Exam 1 Flashcards

1
Q

Atopic Dermatitis (Eczema)

Manifestations:
Pathogenesis;
epidemiology**:
Types (Severity):

A

Manifestations:

a. dry skin and severe pruritic (itching)
b. acute: erythematous papule and vesicles with exudate/ crusting
c. chronic: Dry, scaly excoriated (removal of skin) erythematous papules.

Pathogenesis:

a. Filaggarin deficiency (substance produced by keratinocytes that is broken down to produce natural moisturize factor(NMF)
b. family history of Atopy (eczema, asthma, allergic rhinitis, increased IgE, food allergies, hard water [Calcium carbonate]

epidemiology: more likely to affect black children. les likely to affect black adults. asians least likely to experience

Severity:
a.mild: areas of dry skin, infrequent itching (w. or w.o small areas of redness), little impact on everyday activities, sleep, and psychosocial wellbeing

b. moderate: areas if dry skin, frequent itching, redness (w. or w.o excoriation and localized skin thickening), moderate impact on everyday activities and psychosocial wellbeing, frequently disturbed sleep
severe: widespread dry skin, incessant (continuous) itching, redness (w. or w.o excoriation aextensive skin thickening, bleeding oozing, cracking, and alteration of pigmentation), Severe limitation of everyday activities and psychosocial functioning, nightless loss of sleep

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2
Q

Atopic Dermatitis (eczema)

non pharm/ OTC

A

Non Pharm:

  1. Eliminate Exacerbating factors
    (i. e stress, anxiety, heat, low humidity, contact allergens)
  2. Bathing
    a. warm soaking bath or showers
    b. soap free or mild cleansers
  3. maintain skin hydrations
    a. use lotions with higher oil content (avoid high water to oil content lotions

4.Avoiding Pruritis
a.oral antihistamines-especially if concurrent urticaria/ rhinoconjunctivitis
H1: diphenhydramine, hydroxyzine
H2: fexofenadine, loratadine
b. Topical Doxepin
c, Topical Calicineurin inhibitors

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3
Q

Atopic Dermatitis (Eczema) Treatment

Mild/ Moderate:
a. first line

Severe:

a. non pharm
b. pharm

A
mild-moderate:
a: FIRST LINE:TOPICAL STEROIDS
I. Denoside 0.05% cream/ung
*low potency creams/ung for mild
*BID x 2-4 weeks with emollients

II. Triamcinolone Acetonide oint. 0.5%

  • high potency
  • for moderate
  • 1-2 weeks, taper to low potency creams

III. Face, Flexures
* low potency steroids qd 5-7 days

Severe:

a. Soak and smear
* soak affected area in water for 15 min.
* do not dry, apply high potency steroid (except in face, groin, axillae)

b. Wet wraps
* mid-super potency steroids in an ung. base
* treated areas occluded with wet wraps. Wet pajamas covered by dry pajamas min 4 hrs BID

c. Photo therapy
* 2-3 times weekly
* sometimes combined with coal tar solutions

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4
Q

Allergic Contact dermatitis (General)

Causes: (8 listed)
Manifestations:
General management

:

A

Causes:

  • Latex
  • poison ivy, poison sumac, Poison Oak, Mango (CONTAIN URUSHIOL)
  • metals (nickel, cobalt, cold chromium
  • topical ABX (neomycin, polymyxin B and bacitracin)
  • Topical steroids
  • topical anesthetics (benzocaine, procaine, tetracaine)
  • propylene glycol
  • fragrance

Manifestation:
Erythematous, indurated, scaly plaques

General management:

  1. identify and avoid offending products
  2. treat the skin infammation
  3. restore the skins natural barrier
  4. protect the skin
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5
Q

Allergic Contact dermatitis (General)

Treatment

a. General
b. pharm
c. non pharm

A

a. general
* identify and avoid offending agent
* treat the skin inflammation
* restore the skins natural barrier
* protect the skin

b. PHARM
1. Topical corticosteroids
* first line
* high potency on thick skin or non-face/ flexural areas
* medium potency on face or flexures- no longer than 2 weeks
2. Topical calcineurin inhibitors (TCI)- for chronic localized ACD or ACD involving face or intergrigenous areas.
3. systemic corticosteroids- for patients with ACD >20% of BSA or for acute ACD of face, hands, feet or genetalia
4. drying agents for weeping vesicles
5. soothing agents: oatmeal baths, calamine lotion

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6
Q

Allergic Contact Dermatitis (ACD)

Toxicodendron Dermatitis

What is it:
Cross reactivity:
Presentation:
Prevention:
Treatment:
(also, what will not help)
A

Toxicodendron Dermatitis

What is it: an ACD that occurs after exposure to urushiol, a skin irritating oil produced by members of plant genus toxicodendron.

Causative agent: poison ivy, oak, sumac

Cross reactivity: mango rind, cashew nutshell, etc.

Presentation: redness, itching, swelling, blisters

Prevention:

a. avoidance; protective clothing
b. washing clothes and pets after exposure
c. barrier creams (controversial)

Treatment:
*ANTI HISTAMINES WILL NOT HELP ITCH
*TCI not effective
*but can use..
a. soothing measures, oatmeal baths and cool and wet compress
*calamine lotion for symptomatic relief
b. topical astringents (drying agents)
aluminum acetate: Burows solution
Aluminum sulfate (domeboro)
c.high potency topical steroids for up to a week
d. systemic steroids- for severe facial and genital exposures

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7
Q

Allergic Contact Dermatitis (ACD)

Latex Allergy

Management/prevention
non pharm:
pharm:

A
  1. avoidance (most effective, least expensive

Pharm treatment

a. steroids
b. self admin-epic pen to treat acute reactions

Immunotherapy

a. sub q immunotherapy
b. sub lingual immunotherapy

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8
Q

Seborrheic Dermatitis

Causes:
epidemiology**:
Manifestations

A

Causes: (theory) inflammatory reaction to Malassezia (yeast)
yeast in oil secretion
immune system overeats and causes inflammation and skin changes

epidemiology:
* biphasic incidence: infants btw ages of 2 weeks and 12 months (CRADLE CAP).
* 35% among pts. with early HIV infection, 85% among pts. with aids

manifestations:

