acne, drug induced derm, atopic derm, glaucoma Flashcards
acne formation
- 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!
what are the four mechanisms of acne we are trying to prevent with therapy?
- follicular hyperproliferation/hyperkeratinization
- inc sebum production (androgens)
- inflammation
- bacteria growth
what is the oil of hair follicles called
sebum
what bacteria grows in acne?
Cutibacterium acnes (Propionibacterium acnes)
aka C. acnes
what is acne vulgaris?
common acne
- lesions most common on face, also back, chest, arms, neck
- onset following puberty, could be younger
- males more affected
what factors inc acne vulgaris?
- emotional stress –> CRH
- repetitive stress –> harsh soaps
- occlusions and pressure –> clothing, makeup
- heat, humidity –> topical acne, more oil
- occupational acne –> fryer grease, …
what is the pH of healthy skin? how does this impact drugs?
4.7-5.7
we want soaps/cleansers around this pH, if not could trap more and worsen acne!!
does food affect acne?
very individual –> what impacts one person may not impact another
- chocolate
- fatty food
- milk
- soda
- high sugar foods
acne course
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
drugs that cause acneiform lesison
- glucocorticoids
- oral contraceptives
- androgens
- lithium
- phenytoin
- valproic acid
- cyclosporine
- isoniazid
- azathioprine
- disulfiram
- phentermine
- iodides
- bromides
- danazol
- high dose vitamin B
- high dose vitamin D
goals of acne treatment
- remove keratin plug
- dec sebum production
- dec bacterial inflammation
- reduce scarring
**consider psychological aspects on acne always!!
acne treatment self-care
- gentle cleanser (CeraVe) twice a day
- don’t pick
- stop offending agents (food, harsh cleaners/makeup)
- avoid facial scrubs
- water-based lotions/cosmetics
CI to acne self care
- pregnant, IBD/colitis
- self care fail after 3 months
- moderate-severe acne
- comedogenic drugs (drug causing)
what type of medication (self-care, OTC, Rx) should be used based on skin type/location?
dry: lotion, cream
oily: gels, foams –> allow evaporation
hairy: foam
large area: solutions (are drying tho), pledgets (round applicator)
what do all acne treatments cause?
drying!!!
mild acne
- few-several (<10) papules/pustules
- no nodules
moderate acne
- several-many (10-40) papules/pustules with comedomes
- few-several nodules
severe acne
- numerous-extensive (>40) papules/pustules
- many nodules
what patho does isotretinoin (oral retinoid) target?
- follicular hyperproliferation
- increased sebum production
- inflammation
NOT
- bacterial proliferation
- androgen receptor inhibition
what patho does benzoyl peroxide target?
- bacterial proliferation (C. acnes) –> bc oxidizing, therefore kills
what treatments target follicular hyperproliferation?
- oral retinoids
- topical retinoids
- azelaic acid
- salicylic acid
- hormonal therapy
what treatments target increased sebum production
- oral retinoids
- hormonal therapy
- clascoterone cream
what treatments target bacterial (C. acnes) proliferation?
- benzoyl peroxide
- antibiotics (but HIGH RESISTANCE, need dual therapy)
- azelaic acid
- dapsone topical
what treatments target inflammation?
- topical retinoids
- oral retinoids
- oral tetracyclines
- azelaic acid
- clascoterone cream
- dapsone topical
what treatments target androgen receptor inhibition?
- clascoterone cream
benzoyl peroxide MoA
- antibacterial
- comedolytic
benzoyl peroxide strength
2.5% (up to 10% but no extra benefit)
qd to tid as tolerable
benzoyl peroxide AE
bleaching –> hair, clothes!
