dressing)

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55
Q

clascoterone cream administration and storage

A

NO OCCULSIVE DRESSING

REFRIGERATOR until dispense
room temperature dispensed for 180 days or 30 days after opening

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56
Q

which acne therapy do we not use anymore

A

sulfur

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57
Q

alpha hydroxy acids MoA

A
  • remove top layer of dead skin
  • dec post-inflammatory hyperpigmentation!!
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58
Q

tea tree oil MoA

A
  • inflammation
  • antibiotic
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59
Q

hormonal agent indication

A
  • moderate-severe acne
  • woman
  • not seeking pregnancy
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60
Q

hormonal agent MoA

A

estrogen/ethinyl estradiol (COC)
- dec ovarian androgen production
- dec sebum production

spironolactone, drosperinone
- competitive inhibition of androgen receptors at glands

OVERALL: dec androgen activity at glands

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61
Q

which hormonal agents are not effective for acne

A

progestin only –> POPs: Camila, Micronor (norethindrone)
- bc progestin is androgenic (promotes androgens)

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62
Q

onset for hormonal agents

A

need to wait 3-6 months to see if efficacy

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63
Q

COC AEs and CIs

A
  • thromboembolism

CI: rifampin use (dec efficacy COC)

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64
Q

spironolactone AEs and CIs

A
  • breast tender
  • CNS effects

CI:
- pregnancy (inc feminization of male fetus)
- HF, renal dysfunction, liver dysfunction (K sparing)

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65
Q

drosperinone CI

A

CI:
- renal dysfunction, liver dysfunction (K sparing)

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66
Q

how to monitor spironolactone and drosperinone for renal and liver dysfunction

A

monitor K for first cycle –> baseline, 4-6 weeks later

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67
Q

comparative efficacy of antibiotics, hormone therapy, isotretinoin

A

no data compares –> patient specific treatment
ALWAYS concomitantly use topical retinoids

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68
Q

oral antibiotic MoA

A
  • antibacterial
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69
Q

oral antibiotic consideration and how to prevent

A

RESISTANCE!!
- dec duration
- do not change too quickly
- restart same ones if effective
- do not combine MoAs (even if oral and topical)
- ALWAYS give with BP or topical retinoids

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70
Q

oral antibiotic options

A
  • tetracyclines: tetracycline, doxycycline, minocycline, sarecycline (least resistance)
  • erythromycin
  • azithromycicn
  • TMP/SMX
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71
Q

tetracycline AEs and CIs

A

AE:
- PHOTOCENSITIVITY –> therefore use sunscreen
- GI

CI: pregnancy, young children –> bone deposition

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72
Q

erythromycin AE

A

GI

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73
Q

TMP/SMX AE

A

SJS/TEN

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74
Q

azithromycin AE

A

GI

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75
Q

isotretinoin indication

A

moderate or severe, recalcitrant, nodules

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76
Q

isotretinoin CIs

A
  • pregnancy –> birth defects
  • underlying psychiatric conditions –> worsen
  • vitamin A supplements –> toxicity
  • use with tetracyclines –> pseudomotor cerebri (inc cranial HTN)
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77
Q

isotretinoin MoA

A
  • shrink sebaceous glands, dec sebum
  • inflammation
  • normalize proliferation
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78
Q

isotretinoin options

A

NORMAL: Claravis, Zenatane, Absorica
MICRONIZED: Absorica LD

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79
Q

isotretinoin dosing

A

1) dose
normal: 0.5-1 mg/kg/day, divided, food
micronized: 0.4-0.8 mg/kg/day, BID

2) duration
normal: 120-150 mg/kg cumulative dose OR 15-20 weeks
micronized: 15-20 weeks

3) course
usually 1 will work
refractory 3+
need 8+ weeks between courses

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80
Q

isotretinoin monitoring

A
  • LFT: baseline, 2 months, periodic if abnormal or change dose
  • FLP: baseline, 2 months, periodic if abnormal or change dose
  • CK elevation: ONLY if symptoms of joint/muscle pain
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81
Q

when would you discontinue isotretinoin

A

if LFTs (liver) are 3 x ULN

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82
Q

isotretinoin AEs

A
  • hepatotoxicity
  • joint/muscle pain
  • PHOTOSENSITIVITY
  • depression/suicide
  • night blindness
  • drying
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83
Q

what to avoid doing during/after stopping isotretinoin

A

giving blood –> 1 month after
cosmetic skin smoothing –> 6 months after **bc scar risk!!!