  • well-demarcated erythematous plaques
  • worsens e. stress, cold, dry heat of winter
  • greasy yellow scales
  • distributed on areas rich in sebaceous glands such as
    a. scalp
    b. external ear
    c. center of the face
    d. upper part of the trunk
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9
Q

Seborrheic Dermatitis

pharm Management

A

a. Topical anti fungal agents
* ketoconazole 2%
* selenium sulfide 2.5%
* Zinc Pryithione 1% shampoos
* ciclopirox 1% shampoo, 0.77% ung.

b. topical steroids for symptom management

c. Systemic antifungals (severe)
* itroconazole, ketoconazole, fluconazole, terbinafine

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10
Q

Seborrheic Dermatitis

Selenium sulfide

Class:
Adverse effects:
Formulations:
Notes:

A

Class: Anti-Malessezia activity

Adverse effects: well tolerated with no adverse events

Formulations:
*1% is OTC: >2y.o BIW: apply to wet hair, massage into scalp for several min, rinse

*2.5% is rx: >2y.o BIW: apply to wet hair, massage into scalp for several min. BIW for 2 week. once a week or less there after

Notes:

  • contact time important
  • discoloration of blonde, gray or died hair may occur
  • if pt< 2 y.o consult pediatrician.
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11
Q

Seborrheic Dermatitis

Zinc Pyrothione

Class:
Adverse effects:
Formulations:
Notes:

A

Class: anti-malassezia activity. reached yeast count in scalp and skin and binds exclusively to skin of scalp and hair

Adverse effects: well tolerated, no AE

Formulations:
>2.yo: BIW apply to wet hair, massage into scalp for several min. rinse

Notes: absorption increases w, contact time, temp, conc. and freq. of application.

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12
Q

Seborrheic Dermatitis

Cradle Cap

Causes:
Manifestation:
Treatment

A

Causes: asymptomatic and non inflammatory accumulation of greasy scales (dark to yellowish) on the scalp.

manifestations: can start on face, with erythematous , scaly salmon colored plaques
* in forehead, retroauricular areas, eyebrows, eyelids, cheeks, nasolabial folds

Treatment: a. often spontaneously resolves

b. concervative measures
* baby shampoo, remove scales w. soft brush
* emolient cream (mineral oil, or petroleum jelly), then baby shampoo

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13
Q

Conjunctivitis (pink eye)

What is it:
Types:

A

what is it: inflammation of the conjunctiva of the eye (aka pink eye)

types: 
bacterial
allergic
viral
toxic
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14
Q

Conjunctivtis

General prevention

A

wash hands

keep eyes clean (wash hands b4 changing contacts)

change pillow cases frequently during infection

don’t share eye makeup

avoid allergens

avoid rubbing eyes

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15
Q

Bacterial conjunctivitis

causes:
manifestation:
Treatment:

A

causes: S. aureus, S. Pneumoniae, H influenzae, M catarrhalis

manifestation:

  • starts in one eye, but can spread in both
  • thick pus (meow, white green) at lid margins and corner of eye
  • morning crust that continues throughout the day
  • purulent discharge

Treatment:

  1. Erythromycin 5mg/gram of ung.
    * Dosing: 1/2 inch pid x 5-7 days
  2. Trimethroprim/ polymyxin B 0.1%-10,000 units/ g drops
    * 1-2 drops bid x 5-7 days
  3. IF PT HAS CONTACTS, must possibly cover for pseudomonas. can consider fluoroquinolones.
  4. for special new born ocular bacterial infections such as neisseria gonnorhea and chalmydia trachmatis, use SYSTEMIC TREATMENT.
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16
Q

Viral conjunctivitis

causes:
manifestation:
Treatment:
Counseling points:

A

Viral conjunctivitis

causes:
*most contagious
adenovirus serotypes

manifestation:

  • self limiting. 1-2 weeks
  • apart of viral prodrome: fever, pharyngitis, URI
  • burning, sandy, grit feeling
  • watery or mucous discharge
  • enlarged tender pre-auricular nodes

Treatment:

  1. Vasocontrictor/ antihistamine combo
    * NAphazoline/ Pheniramine (Naphcon-A, Opcon-A)
    * 1-2 gtt bid
  2. antihistamines with mast cell stabilizing properties (only treat symptoms. systemic doesn’t work)
    * Azelastine (Optivar) 1 gtt bid
    * Ketotifen (Zaditor) 1gtt bid
    * olopatadine (Patanol) dose cared by strength
  3. Counseling points
    *symptons get worse b4 they get better
    3 days or so, and may persist
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17
Q

Allergic conjunctivitis

SS:
types:
non pharm/ prevention:
Pharm:

A

SS: intense itching, hyperemia, tearing,chemosis, and eyelid edema

types:
* acute allergic Con. (AAC): fast onset. ends in ~24h
* seasonal acute. con. (SAC): SIMILAR TO AAC+rhinitis. slower onset and takes days-weeks associated w. pollen seasons.
* Perenniam allergic. con. (PAC): mild chronic waxingg and year round symptoms. dust, dandy,mold. etc.

non pharm/ prevention: *refrigerated artificial tears

  • cold compress and avoid contacts if possible
  • allergen reduction: frequent clean, limit outdoor exposure, replace/clean/cover pillows, blankets, mattresses, carpets, curtains

Pharm:

  • vasoconstrictors/ antihistamines: max of 2 weeks due to rebound problems
  • antihistamines w. mast cell stabilizing properties (TOPICAL)
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18
Q

Non allergic conjunctivitis

what is it:
causes:
Treatment

A

what is it: catch all for all other potential causes of conjunctivitis

causes: transient chemical or mechanical grit
* resolves within 24hrs
* dry eye has similar SS

Treatment:

  1. eye lubricant drops: 1-2 gtts up to 6x per day
  2. eye lubricant ung.: 1/2 inch qid pen or hs.
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19
Q

Toxic conjunctivitis

what is it:
causes:
SS:
Treatment:

A

what is it: direct contact to ocular tissues from preservatives or meds

causes:

  • contact lens solutions
  • artificial tears
  • topical eye meds such as
    a. amino glycoside abx
    b. antiviral meds
    c. glaucoma meds
    d. topical anesthetics

SS:redness, edema, mucus discharge, swollen eyelids, thickened eyelids

Treatment:

  • discontinue topical meds containing preservatives (benzalkonium chloride)
  • use of short course loteprednol (topical corticosteroid) qid.
  • use non BAK containing formulations
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20
Q