benzoyl peroxide onset
3-12 weeks
topical retinoid MoA
- normalize follicular hyperkeratosis (sloughing) / dec keratinocyte cohesiveness
- dec inflammation
- enhance penetration of other topical acne medications (adapalene + BP, tretinoin + clindamycin)
- dec hyperpigmentation of scars
topical retinoid onsets
8-12 weeks
topical retinoid CI
pregnancy
topical retinoid administration
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)
topical retinoid AE
- dryness
- PHOTOSENSITIVITY
- acute worsening of acne
topical retinoid allergy
Atralin (micronized tretinoin 0.05%) and soluble fish proteins
which drugs are photosensitive
- topical retinoids
- tetracycline oral antibiotics (tetracycline, minocycline, doxycycline, sarecycline)
- isotretinoin
which drugs help with decreasing hyperpigmentation of scars
- topical retinoids
- azelaic acid
- alpha hydroxy acids (glycolic acid, lactic acid)
topical retinoid order of strength/increasing irritation
adapalene
micro-encapsulated tretinoin
polyolperpolymer-2 tretinoin
tazarotene
types of retinoids
- adapalene
- tretinoin
- tazarotene
- trifarotene
which retinoid is OTC
adapalene 0.1% (differin)
- for 12+ yrs
azelaic acid MoA
- inflammation
- antibacterial
- comedolytic
- dec hyperpigmentation
azelaic acid dose
qd
how does azelaic acid dec hyperpigmentation
inhibit tyrosinase –> dec melanin
salicylic acid MoA
comedolytic, inflammation
topical antibiotic MoA
- antibacterial (kill C. acnes)
- inflammation
how to prevent topical antibiotic resistance
COMBO WITH BP
topical antibiotic options and AE/consideration
BP
clindamycin
erythromycin
dapsone
minocycline
topical BP AE
bleaches hair/clothes
topical clindamycin consideration/AE
add on BP
pseudomembraneous colitis
erythromycin consideration
add BP
topical dapsone AE
yellow-orange skin discolor IF SAME TIME AS BP –> separate!!
minocycline AE
HA
clascoterone cream MoA
- androgen receptor inhibitor
clascoterone cream AE
HPA suppression (if occlusive dressing)
clascoterone cream administration and storage
NO OCCULSIVE DRESSING
REFRIGERATOR until dispense
room temperature dispensed for 180 days or 30 days after opening
which acne therapy do we not use anymore
sulfur
alpha hydroxy acids MoA
- remove top layer of dead skin
- dec post-inflammatory hyperpigmentation!!
tea tree oil MoA
- inflammation
- antibiotic
hormonal agent indication
- moderate-severe acne
- woman
- not seeking pregnancy
hormonal agent MoA
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
which hormonal agents are not effective for acne
progestin only –> POPs: Camila, Micronor (norethindrone)
- bc progestin is androgenic (promotes androgens)
onset for hormonal agents
need to wait 3-6 months to see if efficacy
COC AEs and CIs
- thromboembolism
CI: rifampin use (dec efficacy COC)
spironolactone AEs and CIs
- breast tender
- CNS effects
CI:
- pregnancy (inc feminization of male fetus)
- HF, renal dysfunction, liver dysfunction (K sparing)
drosperinone CI
CI:
- renal dysfunction, liver dysfunction (K sparing)
how to monitor spironolactone and drosperinone for renal and liver dysfunction
monitor K for first cycle –> baseline, 4-6 weeks later
comparative efficacy of antibiotics, hormone therapy, isotretinoin
no data compares –> patient specific treatment
ALWAYS concomitantly use topical retinoids
oral antibiotic MoA
- antibacterial
oral antibiotic consideration and how to prevent
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
oral antibiotic options
- tetracyclines: tetracycline, doxycycline, minocycline, sarecycline (least resistance)
- erythromycin
- azithromycicn
- TMP/SMX
tetracycline AEs and CIs
AE:
- PHOTOCENSITIVITY –> therefore use sunscreen
- GI
CI: pregnancy, young children –> bone deposition
erythromycin AE
GI
TMP/SMX AE
SJS/TEN
azithromycin AE
GI
isotretinoin indication
moderate or severe, recalcitrant, nodules
isotretinoin CIs
- pregnancy –> birth defects
- underlying psychiatric conditions –> worsen
- vitamin A supplements –> toxicity
- use with tetracyclines –> pseudomotor cerebri (inc cranial HTN)
isotretinoin MoA
- shrink sebaceous glands, dec sebum
- inflammation
- normalize proliferation
isotretinoin options
NORMAL: Claravis, Zenatane, Absorica
MICRONIZED: Absorica LD
isotretinoin dosing
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
isotretinoin monitoring
- 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
when would you discontinue isotretinoin
if LFTs (liver) are 3 x ULN
isotretinoin AEs
- hepatotoxicity
- joint/muscle pain
- PHOTOSENSITIVITY
- depression/suicide
- night blindness
- drying
what to avoid doing during/after stopping isotretinoin
giving blood –> 1 month after
cosmetic skin smoothing –> 6 months after **bc scar risk!!!