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84
Q

iPledge goals

A
  • stop patients taking isotretinoin from becoming pregnant
  • stop patients who are pregnant from taking isotretinoin
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85
Q

iPledge patient categories

A

can become pregnant, INLCUDES:
- pre-menstruation
- tubal sterilization

cannot become pregnant, INCLUDES:
- hysterectomy
- bilateral oophorectomy (ovary removal)
- post-menopause

consider sex (trans-male) AND status (above)

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86
Q

three iPledge requirements

A

1) contraception – only if can become pregnant
2) pregnancy test
3) do not dispense to patient after date

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87
Q

contraception requirement

A

primary AND secondary methods
- NOT include POPs (Camille, Micronor)

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88
Q

pregnancy test requirements

A

for whole course = N + 4
N: months on therapy

2 before start, 1 each month during, 2 after stop (1 right after, 1 30 days after)

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89
Q

do not dispense to patient after date requirements

A

can become pregnant –> 7 days after pregnancy test
cannot become pregnant –> 30 days after office visit

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90
Q

legal requirements

A
  • reverse RMA if after do not dispense date or RTS
  • 30 day supply max
  • no refills
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91
Q

acne conglobata

A
  • inflammation, nodules and cysts grow together deep under skin
  • scarring severe
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92
Q

acne conglobata treatment

A

isotretinoin
systemic antibiotics
intralesional steroids (inject)

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93
Q

acne fulminans

A

immune system mediated form of acne conglobata
- ulcers, bleeding, bone lesions

causes: ISOTRETINOIN, spontaneous

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94
Q

acne fulminans treat

A

stop isotretinoin if that is the cause

if not systemic: oral glucocorticoids x 2 weeks –> isotretinoin
if systemic: oral glucocorticoids x 4 weeks –> isotretinoin

*minimum 4 weeks

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95
Q

what is difficult about acne fulminans treatment

A

isotretinoin is a treatment but also could be a cause

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96
Q

post-inflammatory hyperpigmentation (PIH)

A

excess/uneven melanin distribution
caused by acne
improves overtime and may not need to treat

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97
Q

PIH treatment

A

non-pharm:
photoprotection

1st line:
hydroquinone BID –> avoid spot treatment, decreases formation and melanization of melanosomes

2nd line: **the same drugs
topical retinoids
azelaic acid
glycolic acid

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98
Q

when does a new drug rash require immediate ER attention vs calling PCP?

A

new drug rash + fever = ER
new drug rash + no fever = PCP

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99
Q

macules

A

defined flat lesions of any shape/size that are a different color from the rest of the skin

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100
Q

papules

A

small, raised lesions
*pimples

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101
Q

nodules

A

raised, solid, round, oval lesions

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102
Q

drug eruption

A

multiple, defined, red macules, blanch upon pressure, due to inflammatory vasodilation

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3
4
5
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103
Q

vesicles and bullae

A

blisters
- vesicles: defined (circumscribed)
- bullae: >0.5cm diameter

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104
Q

wheals

A

rounded, flat-topped papule/plaque, disappear quickly

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105
Q

what is the distinguishing factor of if a drug eruption is mild or severe?

A

FEVER!!