Flea bites

TReatments

a. non pharm
b. pharm

A

treatment:

  • avoid scratching
  • wash area
  • oral antihistamines such as cetirizine, loratadine, fezofenadine
  • topical steroids
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21
Q

Bed bug bite

Treatments

A
  1. avoid scratching
  2. low or medium potency topical steroid
  3. systemic antihistamine
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22
Q

Pediculosis humanus captious (head lice)

transmission:
manifestation:
Treatment:

A

transmission: head ot head. hand to head
vectors. hats, pillows

manifestation: itching

Treatment:

  1. Permethrin 1%
  2. Pyrethrins and piperonyl butoxide
  3. Wet combing
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23
Q

Permethrin (Nix)

indication: 
MOA:
age group:
Regimen:
Precautions:
general treatment guidance:
A
indication: Head lice
MOA: neurotoxin
age group: >/=2 months
Regimen: 
*wash hair
* do NOT use conditioner
*leave on hair for 10 min, rinse
*repeat on day 9

Precautions:

  • skin irritation
  • induc difficulty breathing in pts . ragweed allergy
  • avoid in chrysanthemum allergy
general treatment guidance:
* do not use conditioners
Rinse over sink instead of in shower
rinse w. warm water not hot to prevent vasodilation
*treat bedmates prohpyllactly
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24
Q

Pyrethin/ piperonyl butoxide (Rid)

indication: 
MOA:
age group:
Regimen:
Precautions:
general treatment guidance:
A
indication: head lice 
MOA: neurotoxin
age group:>/= 2 years
Regimen:
*apply to dry hair or other affected area
*don't use conditioner
*leave o hair for 10 min
*rinse with warm water
* repeat in 7-10 days

Precautions: skin irritation

general treatment guidance:
* do not use conditioners
Rinse over sink instead of in shower
rinse w. warm water not hot to prevent vasodilation
*treat bedmates prohpyllactly
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25
Q

Wet combing

what is it used for:
how to do it:

A

what is it used for:
alternaive to meds for removal lice

how to do it:

  • wash hair w. shampoo
  • apply conditioner
  • detangle
  • use head lice detection *comb, draw comb to ends of hair starting from roots
  • wipe and rinse comb
  • work in sections
  • repeat
  • can take 10-30 min
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26
Q

Body Lice (pediculosis corporis)

general treatment:

A
  1. ensure regular change of clean clothes
  2. throughly bathe
  3. wash clothing in hot water or throw away
  4. ironing with hot flat iron
  5. vacuums area well
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27
Q

Pubic Lice (phthirus pubs)

transmission:
SS:
treatment: (including household contacts)

also what is ciliaris, and what is the pharm treatment

A

transmission: sexual contact

SS: usually asymptomatic . if ss, USUALLY urticaria in pubic areas, maculae ceruleae (red macule)
CILARIS: reddish crusting

Treatment: 
Pubis
*topical permethrin 1% or pyrethrins+ piperonly butoxide
a. apply on cool and dry skin
b. apply. wash off after 10min
c. put on clean clothing
d.treat after 9-10 days

Ciliaris:
1. manual removal or apply ophthalmic grade Vaseline bid-qid x 10 days

household contacts:

a. avoid sex contact until both partners treated
b. don’t need to treat non sex contacts
c. evaluate for other std’S
d. machine wash clothes w. hot water
e. fumigation not necessary

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28
Q

Scabies

what is it:
manifestations :
Dx:
treatment:
Counseling:
control of transmission
A

what is it: itchy skin condition caused by a burrowing mite

manifestations :

  • intense pruritis, worse at night. w. onset of SS 3-6 weeks after infestation.
  • burrow: slightly elevated 1-2 mm long
  • crusted/ Norwegian area: pathes-> fissures->secondary bacterial, sepsis

Dx: finding mite or burrow

treatment:
NO OTC
a.Mites
1. Permethrin 5% (Elimite) cream (kills mites and eggs)
2. crusted scabies: Permethrin 5% cream + oral ivermectin
b. itching: antihistamines for up to 2 weeks

Counseling:

  1. Permethrin 5%
    * aply throughout body into skin from neck to soles of feet
    * include under fingernails and toes
    * 30g per average adult
    * include hairline, neck, temples, and forehead in geriatrics and infants
    * remove by washing after 8-14 hrs
    * apply 1-2 weeks later
    * >2 mo. old
    * if breast feeding, D/c breast feeding temporarily.

control of transmission: *treat all members of family or ppl w. close ocntact

  • machine wash fomites
  • place items in plastic bags x3 days (mites cant survive w.o human contact more than 2 days
  • fumigation not indicated
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29
Q

Chiggers

What is it:
Treatments:

A

what is it: skin disease secondary to bite of mites most common in summer and fall

fun fact: cluster of bites in certain areas due to barriers of migration such as belts, waist bands, etc.
precludes wandering

treatment:
1. vigorous soap and water
2. Repel with DEET
3. symptomatic treatment; topical antipyretics such as menthol or calamine, topical steroids, oral sedating antihistamines

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30
Q

Mosquitos

transmission:
treatment:

A

transmission: inject anticoagulant saliva: welt, pain, and itching. some pts get symptomatic fever and joint swelling

treatment: (if needed)
1. antihistamine (cetirizine, loratadine, fexofenadine)
2. topical glucocorticoid x 5-10 days
3. oral glucocorticoid

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31
Q

Ticks

what is it:
disease transmission:
How to remove tick:
Treatment:

A

what is it: parasite

disease transmission: feed on blood of humans and animals. takes about 36 hrs to transmit lyme disease
a. rocky mountain spotted fever: headache, rash, high fever, extreme exhaustion
Lyme disease: erythema migrant (bulls eye) transmitted by spirochete
long term complications: neurologic, cardiovascular, musculoskeletal, arthritis

How to remove tick:
1. sanitize bite area and tweezers
2. grab tick close to head
pull up slowly and carefully
sanitize bite area again

Treatment:
insect repellents
1. Topical N,N- diethyl-m-toluamide, commonly called DEET (most efficacious repellant