iPledge goals
- stop patients taking isotretinoin from becoming pregnant
- stop patients who are pregnant from taking isotretinoin
iPledge patient categories
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)
three iPledge requirements
1) contraception – only if can become pregnant
2) pregnancy test
3) do not dispense to patient after date
contraception requirement
primary AND secondary methods
- NOT include POPs (Camille, Micronor)
pregnancy test requirements
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)
do not dispense to patient after date requirements
can become pregnant –> 7 days after pregnancy test
cannot become pregnant –> 30 days after office visit
legal requirements
- reverse RMA if after do not dispense date or RTS
- 30 day supply max
- no refills
acne conglobata
- inflammation, nodules and cysts grow together deep under skin
- scarring severe
acne conglobata treatment
isotretinoin
systemic antibiotics
intralesional steroids (inject)
acne fulminans
immune system mediated form of acne conglobata
- ulcers, bleeding, bone lesions
causes: ISOTRETINOIN, spontaneous
acne fulminans treat
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
what is difficult about acne fulminans treatment
isotretinoin is a treatment but also could be a cause
post-inflammatory hyperpigmentation (PIH)
excess/uneven melanin distribution
caused by acne
improves overtime and may not need to treat
PIH treatment
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
when does a new drug rash require immediate ER attention vs calling PCP?
new drug rash + fever = ER
new drug rash + no fever = PCP
macules
defined flat lesions of any shape/size that are a different color from the rest of the skin
papules
small, raised lesions
*pimples
nodules
raised, solid, round, oval lesions
drug eruption
multiple, defined, red macules, blanch upon pressure, due to inflammatory vasodilation
vesicles and bullae
blisters
- vesicles: defined (circumscribed)
- bullae: >0.5cm diameter
wheals
rounded, flat-topped papule/plaque, disappear quickly
what is the distinguishing factor of if a drug eruption is mild or severe?
FEVER!!
four categories of cutaneous (skin) drug eruptions
- exanthematous (eruptive rash)
- urticarial (itchy, red)
- blistering
- pustular
exanthematous drug eruption types
no fever –> maculopapular rash
fever –> DRESS (hypersensitivity syndrome reaction)
urticarial drug eruption types
no fever –> urticaria
fever –> serum-sickness
blistering drug eruption types
no fever –> fixed drug eruption
fever –> SJS/TEN
pustular drug eruption types
no fever –> acneiform
fever –> AGEP
which is the most common cutaneous drug eruption
exanthematous –> maculopapular rash, DRESS
maculopapular rash presentation
flat, red, defined, diffuse, edges slight raised
maculopapular rash onset and resolution
onset: 7-10 days (faster if already sensitized)
resolution: 7-14 days after stop
maculopapular rash offending drugs
pencillins, cephalosporins
sulfonamides (bactrim)
anticonvulsants
maculopapular rash treatment
stop offending agent
DRESS presentation
exanthematous eruptions
PLUS
fever, lymphadenopathy, esosinophilia, multiogan involvement (kidney, liver, lungs)
DRESS onset and recovery
onset: 1-6 weeks after drug
recover: 6-8 weeks, relapse from bet-lactams possible
DRESS s/s
> 50% BSA affected
facial edema and rash
RegiSCAR scoring system to see Dx (not help treat)
DRESS offending agents
ALLOPURINOL
LAMOTRIGINE
other anticonvulsants
sulfonamides
dapsone
most common DRESS cause
allpurinol
allopurinol DRESS risk factors
- high dose
- renal dysfunction
- HTN
- thiazide use
- ASIAIN (HLA-B* 58:01)
allopurinol renal dysfunction max dose
1.5mg x eGFR
DRESS treatment
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
which anticonvulsant is a good option if you need to stop one as an offending DIDD agent?