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106
Q

four categories of cutaneous (skin) drug eruptions

A
  1. exanthematous (eruptive rash)
  2. urticarial (itchy, red)
  3. blistering
  4. pustular
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107
Q

exanthematous drug eruption types

A

no fever –> maculopapular rash
fever –> DRESS (hypersensitivity syndrome reaction)

108
Q

urticarial drug eruption types

A

no fever –> urticaria
fever –> serum-sickness

109
Q

blistering drug eruption types

A

no fever –> fixed drug eruption
fever –> SJS/TEN

110
Q

pustular drug eruption types

A

no fever –> acneiform
fever –> AGEP

111
Q

which is the most common cutaneous drug eruption

A

exanthematous –> maculopapular rash, DRESS

112
Q

maculopapular rash presentation

A

flat, red, defined, diffuse, edges slight raised

113
Q

maculopapular rash onset and resolution

A

onset: 7-10 days (faster if already sensitized)
resolution: 7-14 days after stop

114
Q

maculopapular rash offending drugs

A

pencillins, cephalosporins
sulfonamides (bactrim)
anticonvulsants

115
Q

maculopapular rash treatment

A

stop offending agent

116
Q

DRESS presentation

A

exanthematous eruptions
PLUS
fever, lymphadenopathy, esosinophilia, multiogan involvement (kidney, liver, lungs)

117
Q

DRESS onset and recovery

A

onset: 1-6 weeks after drug
recover: 6-8 weeks, relapse from bet-lactams possible

118
Q

DRESS s/s

A

> 50% BSA affected
facial edema and rash
RegiSCAR scoring system to see Dx (not help treat)

119
Q

DRESS offending agents

A

ALLOPURINOL
LAMOTRIGINE
other anticonvulsants
sulfonamides
dapsone

120
Q

most common DRESS cause

A

allpurinol

121
Q

allopurinol DRESS risk factors

A
  • high dose
  • renal dysfunction
  • HTN
  • thiazide use
  • ASIAIN (HLA-B* 58:01)
122
Q

allopurinol renal dysfunction max dose

A

1.5mg x eGFR

123
Q

DRESS treatment

A

non-pharm
- stop offending
- do not start anything
– beta-lactams can relapse!
– valproic acid good alternative
- fluids, electrolytes, nutrition

pharm: depends on organ involvement
- not involvement: high potency topical steriods, bid-tid, 1 week
- involvement: systemic corticosteriods 0.5-2 mg/kg/day prednisone, 8-12 weeks taper

124
Q

which anticonvulsant is a good option if you need to stop one as an offending DIDD agent?

A

valproic acid –> low risk

125
Q

high potency topical steriods

A
  • triamcinolone 0.5%
  • clobetasol
  • fluocinoninde
  • halobetasol
  • betamethasone dipropionate
  • halcinonide
  • desoximetasone
126
Q

medium potency topical steriods

A
  • triamcinolone 0.1%
  • mometasone
  • hydrocortisone valerate
  • betamethasone valerate
127
Q

low potency topical steriods

A
  • triamcinolone 0.025%
  • hydrocortisone
  • desonide
128
Q

urticaria patho

A

type 1 hypersensitivity –> IgE mediated

129
Q

urticaria presentation

A

hives, red, itchy (pruritic), raised wheals
angioedema and swelling of mucous membranes
can be first sign of anaphylaxis

130
Q

urticaria onset

A

minutes-hours

131
Q

urticaria offending agents

A
  • penicillin
  • sulfonamides
  • aspirin
  • opiates
  • latex
132
Q

urticaria treatment

A

stop drug
anaphylaxis treatment as needed

133
Q

serum sickness like reactions presentation

A

urticaria, fever, arthralgia

**not a true type iii serum sickness

134
Q

serum sickeness like onset and resolution

A

onset: 1-3 weeks
resolution: 1-2 weeks

135
Q

serum-sickness like offending agents

A

penicillins, cephalosporins
sulfonamides

136
Q

fixed drug eruptions presentation

A

simple eruption, raised, red, defined, itchy, blister, skin hyperpigmentation!!