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32
Q

DEET

indication:
available dosage forms and strength:
how to use:
age indication

A

DEET

indication: repellant

available dosage forms and  strength:
sprays, solutions, creams, and wipes
conc. 10-35 % for most situations
conc. >/= 20% for ticks
conc. <30% for children

how to use: usually no ore frequently than q4-8hrs

age indication: > 2 months old

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33
Q

Exclusions for self-treatment for bites

A
  1. hypersensitivity to insect bites. resulting in systemic symptoms or symptoms away from bite area
  2. <2 years of age
  3. hx tick bite and systemic c effects indicating possible infection
  4. suspected spider bite requiring medical attention
  5. SS of secondary infection of bite area
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34
Q

Exclusions for self-treatment for stings

A
  1. Hives, excessive swelling, dizziness, weakness, N&V, difficulty breathing
  2. significant allergic response away from site of sting
  3. previous sting by honeybee, wasp or horney ( need to evaluate possible development of hypersensitivity
  4. previous severe reaction to insect bites
  5. Personal or family hx significant allergic reactions (eg. hay fever)
  6. <2 y.o
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35
Q

Patho of acne

A
  1. excess keratin cells and blockage of folic entrance due to sebum
  2. blockage of pore due to sweat, makeup, etc.
  3. WBC flow to cause inflammation
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36
Q

pH of health skin

A

~4.7-5.7

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37
Q

types of acne lesions

A
  1. white head (close comedones
  2. black head (open comedones)
  3. papules (pinhead)
  4. cysts
  5. nodules
  6. pustules (pimple)
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38
Q

Acne Treatment:

Mild:
Moderate:
Severe:

A

Mild:
a. first line: Benzoyl peroxide (BP) OR topical retinoid

Moderate:
1st line: Topical combo therapy
ex: BP+ retinoid

Severe: Oral isotretinoin

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39
Q

acne classifications

mild:
moderate:
severe:

A

mild: few -several papules/ pustules (generally <10) and no nodules
moderate: several- many papules/ pustules (10-40) along with comedones (10-40) and few to several nodules
severe: numerous or extensive papules/ pustule and many nodules

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40
Q

Home care of acne

A

gentle synthetic clearers twice a day

wash with fingers not cloths

avoid scrubs- apricot or otherwise

use water-based lotions, cosmetics, and hair products

don’t pick at lesions

skin should be dry before applying topicals

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41
Q

vehicles used for skin types

dry skin: 
oily skin:
hairy areas:
also...
solutions:
pledgets:
A

dry skin: lotions or creams

oily skin: gels or foams

hairy areas: foams

also. ..
solutions: drying but cover large areas

pledgets: cover large areas

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42
Q

Targeted treatment Factors for acne

Follicular/ hyperpoliferation

A

oral/ topical retinoids

azalea acid

salicylic acid

hormonal therapies

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43
Q

Targeted treatment Factors for acne

Increased sebum production

A

oral retinoids

hormonal therapies

clascoterone cream

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44
Q

Targeted treatment Factors for acne

C. acnes proliferation

A

benzoyl peroxide

ABX

azaleic acid

dapsone topical

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45
Q

Targeted treatment Factors for acne

inflammation

A

oral/opical retinoids

oral tetracyclines

azalea acid

clascoterone cream

dapsone topical

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46
Q

Targeted treatment Factors for acne

androgen receptor inhibitor

A

clascoterone cream

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47
Q

Topical Retinoids

ex:
effects:
side effects:
notes:

A

ex: Tretinoin, Tazarotene, etc.
effects: decrease cohesiveness of keratinocytes

side effects:
irritation
dryness
flaking of skin
transient worsening of acne
"photosensitivity
avoid OTC irritating products

avoid use in pregnancy (especially tazarotene)

allergy info: atralin -soluble fish proteins

notes: start low, go slow

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48
Q

Clascoterone cream

class:

ADVERSE EFFECTS

A

class: androgen receptor inhibitor

Adverse effects: HPA suppression has been reported (concern w. occlusive dressings)

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49
Q

topical antimicrobials for treatment of acne

action:

adverse effects:

how to use;

product:

A

action: decrease number of C. acnes colonizing skin. comedolytic

reduce inflammatory response

adverse effects: may bleach hair or clothing
erythema, scaling, xerosis, stinging/ burning
reports of life threatening hypersensitivity

how to use: apply qd, may be increased to bid or did after 2 weeks if tolerated.
benefits w.in 3 weeks max within 12 weeks

products: DIFFERIN CLEANSER: BP cleanser (don’t confuse with differin gel which is adapalene)

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50
Q

oral abx for acne

ex:
adverse effects

A

ex. tetracycline, doxycycline, minocycline.

ae:
TETRA + DOXY: photosensitivity, GI distress, CI in pregnancy and young children

mino: dizziness, drug induced lupus, skin discoloration, ci in pregnancy and young children

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51
Q

Salicylic acid

Moa:

A

moa: BHA: desquaming agent. lipophylic

synergistic effect with BP

52
Q

other acne meds

A

sulfur

AHA’s

tea tree oil

Azaleic acid

53
Q

Hormonal acne agents

moa:
ex:
adverse effects:
notes:

A

moa: inhibit androgen action in sebaceous gland

estrogen surpasses ovarian androgen production (androgen produces oil). low dose COC (contains ethynil estradiol)

sprinolactone: inhibit binding of androgens to receptors on sebaceous unit

adverse effects:
COC: thrombocytopenia embolim, esp. in smokers

spironolactone: menstrual irregularities, breast tenderness, GI upset, orthostatic hypotension, headache, dizziness, fatigue

K+ sparing diuretics: CI in renal insufficiency and hepatic dysfunction

notes: Progestin only contraception is NOT effective for acne. (they are androgenic)

54
Q

Oral isotretinoin

ex:
indication:
moa:
ci:
DDI:
A

EX: ZENATANE, AMNESTEEM, CLARAVIS, ABSRICA, ABSORICA LD is miconized

indication : moderate and severe, recalcitrant nodular acne

moa: shrinks sebaceous glands

ci: PRENANCY: category X
underlying psychiatric condition

DDI:

  • tetracyclines/doxy/mino: psudotumor cerebi( increased pressure in brain)
  • do not take w. vitamin supplements (vit. A toxicity )
55
Q

Oral isotretinoin

daily dose calculation

cumulative dose calculation

micronized dose calculation

A

daily dose calculation:
0.5 mg/kg/day in divided doses w. food

cumulative 20 week dose calculation: 120-150 mg/kg

micronized dose calculation:
0.4-0.8 mg/kg/day in divided doses (15-20 weeks max)

56
Q

Oral isotretinoin

adverse effects

A

night blindness

skin photosensitivity

eczema like rash

sry lips and cheilitis

dry eyes

muscle pain

thinning of hair, may be irreversible

dry nasal passages

headaches

stunted growth

bone marrow suppression

IBS

57
Q

GOAL OF IPLedge program

A

prevent pregnancies in pts. taking isotretinoin

prevent pregnant patient from taking isotretinoin

58
Q

equation for # of pregnancy tests over course of therapy

A

N+4.