valproic acid –> low risk
high potency topical steriods
- triamcinolone 0.5%
- clobetasol
- fluocinoninde
- halobetasol
- betamethasone dipropionate
- halcinonide
- desoximetasone
medium potency topical steriods
- triamcinolone 0.1%
- mometasone
- hydrocortisone valerate
- betamethasone valerate
low potency topical steriods
- triamcinolone 0.025%
- hydrocortisone
- desonide
urticaria patho
type 1 hypersensitivity –> IgE mediated
urticaria presentation
hives, red, itchy (pruritic), raised wheals
angioedema and swelling of mucous membranes
can be first sign of anaphylaxis
urticaria onset
minutes-hours
urticaria offending agents
- penicillin
- sulfonamides
- aspirin
- opiates
- latex
urticaria treatment
stop drug
anaphylaxis treatment as needed
serum sickness like reactions presentation
urticaria, fever, arthralgia
**not a true type iii serum sickness
serum sickeness like onset and resolution
onset: 1-3 weeks
resolution: 1-2 weeks
serum-sickness like offending agents
penicillins, cephalosporins
sulfonamides
fixed drug eruptions presentation
simple eruption, raised, red, defined, itchy, blister, skin hyperpigmentation!!
fixed drug eruption unique characteristic
WILL OCCUR IN SAME AREA EACH TIME OFFENDING DRUG GIVEN
fixed drug eruption onset and resolution
onset: minutes-days
resolution: days
fixed drug eruption offending agents
- barbituates
- sulfonamides
- tetracyclines
- codeine
- APAP
- NSAIDs
- phenolphthalein
SJS/TEN presentation
bullous blisters, systemic signs –> fever, HA< respiratory
**MUCOUS MEMBRANE INVOLVEMENT! (eyes, mouth, nose)
skin lesions spread quickly, necrosis, epidermal detachment, sloughing
SJS vs TEN
SJS < 10% slough
TEN > 30% slough
SJS/TEN onset and resolution
onset: 7-14 days
resolution: 1 month to regrow
SJS/TEN patho
immune systemic activation, inc t cells, mucocutaneous disorder
biggest risk factor for SJS/TEN
HIV infection!!
biggest cause of SJS/TEN mortality
bacteremia
other SJS/TEN risk factors
- SLE
- malignancy
- UV radiation
- female
- Asian HLA-B* 15:02 –> carbamazeipine, phenytoin, phenobarbital
SJS/TEN offending agents
- sulfonamides
- penicillin
- anticonvulsants
- NSAIDS (oxicams)
- allopurinol
SJS/TEN complications
- fluid loss
- electrolyte imbalance
- secondary infection bc no skin barrier
- blindness if eye impacted
- bacteremia
- pain
SJS/TEN supportive treatment
supportive:
- stop offending –> cross-reactivity
- supportive: pain, fluids, electrolytes
- TOPICAL ANTISEPTICS/WOUND CARE (prevent infection)
- OPTHALMOLOGY (prevent blindness)
topical antiseptic options
- chlorhexidine
- silver nitrate
- silver sulfadiazine –> NOT IF SULFA CAUSE!
- gentamicin
opthalmic options
mild: artificial tears/ointment multiple times a day
severe: corticosteroid-antimicrobial eye drops
SJS/TEN treatment
if no systemic infection
1st: IVIG
2nd: systemic corticosteriods, cyclosporine
if systemic infection
1st IVIG
NEVER
thalidomide
systemic corticosteriod CI
systemic infection
cyclosporine CI
systemic infection
thalidomide CI
SJS/TEN (bc inc mortality)
IVIG BBWs
- thromboembolic events
- AKI
hyperpigmentation offending agents
- tetracyclines
- amiodarone
- phenytoin
- silver, mercury, antimalarials
photosensitivity offending agents
- tetracyclines
- sulfonamides
- amiodarone
- coal tar
photosensitivity prevention
- SPF 30
- dec sun exposure
general DIDD management
- stop offending
- avoid cross-reactivity
- supportive – itchy, fever
- if severe, consider short course systemic corticosteroids
sulfa allergy considerations
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
sulfa non-antibiotics
- loop diuretics
- thiazide diuretics
- dapsone
- sulfonylureas
- sulfasalazine
penicillin allergy considerations
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!!!!
types of glaucoma
1) primary open-angle glaucoma
- glaucoma
- ocular HTN
- normal tension (N-T) glaucoma
2) primary closed-angle glaucoma
glaucoma patho
- ocular disease
- gradual progression of optic neuropathy (PNS damage)
- two loses: field (scope) AND sensitivity (contrast at night)
**narrowing of visual field
what is damaged in glaucoma
optic nerve (which innervates the retina and allows for sight)
optic disc/optic nerve head
the nerve fibers converge into a bundle and exit through sclera
**anatomical blindspot
- needs to be intact for vision!