137
Q

fixed drug eruption unique characteristic

A

WILL OCCUR IN SAME AREA EACH TIME OFFENDING DRUG GIVEN

138
Q

fixed drug eruption onset and resolution

A

onset: minutes-days
resolution: days

139
Q

fixed drug eruption offending agents

A
  • barbituates
  • sulfonamides
  • tetracyclines
  • codeine
  • APAP
  • NSAIDs
  • phenolphthalein
140
Q

SJS/TEN presentation

A

bullous blisters, systemic signs –> fever, HA< respiratory
**MUCOUS MEMBRANE INVOLVEMENT! (eyes, mouth, nose)
skin lesions spread quickly, necrosis, epidermal detachment, sloughing

141
Q

SJS vs TEN

A

SJS < 10% slough
TEN > 30% slough

142
Q

SJS/TEN onset and resolution

A

onset: 7-14 days
resolution: 1 month to regrow

143
Q

SJS/TEN patho

A

immune systemic activation, inc t cells, mucocutaneous disorder

144
Q

biggest risk factor for SJS/TEN

A

HIV infection!!

145
Q

biggest cause of SJS/TEN mortality

A

bacteremia

146
Q

other SJS/TEN risk factors

A
  • SLE
  • malignancy
  • UV radiation
  • female
  • Asian HLA-B* 15:02 –> carbamazeipine, phenytoin, phenobarbital
147
Q

SJS/TEN offending agents

A
  • sulfonamides
  • penicillin
  • anticonvulsants
  • NSAIDS (oxicams)
  • allopurinol
148
Q

SJS/TEN complications

A
  • fluid loss
  • electrolyte imbalance
  • secondary infection bc no skin barrier
  • blindness if eye impacted
  • bacteremia
  • pain
149
Q

SJS/TEN supportive treatment

A

supportive:
- stop offending –> cross-reactivity
- supportive: pain, fluids, electrolytes
- TOPICAL ANTISEPTICS/WOUND CARE (prevent infection)
- OPTHALMOLOGY (prevent blindness)

150
Q

topical antiseptic options

A
  • chlorhexidine
  • silver nitrate
  • silver sulfadiazine –> NOT IF SULFA CAUSE!
  • gentamicin
151
Q

opthalmic options

A

mild: artificial tears/ointment multiple times a day
severe: corticosteroid-antimicrobial eye drops

152
Q

SJS/TEN treatment

A

if no systemic infection
1st: IVIG
2nd: systemic corticosteriods, cyclosporine

if systemic infection
1st IVIG

NEVER
thalidomide

153
Q

systemic corticosteriod CI

A

systemic infection

154
Q

cyclosporine CI

A

systemic infection

155
Q

thalidomide CI

A

SJS/TEN (bc inc mortality)

156
Q

IVIG BBWs

A
  • thromboembolic events
  • AKI
157
Q

hyperpigmentation offending agents

A
  • tetracyclines
  • amiodarone
  • phenytoin
  • silver, mercury, antimalarials
158
Q

photosensitivity offending agents

A
  • tetracyclines
  • sulfonamides
  • amiodarone
  • coal tar
159
Q

photosensitivity prevention

A
  • SPF 30
  • dec sun exposure
160
Q

general DIDD management

A
  1. stop offending
  2. avoid cross-reactivity
  3. supportive – itchy, fever
  4. if severe, consider short course systemic corticosteroids
161
Q

sulfa allergy considerations

A

1) category
- low cross-reactivity between sulfa antibiotics and sulfa non-antibiotics –> therefore can have other type

2) severity of reaction
- mild: can have other type
- severe: AVOID ALL

162
Q

sulfa non-antibiotics

A
  • loop diuretics
  • thiazide diuretics
  • dapsone
  • sulfonylureas
  • sulfasalazine
163
Q

penicillin allergy considerations

A

1) R1 side chain
*responsible for cross-reactivity
- aminopenicillins (amoxicillin, ampicillin) SIMILAR to 1st and 2nd gen cephalosporins (cephalexin, cefadroxil, cefaclor, cefprozil)
- 3rd, 4th, 5th gen cephalosporins (cefepime, ceftriaxzone) NOT SIMILAR to any pencillin

2) severity of reaction
- mild: consider R1 side chain rules
- severe: AVOID ALL BETA-LACTAMS!!!!