N= # of months on oral isotretinoin

59
Q

ipledge program

do not dispense oral isotretinoin to pt after

A

more than 30 days beyond date of office visit

more than 7 days after pregnancy test

no automatic refills.

non compliance= pharmacy may be permanently deactivated from the program

60
Q

non allowable forms of BC for ipledge

A

progesterone only mini pills

female condoms

natural family planning (rhythm method or fertility awareness)

breastfeeding

withdrawal

cervicle shield

61
Q

oral isotretinonin monitoring

A

take baseline LFT and FLP

  • hepatotoxicity
  • levels decrease w. reduction of dose
  • 3xULN- recommend d/c drug

if normal, take again in 2 months

if still normal, no monitoring unless dose increases.
if abnormal, then periodically monitor

monitor CK:: if symptoms present(joint/ muscle pain), monitor for 15-50% ck elevation

62
Q

oral isotretinoin warnings

A

association w. depression/ suicide (top 10 drugs w. psychiatric effects

psychological distress

avoid dermabrasion, laser, epilation for at least 6 mo after stopping med-> risk of scarring

63
Q

4 main Categories of Allergic Dermatologic drug reactions

A

exanthematous

urticarial

blistering

pustular

64
Q

cutaneous drug eruptions

exanthematous

A

if no fever: simple maculopapular rash

if fever: hypersensitivity syndrome reaction (aka DRESS)

65
Q

cutaneous drug eruptions

Urticartial

A

if no fever: urticaria/ angioedema

if fever: serum sickness-like

66
Q

cutaneous drug eruptions

blistering

A

if no fever: fixed drug eruption

fever: SJS, TEN

67
Q

cutaneous drug eruptions

pustular

A

if no fever: acneiform

fever:AGEP

68
Q

what is the first thing you ask a pt when they present with a drug induced dermatologic problem? why?

A

“do you have a fever?”

fever is a hallmark sign of a severe drug reaction

69
Q

Maculopapular Rash

Onset time:
Offending agents:
SS:
Risk factors: --
Treatment:
A

Onset time: 7-10 days after drug initiation. (may be more rapid if prior sensitization)

Offending agents:

  • Penicillins (aminopenicillins most commonly)
  • sulfonamides
  • anticonvulsants

SS: (rash with both flat and raised parts)(basically definition)

Risk factors: –

Treatment:

  • resolves w.in 7-14 days of stopping drug.
  • aminoPCN rash can resolve spontaneously while on therapy
70
Q

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

Onset time:
Offending agents:
SS:
Risk factors:

A

Onset time: Delayed onset of 1-6 weeks after starting drug (average latency of 2-3 weeks)

Offending agents:
*allopurinol (most common)
*sulfonamides
anticonvulsants (phenobarbital, phenytoin, carbaezapine, lamotrigine
*Dapsone

SS: Exanthematous eruption plus…

  • fever
  • lymphadenopathy
  • hematologic abnormalities such as eosinophilia
  • Multiorgan involvement such as LIVER, kidneys, lung
  • affects >50% of BSA
  • facial edema in ~50% of cases
Risk factors: 
(for DRESS caused by allopurinol)
*excessive allopurinol dose
*renal dysfunction
*concamitant thiazide diuretic
*HTN
*asian ethnicity
71
Q

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

Treatment

  1. main
  2. specific treatments
  3. notes
A

MAIN

  1. stop the offending drug
  2. avoid starting new medications
    * avoid beta lactams
    * valproic acid good alternative if offending agent is another anti-epileptic
  3. Fluid electrolyte, nutrition management

SPECIFIC
is there organ involvement?
NO: high potency topical steroids 2-3 times per day for 1 week

YES: systemic steroids 0.5-2 mg/kg/day prednisone equivalents, tapered over 8-12 weeks

NOTES:
When dosing, start low and go slow

Max starting dose of allopurinol (1.5mg x eGFR( in ml/min/1.73 m^2

72
Q

topical steroids potency

I. Super high
II. high
III. high

A
I. Super high
*Clobetasol 0.05%
*Fluocinonide 0.1%
*Betamethasone sipropionate augmented 0.05%
Halobtasol 0.05%

II. High
Fluocinonide 0.05%
Halcinonide 0.1%
Betamethasone diproprionate 0.05%

III. High
Triamcinolone cream or ointment 0.5%
Desoximetasone 0.05%

73
Q

Urticartia

Onset time:
Offending agents:
SS: (including type of reaction)
Risk factors: --
Treatment:
A

Onset time:minutes-hours

Offending agents:

  • PCNS and related abx
  • sulfonamides
  • aspirin
  • opiates
  • latex

SS: Type 1 hypersensitivity reaction (IgE meidated)hives, pruritic red raised wheals

Risk factors: –

Treatment:
antihistamines (ex: diphenhydramine)

74
Q

Serum Sickness-Like reactions

Onset time:
Offending agents:
SS:
Risk factors: --
Treatment:--
A

Onset time: 1-3 weeks after starting drug. resolves in 1-2 weeks

Offending agents:

  • PCN/ cephalosporins
  • Sulfonamides

SS: urticaria, fever, arthralgias (not a true serum sickness (not a type III hypersensitivity reaction)

Risk factors: –
Treatment: –

75
Q

Fixed Drug Eruptions

Onset time:
Offending agents:
SS:
Risk factors: --
Treatment: --
A

Onset time: minutes-days. resolves win days after drug DC/

Offending agents:

  • Tetracyclines
  • Barbiturates
  • sulfonamides
  • codeine
  • phenolpthalein
  • acetominophen
  • NSAIDS

SS: simple eruptions with pruritic, erythematous, raised lesions that can blister. reoccur in same area each time drug is given. skin hyperpigmentation can last for months

Risk factors: –
Treatment: –

76
Q

Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)