cup:disc ratio
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
how can the optic disc change?
mechanical: compression, axonal tissue necrosis
vascular: dec blood flow –> destroy axonal tissue
normal cup:disc ratio range
0.1-0.2
function of the aqueous humor
(the liquid in the eye)
- maintain intraocular pressure (IOP)!!**
- nutrient
- waste
- immune response
- paracrine signal
what does maintaining IOP prevent
- corneal collapse
- damage to optic nerve
aqueous humor pathway
produced in ciliary body –> posterior chamber –> anterior chamber –> trabecular meshwork –> angle –> circulation
two ways for aqueous humor outflow
- trabecular network/schlemm’s canal
- uveoscleral outflow (sclear)
which route of AH outflow is major
trabecular network/schlemm’s canal
which route of AH outflow is IOP-dependent (higher IOP leads to more outflow)
trabecular meshwork/schlemm
which route of AH outflow is IOP-independent (same outflow amount no matter how much IOP)
uveoscleral outflow
what is the result of blocked AH outflow
inc IOP!
three ways for AH outflow obstruction
- trabecular meshwork obstruction
- collapsed schlemm’s canal
- changes in AH composition
normal IOP
13-21 mmHg
high IOP
> 21 mmHg
higher IOP means…
inc risk of nerve damage
higher IOP does NOT mean…
glaucoma
normal IOP does NOT mean…
cannot get glaucoma
what is the only modifiable risk factor for glaucoma?
aqueous humor dynamics/IOP
lowering IOP…
dec risk for glaucoma progression
what determines if glaucoma or not?
glaucomatous changes!
- field, sensitvitiy, maybe cup:disc ratio?
normal IOP, glaucoma changes
NT glaucoma
high IOP, glaucoma changes
glaucoma
normal IOP, no glaucoma change
normal
high IOP, no glaucoma change
ocular HTN
risk factors for developing open angle glaucoma
- 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
is HTN a risk factor for POAG?
NOOOO
is smoking a risk factor for POAG?
NO
what are glaucomatous changes?
- disc change
- field defects
who to treat for glaucoma
high IOP + glaucomatous changes (disc, field)
glaucoma treatment goals
- preserve the nerve (stop damage)
- dec IOP by 25% or more vs pretreatment
is medication or surgery more effective at lowering IOP?
surgery
surgery vs medication?
can be equally effective, just need to dec IOP
surgery: invasive, one time, inc cataract risk
medication: non invasive, every day, dec cataract risk
prostaglandin Fa2 analog MoA
inc sclearal permeability –> inc uveoscleral outflow
prostaglandin Fa2 IOP reduction
25-33%
**very effective!!
prostaglandin F2a AEs
- ocular irritation (red)
- eyelash growth
- iris pigment change
which prostaglandin F2a have best efficacy
bimatoprost
latanoprost bunod
which prostaglandin analog has fewest AE
omidenepeg
then
latanoprost
which prostaglandins are generic
bimatoprost 0.03%
latanoprost
prostaglandin EP2 antagonist MoA
inc uveosclearal AND trabecular outflow
omidenepeg!
prostaglandin F CI
existing ocular inflammation
beta blocker MoA
decrease aqueous humor production
beta blocker IOP reduction
20-25%
beta blocker AE
less ocular irritation
SYSTEMIC –> cardiac, respiratory, CNS
beta blocker CI
absolute: HF, sinus bradycardia, heart block
relative: pulmonary disease
beta blocker options
timolol
carteolol
betaxolol
levobunolol
metipranolol
beta blocker best efficacy
all equal
beta blcoker with qd dosing
timolol
levobunolol
beta blocker with dec AR
betaxolol
beta blocker for asthma/copd
betaxolol —> highly selective
eye drop adminstration to dec systemic effects
hold eye duct while use
alpha 2 agonist MoA
reduce aqeuous humor production, small effect on uveosclearal outflow
alpha 2 agonist AE
ocular irritation
XEROSTOMIA (dry mouth) –> hold lacrimal duct
alpha 2 agonist options
brimonidine
brimonidine-timolol fixed combination (BTFC)
alpha 2 agonist IOP reduction
20-25%, closer to 20%
carbonic anhydrase inhibitor MoA
reduce aqueous humor production vis dec bicarbonate ion secretion
carbonic anhydrase inhibitors
topical: 15-20%
carbonic anhydrase inhibitor AE
none
carbonic anhydrase inhibitor options
brinzolamide
dorzolamide
dorzolamide-timolol FC (DTFC) –> prefer
brinzolamide-brimonidine FC (BBFC)
DTFC or bimatoprost have better diurnal control?