164
Q

types of glaucoma

A

1) primary open-angle glaucoma
- glaucoma
- ocular HTN
- normal tension (N-T) glaucoma

2) primary closed-angle glaucoma

165
Q

glaucoma patho

A
  • ocular disease
  • gradual progression of optic neuropathy (PNS damage)
  • two loses: field (scope) AND sensitivity (contrast at night)

**narrowing of visual field

166
Q

what is damaged in glaucoma

A

optic nerve (which innervates the retina and allows for sight)

167
Q

optic disc/optic nerve head

A

the nerve fibers converge into a bundle and exit through sclera
**anatomical blindspot
- needs to be intact for vision!

168
Q

cup:disc ratio

A

cup: the top of the neuron bundle
disc: the opening in sclera where the bundle is

can be increased due to:
optic disc changes
axons dying off –> inc cup

**usually just an inc in cup

169
Q

how can the optic disc change?

A

mechanical: compression, axonal tissue necrosis
vascular: dec blood flow –> destroy axonal tissue

170
Q

normal cup:disc ratio range

171
Q

function of the aqueous humor

A

(the liquid in the eye)
- maintain intraocular pressure (IOP)!!**

  • nutrient
  • waste
  • immune response
  • paracrine signal
172
Q

what does maintaining IOP prevent

A
  • corneal collapse
  • damage to optic nerve
173
Q

aqueous humor pathway

A

produced in ciliary body –> posterior chamber –> anterior chamber –> trabecular meshwork –> angle –> circulation

174
Q

two ways for aqueous humor outflow

A
  1. trabecular network/schlemm’s canal
  2. uveoscleral outflow (sclear)
175
Q

which route of AH outflow is major

A

trabecular network/schlemm’s canal

176
Q

which route of AH outflow is IOP-dependent (higher IOP leads to more outflow)

A

trabecular meshwork/schlemm

177
Q

which route of AH outflow is IOP-independent (same outflow amount no matter how much IOP)

A

uveoscleral outflow

178
Q

what is the result of blocked AH outflow

179
Q

three ways for AH outflow obstruction

A
  1. trabecular meshwork obstruction
  2. collapsed schlemm’s canal
  3. changes in AH composition
180
Q

normal IOP

A

13-21 mmHg

181
Q

high IOP

182
Q

higher IOP means…

A

inc risk of nerve damage

183
Q

higher IOP does NOT mean…

184
Q

normal IOP does NOT mean…

A

cannot get glaucoma

185
Q

what is the only modifiable risk factor for glaucoma?

A

aqueous humor dynamics/IOP

186
Q

lowering IOP…

A

dec risk for glaucoma progression

187
Q

what determines if glaucoma or not?

A

glaucomatous changes!
- field, sensitvitiy, maybe cup:disc ratio?

188
Q

normal IOP, glaucoma changes

A

NT glaucoma

189
Q

high IOP, glaucoma changes

190
Q

normal IOP, no glaucoma change

191
Q

high IOP, no glaucoma change

A

ocular HTN

192
Q

risk factors for developing open angle glaucoma

A
  • elevated IOP
  • age > 60, >40 for black
  • black, hispanic
  • family history/genetics
  • T2 DM
  • thinner CCT (central corneal thickness)
  • increased cup:disc ratio
  • myopia (near-sighted)
  • lower ocular perfusion pressure
193
Q

is HTN a risk factor for POAG?

194
Q

is smoking a risk factor for POAG?

195
Q

what are glaucomatous changes?

A
  • disc change
  • field defects
196
Q

who to treat for glaucoma

A

high IOP + glaucomatous changes (disc, field)

197
Q

glaucoma treatment goals

A
  1. preserve the nerve (stop damage)
  2. dec IOP by 25% or more vs pretreatment
198
Q

is medication or surgery more effective at lowering IOP?

199
Q

surgery vs medication?