Onset time:
Offending agents:
SS: (also diff btw, SJS & TEN)
Risk factors: 
Sequelae:
A

LIFE THREATENING

Onset time: 7-14 days of drug exposure

Offending agents:

  • sulfonamides
  • PCNs
  • anticonvulsants: phenytoin, carbamezapine, barbiturates, lamotrigine
  • NSAIDS
  • allopurionol

Sequelae:

  • fluid loss
  • electrolyte imbalance
  • hypotension
  • scondary infection- S. Epidermis, MRSA
  • treated w. topical wound care and topical ABX

SS: Painful bullous formation with systemic SS…

  • fever
  • headache
  • respiratory symptoms
  • mucous membrane involvement
  • Rapid spread of skin lesions causing epidermal necrosis, detachment and sloughing
  • SJS: <10% epidermal attachment
  • TEN:>30% epidermal attachment:

Risk factors:

  • HIV infection
  • Lupus (SLE)
  • malignancy
  • UV light or radiation therapy
  • genetic: HLA-B*15:02 increased risk of SJS/TEN w. carbamezapine, phenytoin, and phenobarbital (FDA recommends screen pts of asian ethnicity prior to carbamezapine
77
Q

acute phase SJS/TEN complications that require pharmacotherapy

A

fluid loss/ electrolyte imbalance

severe pain

hypovolemic shock and associated AKI

bacteremia (MRSA, pseudomonas)

hyper catabolic state

insulin resistance

pulmonary dysfunction requiring mechanical ventilation

GI dysfunction due to mucosal ulceration (poor PO intake)

multiple organ dysfunction syndrome

78
Q

Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)

General Treatment

A
  1. Withdraw offending Drug
    (check fr cross reactivities w. sulfas, PCNs.
  2. supportive care (pain management, fluid/electrolytes, nutrition
  3. Wound Care (topical antiseptics i.e chlorhexidane, silver nitrate, silver sulfadiazine, gentamicin
  4. Ophamology consult (artificial tears or ung. , corticosteroid/ antimicrobial combo drops for severe)
79
Q

Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)

Summary of Treatments for SJS/TEN

  1. systemic corticosteroids
  2. IVIG
  3. Cyclosporine
  4. Thalidomide
A
  1. systemic corticosteroids
    general observation: possible harm due to increased infectious risk and poor wound healing. beneficial w.in 24-48 hrs of onset
    take home: generally avoided unless early in course
80
Q

Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)

Summary of Treatments for SJS/TEN

IVIG

  1. BENEFITS:
  2. RISKS
  3. TAKE HOME:
A

IVIG:
benefits: 1g/kg/day x 3 days within 24-48hrs of SS onset may be beneficial
risks: doesn’t treat underlying pathology (to our knowledge), cost, BBW thromboembolic events and AKI
take home: generally not used unless severe disease early in the course

81
Q

Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)

Summary of Treatments for SJS/TEN

Cyclosporine

  1. BENEFITS:
  2. RISKS
  3. TAKE HOME:
A

Cyclosporine

benefit: 3-5 mg/kg/day has shown o slow progression of SJS/TEN but limited to case series
risks: normal side effect profile, (HTN, renal injury) but limited by short course of therapy. increased infection risk

take home: Generally not used.second line to IVIG.

82
Q

Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)

Summary of Treatments for SJS/TEN

Thalidomide

  1. BENEFITS:
  2. RISKS
  3. TAKE HOME:
A

Thalidomide
benefit: targets TNF-alpha which is involved in up regulation of immune response in SJS/TEN
risk: increased mortality in pts. with TEN.
take home: DO NOT USE for SJS/TEN! ABSOLUTELY CONTRAINDICATED.

83
Q

Hyperpigmentation

Onset time:--
Offending agents:
SS:--
Risk factors: --
Treatment: --
A

Onset time:–

Offending agents:

  • phenytoin: increased melanin
  • tetracyclines, silver, mercury, antimalarials-dirt deposition
  • amiodarone: direct deposition and/or dermal lipofuscinosis (macrophage deposition of brown pigment granules that result from lysosomal digestion).

SS:–
Risk factors: –
Treatment: –

84
Q

Acute Generalized Exanthematous Pustulosis

Onset time:
Offending agents:--
SS:
Risk factors: --
Treatment: --
A

Onset time: < 3 days

Offending agents: –

SS: widespread erythema, pustules (small numerous), high fever, leukocytosis with neutrophilic

Risk factors: –
Treatment: –

85
Q

Photosensitivity

Onset time: --
Offending agents:
SS:--
Risk factors: --
Treatment:
A

Onset time:–

Offending agents:

  • sulfonamides
  • tetracyclines
  • amiodarone
  • Coal tar

SS:–

Risk factors: –

Treatment:
*prevention; pt education about avoiding sun exposure , minimum SPF 30 sunscreen.

86
Q

General management of drug induced dermatologic disorders

A
  1. stop the offending drug
  2. avoid cross- reacting drugs
  3. supportive care (pruritis, fever)
  4. consider a short course of systemic corticosteroids for more severe manifestations.
87
Q

Cross reactivity of sulfa drugs and ex: of sulfa non ABX

A

cross reactivity btw sulfa ABX and sulfa non ABX are minimal.

ex:
* loop diuretics
* thiazide diuretics
* sulfonylureas
* sulfasalazine
* dapsone

88
Q

Cross reactivity btw PCNs and Cephalosporins.

A

85-90% of pts. who are reported to have PCN allergy will tolerate pcn.
* NEVER WERE ALLERGIC OR RESOLUTION OF HYPERSENSITIVITY OVER TIME

  • crossreactivity btw PCN and ceph. are 1-2% not 10%.
  • largely dependent on R1 side chain structure, not beta lactam ring
  • so cross reactivity is determined by side chain moieties, not beta lactam ring
    note: aminoPCNS (amoxicillin, ampicillin) have higher cross reactivity with cefadroxil, cephalexin, cefaclor, and cefprozil due to similarities in R1 side chains.