bimatoprost
rho kinase inhibitor MoA
- inc trabecular outflow
rho kinase IOP reduction
20% IF high initial IOP > 27 mmHg
rho kinase AE
many
conjunctival hemorrhaging
rho kinase options
netarsudil
when to switch drug class?
adherence, tolerance, poor efficacy
when to add another drug?
the current drug is almost there but not quite at goal
time to follow up
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
what is nasolacrimal occlusion
holding the lacrimal duct to prevent systemic absorption and AEs
risk factors for progression of glaucoma
- 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
which medications dec uveoscleral outflow?
- prostaglandin F2
- prostaglandin EP2
which medications dec aqueous humor production?
- beta-blockers
- alpha 2 agonist
- carbonic anhydrase inhibitors
which medcations inc trabecular outflow?
- prostaglandin E2P
- rho kinase inhibitors
why do we treat ocular HTN
delay progression to glaucoma
who do we treat for ocular HTN
ocular HTN + risk factors
risk factors:
- black/hispanic
- IOP> 25mmHg
- family Hx
- thin central cornea
- large cup/disc ratio
why do we treat NT glaucoma
preserves visual field, preserved optic disc
*same treatment goals of dec 25%
who do we treat for NT glaucoma?
NT glaucoma + documnted visual field loss (glaucoma changes)
overall, treat
- glaucoma
- NT galucoma
- ocular HTN + risk factors
goals of therapy for acute angle closure crisis
break attack to
1. preserve vision
2. prep eye for LPI (laser peripheral iridotomy) –> dec IOP, open angle, dec inflammation
first line treatments for AACC
for IOP lower:
1. acetazolamide IV or PO 500mg
2. topical beta blocker
3. topical apraclonidine
for angle opening
4. topical pilocarpine
how long do you wait to add more therapy
1 hour no change
what do you add
to dec IOP:
5. hyperosmotic –> mannitol IV, glycerin/isosorbide PO
to dec inflammation:
6. ophthalmic steroid
goal of chronic closed angle treatment
keep angle open, prevent acute attacks
chronic closed angle treatment
- same meds as open angle
- iridotomy
- counsel on acute s/s, avoid OTC that dilate pupils
atopic dermatitis patho
filaggrin deficiency –> dec natural moisturizer factor (NMF)
atopic derm non-pharm
- dec exacerbating factors
- bathing
- skin hydration
- prevent itching
JAKi drugs
-inibs
ruloxitinib – cream
abrocitinib – tab
upacitinib – tab
monoclonal antibody durgs
dupilumab
tralokinumab
immunosupressant drugs
methotrexate
cyclosporine
azathioprine
face/flexure first line
LOW POTENCY topical corticosteriods
5-7 day course!!
JAKi avoid/CI
- thrombosis
- > 50 and CV risk
- MACE
- herpes, pneumonia
- malignancy
JAKi monitoring
- liver
- kidney
- lipid
- neutrophil, hemoglobin
- viral hepatitis, TB
JAKi kidney dosing
ruloxitinib – none
abrocitinib – CI if CrCl < 30
upacitinib – CI if CrCl < 15
allergic contact dermatitis causes
- latex
- posion ivy
- metal
- TOPICAL STERIODS –> difficult bc that is the treatment
…
poison ivy causitive agent
urushiol
- mango
- unroasted cashew nuts
what do you avoid when treating toxicodendron dermatitis
- antihistamines
- topical calcineurin inhibitors
- medrol dose pack
cause of seborrheic dermatitis
Malassezia (fungus, yeast)
cradle cap
biphasic seborrheic derm (2 weeks then 12 months)
- greasy, yellow scales inscalp, forehead
first line for seborrheic derm
topical antifungal!!
- selenium sulfide
- zinc pyrithione
- ketoconazole shampoo
- ciclopirox
- coal tar
second line seborrheic derm
topical corticosteriods
topical CI
systemic antifungal
cradle cap treat
bady shampoo
soft brush
petroleum jelly, mineral oil