A

can be equally effective, just need to dec IOP

surgery: invasive, one time, inc cataract risk
medication: non invasive, every day, dec cataract risk

200
Q

prostaglandin Fa2 analog MoA

A

inc sclearal permeability –> inc uveoscleral outflow

201
Q

prostaglandin Fa2 IOP reduction

A

25-33%
**very effective!!

202
Q

prostaglandin F2a AEs

A
  • ocular irritation (red)
  • eyelash growth
  • iris pigment change
203
Q

which prostaglandin F2a have best efficacy

A

bimatoprost
latanoprost bunod

204
Q

which prostaglandin analog has fewest AE

A

omidenepeg
then
latanoprost

205
Q

which prostaglandins are generic

A

bimatoprost 0.03%
latanoprost

206
Q

prostaglandin EP2 antagonist MoA

A

inc uveosclearal AND trabecular outflow

omidenepeg!

207
Q

prostaglandin F CI

A

existing ocular inflammation

208
Q

beta blocker MoA

A

decrease aqueous humor production

209
Q

beta blocker IOP reduction

210
Q

beta blocker AE

A

less ocular irritation
SYSTEMIC –> cardiac, respiratory, CNS

211
Q

beta blocker CI

A

absolute: HF, sinus bradycardia, heart block
relative: pulmonary disease

212
Q

beta blocker options

A

timolol
carteolol
betaxolol
levobunolol
metipranolol

213
Q

beta blocker best efficacy

214
Q

beta blcoker with qd dosing

A

timolol
levobunolol

215
Q

beta blocker with dec AR

216
Q

beta blocker for asthma/copd

A

betaxolol —> highly selective

217
Q

eye drop adminstration to dec systemic effects

A

hold eye duct while use

218
Q

alpha 2 agonist MoA

A

reduce aqeuous humor production, small effect on uveosclearal outflow

219
Q

alpha 2 agonist AE

A

ocular irritation
XEROSTOMIA (dry mouth) –> hold lacrimal duct

220
Q

alpha 2 agonist options

A

brimonidine
brimonidine-timolol fixed combination (BTFC)

221
Q

alpha 2 agonist IOP reduction

A

20-25%, closer to 20%

222
Q

carbonic anhydrase inhibitor MoA

A

reduce aqueous humor production vis dec bicarbonate ion secretion

223
Q

carbonic anhydrase inhibitors

A

topical: 15-20%

224
Q

carbonic anhydrase inhibitor AE

225
Q

carbonic anhydrase inhibitor options

A

brinzolamide
dorzolamide

dorzolamide-timolol FC (DTFC) –> prefer
brinzolamide-brimonidine FC (BBFC)

226
Q

DTFC or bimatoprost have better diurnal control?

A

bimatoprost

227
Q

rho kinase inhibitor MoA

A
  • inc trabecular outflow
228
Q

rho kinase IOP reduction

A

20% IF high initial IOP > 27 mmHg

229
Q

rho kinase AE

A

many
conjunctival hemorrhaging

230
Q

rho kinase options

A

netarsudil

231
Q

when to switch drug class?

A

adherence, tolerance, poor efficacy

232
Q

when to add another drug?

A

the current drug is almost there but not quite at goal

233
Q

time to follow up

A

gluacomatous changes –> 1-2 months

no changes, not at goal –> 3-6 months
no changes, at goal for 6 months or less –> 6 months
no changes, at goal for more than 6 months –> 6-12 months

234
Q

what is nasolacrimal occlusion

A

holding the lacrimal duct to prevent systemic absorption and AEs

235
Q

risk factors for progression of glaucoma

A
  • higher IOP
  • older age
  • disc hemorrhage
  • larger cup:disc ratio
  • bilteral disease
  • thinner central cornea
  • lower ocular perfusion pressure
  • untreated disease, poor adherence
  • progression in other eye
236
Q

which medications dec uveoscleral outflow?

A
  • prostaglandin F2
  • prostaglandin EP2
237
Q

which medications dec aqueous humor production?