MUST PERFORM THOROUGH HX AND ASSESSMENT

89
Q

Pharmacists role in drug-induced dermatologic disorders

A
  1. identify culprit
  2. identify cross reacting drugs to also avoid
  3. sect alternative treatments for he patients underlying disroder
  4. educate patients and care givers about drug avoidance in the future
  5. differentiate and triage mild and serious drug eruptions
  6. provide pharmacotherapy recommendations for treating DIDD including supportive care measures
  7. develop monitoring plans for patients with DIDD
90
Q

Primary Open Angle Glaucoma (POAG)

PAtho:

A

patho: gradual destruction of the optic nerve due to mechanical compression on the optic nerve by aqueous humor outflow obstruction, increasing intraoccular pressure (IOP).

the higher the IOP, the worsening of glaucomatous damage

91
Q

IOP as a risk factor

A

elevated IOP does not mean you will develop glaucome

normal IOP doesn’t mean you wont develop glaucoma.

Lowering IOP reduces risk of glaucomatous progression.

92
Q
  1. IOP glaucoma continuum pressure classifications
  2. normal cups to disk ratio
  3. Visual acuity
A
  1. 13-21 mmHg: normal

> 21 mmHg: elevated.

If + glaucomatous changes:

  • 13-21 mmHg: Normal tension (N-T) glaucoma
  • > 21: glaucoma

if - glaucomatous changes

  • 13-21 mmHg: normal
  • > 21 mmHg: Occular hypertension
  1. normal cup to disk ratio: 0.3
  2. visual acuity: if acuity < 20/20, myopia (nearsightedness could be developing)
93
Q

POAG risk factors for developing

A
  1. Elevated IOP
    * >21 mmHg vs. <16mmHg=16x the risk
  2. Age (>60, >40 for black patients
  3. Family history/ genetics
  4. Race/ethnicity (black, hispanic)
  5. increased cup to disk ratio
  6. central corneal thickness (thinner CCT= elevated risk)
  7. Occular perfusion pressure (SBP or DBP minus IOP; lower=more risk
  8. T2DM
  9. Myopia (nearsightedness)
94
Q

Who should be treated for glaucoma

A
  1. all patients with elevated IOP ANDDDD glaucomatous changes
95
Q

Goals of treatment for Glaucoma

A
  1. Preserve the nerve
    * stabillize visual fields
  2. Lower IOP
    * control of target pressure: >/= 25% below pretreatment IOP. (NOT a “normal IOP)
    * readjust goal based on clinical progression
    * reassess if “target” not achieved
    * maintain adherence
96
Q

Main drug classes used in POAG

A
  1. Prostalglandin analogs
  2. Beta Blockers
  3. Alpha Agonists
  4. Carbonic anhydrase inhibitors
  5. Rho kinase inhibitors
97
Q

Drug classes used in POAG

Prostalglandin Analogs

examples:
MOA:
effectiveness:
adverse effects:
CI:
A

examples:
* Bimatoprost (BIM)
* Latanoprost (LTN)
* Latanoprostene bunod (LBN)

MOA:unconfirmed, but believed to be either uvosclerl or trabecular outflow

effectiveness: all reduce IOP by 25-33%

adverse effects:

  • local: 15-45% conjunctival hyperemia (red eyes), hypertrichosis (hair growth), periocular/ iris pigmentation changes
  • systemic: headache

CI: existing ocular inflammation (keratitis, iritis,uveitis, macular edema)

98
Q

Drug classes used in POAG

class comparison of prostaglandin analogs

A
  1. Efficacy
    a. preffered: BIM-LLBN
    b. alternative: others
  2. Burning/stinging/hyperemia
    a. prefered: LB=LTN (least likely to cause these side effects)
    b. alternatives: others (BIM most likely to cause these sideeffects
  3. Generic availability
    a. preferred: BIM 0.03%, LTN, TRV
    b. alternatives: bim 0.01%, LBN, others
99
Q

Drug classes used in POAG

Beta Blockers

examples:
MOA:
effectiveness:
adverse effects:
CI:
A

examples: betaxalol(BTX), carteolol(CAR), levobunolol(LVB), metipranolol (MTP), timolol(TIM)

MOA: decrease aqueous humor production

effectiveness: reduce IOP 20-25% (all agents about equally efficacious

adverse effects:

  • local irritation (switch product/ form)
    systemic: cardiac (conduction, contractility, pressure), pulmonary, CNS
  • tachyphylaxis (20-25%)

CI:
sinus bradycardia, heart block, HF (absolute), pulmonary disease (relative)

100
Q

Drug classes used in POAG

BEta Blocker Class comparison

A
  1. convenience
    a. preffered: LVB,TIM QD sol, gel
    b. alternatives: other
  2. systemic side effect risk:
    a. preffered (lower risk): BTX, CAR
    b. alternative: others
  3. generic availability: a. preferred: BTX sol, CAR, LVB, MTP, TIM
    b. BTX susp.
101
Q

Drug classes used in POAG

Alpha-2 adrenergic agonists

examples:
MOA:
effectiveness:
adverse effects:
Precautions:
A

examples: brimonidine

MOA: reduce aqueous humor production by the cilia body. bromonidine also has a weak effect on uveoscleral aqueous humor outflow

effectiveness: reduces IOP by 20-25% (depends on how long vs last dose). proposed neuroprotective effect

adverse effects:

  • local irritation and side effects: conjunctival hyperemia, irritation, (burning and stinging), allergic reactions
  • systemic: drowsiness, xerostomia[ (dry mouth), (up to 30%)
  • tachyphylaxis

Precautions: cardiovascular diseases

102
Q

Brimonidine-timolol combo vs latanoprost

A

iop reduction:, no difference

diurnal control similar

latanoprost cheaper at this time

103
Q

Drug classes used in POAG

Carbonic anhydrase inhibitors

examples:
MOA:
effectiveness:
adverse effects:
Precautions:
A

examples: acetazolamide (oral)
brinzolamide
dorzolamide
methazolamide (oral)

MOA: reduced aqueous humor production by the ciliary body via decrease in bicarbonate ion secretion.
(topical chi ARE SPECIFIC FOR THE ISOZOME carbonic anhydrase II

effectiveness: reduce IOP 15-20% (topical), 20-30% (oral)

favorable adverse event profile

104
Q

Drug classes used in POAG

Rho Kinase Inhibotor

examples:
MOA:
effectiveness:
adverse effects:
Precautions:--
A

examples:
Netarsudil

MOA: postulated mechanism of improving trabecular outflow. decreased actin-myosin contractions

effectiveness: ~20% IOP decreases if IOP <27 mmHg

adverse effects:
high rate of undesirable AE; hyperemia (53%), conjunctival hemorrhage (20%)

Precautions:–

105
Q

First, second line options for POAG

A

first line:

  • prostaglandin analogs (1A preferred)
  • beta-blockers (1b alternative)

second line:

  • dorzolamide: using (DTFC)
  • brimonidine (alt 1st-line if other agents contraindicated)
  • 2C brinzolamide, dorzolamide alon or oral CAIs
  • 2D: netarsudil
106
Q

Treatment Suggestions for POAG

A
  1. fewest drugs, lowest concentrations
  2. stress convenience for pt. (simple regimen)
  3. stress adherence to pt.
  4. educate on nasolacrimal occlusion (decreases systemic absorption)
  5. not at goal?
    * switch: adherence or tolerance issues, poor efficacy
    * add: one drug helps but not quite at goal
107
Q

time to follow up with pt in POAG

A

1.glaucomatous progression : follow up in 1-2 months

  1. no glaucomatous progression
    a; IOP target not achieved-> followup in 3-6 months
    b. IOP target achieved:
    I. target met for>6 mo.-> follow up in 6-12 months
    II. target met for = 6 mo.-> follow up in 6 months.
108
Q

Early Manifest Glaucoma Trial (EMGT) talking points

A
  1. reducing IOP reduces risk of progression (but decreasing by 25% doesn’t stop progression all together)
  2. there are clear risk factor for progression (age, high baseline IOP, bilateral disease, untreated disease), however large interpt. variability.
109
Q

Risk factors for progression of POAG

A
  1. iOP
    * higher at baseline
    * higher at follow up
    * higher yearly mean
  2. older age
  3. disc hemmorhage
  4. large cup to disk ratio
  5. thinner central cornea
  6. lower ocular perfusion pressure
  7. poorer adherence to medications
  8. progression in fellow eye
110
Q

Ocular hypertension

definition

A

definition: elevated IOP (>21 mmHg) and no glaucomatous changes

111
Q

In considering treatment for pt with Ocular hypertension, who should be treated

A
  1. all patients with elevated IOP ANDDD confirmed disc changes/ field defects
  2. those with OH ANDDD risk factors such as ethnicity, family hx, thin central cornea, large cup to disk ratio, IOP> 25 mmHg
112
Q

Normal Tension Glaucoma definition

A

normal intraoccular pressure (13-21 mmHg) with signs of glaucomatous changes

113
Q

In considering treatment for pt with Normal tension glaucoma, who should be treated

A
  1. all patients with elevated IOP ANDDD confirmed disc changes/ field defects
  2. those with OH ANDDD risk factors such as ethnicity, family hx, thin central cornea, large cup to disk ratio, IOP> 25 mmHg
  3. those with NTG AND documented progression of visual field loss
114
Q

Primary Angle Closure Glaucoma

patho:

A

pupillary block (len contacts iris at pupillary margin, preventing outflow of aqueous humor

115
Q

types of angle closure glaucoma

A
  1. normal/high IOP, but no subacute attacks
  2. normal/high IOP with infrequent Acute Angle Closure Crisis (AACC)
    * rapid vision damage
    * wild IOP fluctuations (up to 80 mmHg)
    * medical emergency
    * typically unilateral
116
Q

risk factors for developing angle closure glaucoma

A

shallow anterior chamber depth (including eastern asian ancestry), family hx, hyperopia (far sightedness), age

117
Q

types of attacks for acute angle closure glaucoma

A
  1. subacute: self limiting
  2. Acute angle closure crisis (AACC)
    * typically signaled by prodrome..
    * opthalmic emergency
118
Q

Goals of treatment for Acute Angle Closure Crisis (AACC)

A

medically break attack quickly to..

  1. preserve vision (reduce damage to optic nerve)
  2. prep eye for laser peripheral iridotomy (LPI)
    * redcue IOP
    * open angle
    * reduce inflammation/ edema/ pain

Treat contralateral eye

119
Q

AACC pharm treatments

IOP

A
  1. carbonic anhydrase inhibitor
  2. beta blocker
  3. alpha agonist
  4. hyper osmotic (last line)
120
Q

AACC pharm treatments

angle

A

Pilocarpine

121
Q

AACC pharm treatments

inflammation

A

ophthalmic steroid (used only after first lines used or could make it worse)

122
Q

first lines used for AACC

A
  1. carbonic anhydrase inhibitors
  2. beta blockers
  3. alpha agonist
  4. pilocarpine
123
Q

Specific AACC treatment

A

Drug for IOP

  1. IV or PO CAI
    * 500 mg acetazolamide (not ER)
    * IV can drop IOP in little as 2 min, PO has 2 hr onset. generally use iv if severe and pt is N&V, PO for less severe
  2. Topical beta blocker
  3. Topical alpha agonist
    * apraclonidine preffered

drug for ANGLE
1. Pilocarpine
induces mitosis (constricts)
constricts iris and pulls it away from touching lens
side effects: spasm, headache, brow ache, lid twitch

124
Q

what is the Problem with pressure induced ischemia in AACC

what do we do about it ?

A

so much pressure that there is no bloodflow, causing decreased delivery of medications used to treat

if first line drugs do not work after 1 hour, use hyperosmotics

125
Q

Hyperosmotics in AACC

effects:
examples:

A
  • reduce virtuous volume
  • will produce quickest and largest IOP decreases
  1. glycerin or isosorbide 1-2g/kg
    * glycerin: keto acidosis in diabetic patients
  2. IV mannitol 1.5-2 g/kg
    * circulatory overload (hospital setting)
126
Q

AACC Treatment confirmation (How to know meds are working )

A
  1. IOP low, angle open, pupil miotic
    * clinician check IOP q 15-30 min
    * check angle when IOP drops into normal range
  2. at 1 hour
    * hyperosmotic prn high IOP
    * repeat doses of BB, alpha agonist, pilocarpine,
    * may add apthalmic steroid
127
Q

Chronic Primary AngleClosure Glaucoma (PACG)

goal of treatment:
treatment:

A

GOAL: KEEP ANGLE OPEN, REDUCE RISK OF ATTACH

treatment: similar to/ treated same way as POAG
* OPTHALMIC PROSTALGLANDINS
* beta blockers

*iridotomy

  • counsel pt about importance of emergent acute attacks (seek medical attention if symptoms)
  • avoid OTC drugs that can cause pupil dilation