A
  • beta-blockers
  • alpha 2 agonist
  • carbonic anhydrase inhibitors
238
Q

which medcations inc trabecular outflow?

A
  • prostaglandin E2P
  • rho kinase inhibitors
239
Q

why do we treat ocular HTN

A

delay progression to glaucoma

240
Q

who do we treat for ocular HTN

A

ocular HTN + risk factors

risk factors:
- black/hispanic
- IOP> 25mmHg
- family Hx
- thin central cornea
- large cup/disc ratio

241
Q

why do we treat NT glaucoma

A

preserves visual field, preserved optic disc

*same treatment goals of dec 25%

242
Q

who do we treat for NT glaucoma?

A

NT glaucoma + documnted visual field loss (glaucoma changes)

243
Q

overall, treat

A
  • glaucoma
  • NT galucoma
  • ocular HTN + risk factors
244
Q

goals of therapy for acute angle closure crisis

A

break attack to
1. preserve vision
2. prep eye for LPI (laser peripheral iridotomy) –> dec IOP, open angle, dec inflammation

245
Q

first line treatments for AACC

A

for IOP lower:
1. acetazolamide IV or PO 500mg
2. topical beta blocker
3. topical apraclonidine

for angle opening
4. topical pilocarpine

246
Q

how long do you wait to add more therapy

A

1 hour no change

247
Q

what do you add

A

to dec IOP:
5. hyperosmotic –> mannitol IV, glycerin/isosorbide PO

to dec inflammation:
6. ophthalmic steroid

248
Q

goal of chronic closed angle treatment

A

keep angle open, prevent acute attacks

249
Q

chronic closed angle treatment

A
  • same meds as open angle
  • iridotomy
  • counsel on acute s/s, avoid OTC that dilate pupils
250
Q

atopic dermatitis patho

A

filaggrin deficiency –> dec natural moisturizer factor (NMF)

251
Q

atopic derm non-pharm

A
  1. dec exacerbating factors
  2. bathing
  3. skin hydration
  4. prevent itching
252
Q

JAKi drugs

A

-inibs

ruloxitinib – cream
abrocitinib – tab
upacitinib – tab

253
Q

monoclonal antibody durgs

A

dupilumab
tralokinumab

254
Q

immunosupressant drugs

A

methotrexate
cyclosporine
azathioprine

255
Q

face/flexure first line

A

LOW POTENCY topical corticosteriods

5-7 day course!!

256
Q

JAKi avoid/CI

A
  • thrombosis
  • > 50 and CV risk
  • MACE
  • herpes, pneumonia
  • malignancy
257
Q

JAKi monitoring

A
  • liver
  • kidney
  • lipid
  • neutrophil, hemoglobin
  • viral hepatitis, TB
258
Q

JAKi kidney dosing

A

ruloxitinib – none

abrocitinib – CI if CrCl < 30
upacitinib – CI if CrCl < 15

259
Q

allergic contact dermatitis causes

A
  • latex
  • posion ivy
  • metal
  • TOPICAL STERIODS –> difficult bc that is the treatment
    …
260
Q

poison ivy causitive agent

A

urushiol

  • mango
  • unroasted cashew nuts
261
Q

what do you avoid when treating toxicodendron dermatitis

A
  • antihistamines
  • topical calcineurin inhibitors
  • medrol dose pack
262
Q

cause of seborrheic dermatitis

A

Malassezia (fungus, yeast)

263
Q

cradle cap

A

biphasic seborrheic derm (2 weeks then 12 months)
- greasy, yellow scales inscalp, forehead

264
Q

first line for seborrheic derm

A

topical antifungal!!
- selenium sulfide
- zinc pyrithione
- ketoconazole shampoo
- ciclopirox
- coal tar

265
Q

second line seborrheic derm

A

topical corticosteriods
topical CI
systemic antifungal

266
Q

cradle cap treat

A

bady shampoo
soft brush
petroleum jelly, mineral oil

p2 year (9 decks)

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