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
2
Q
Atopic Dermatitis (eczema)
non pharm/ OTC
A
Non Pharm:
- Eliminate Exacerbating factors
(i. e stress, anxiety, heat, low humidity, contact allergens) - Bathing
a. warm soaking bath or showers
b. soap free or mild cleansers - 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
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
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:
- identify and avoid offending products
- treat the skin infammation
- restore the skins natural barrier
- protect the skin
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
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
7
Q
Allergic Contact Dermatitis (ACD)
Latex Allergy
Management/prevention
non pharm:
pharm:
A
- 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
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
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
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.
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.
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
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
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
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:
- Erythromycin 5mg/gram of ung.
* Dosing: 1/2 inch pid x 5-7 days - Trimethroprim/ polymyxin B 0.1%-10,000 units/ g drops
* 1-2 drops bid x 5-7 days - IF PT HAS CONTACTS, must possibly cover for pseudomonas. can consider fluoroquinolones.
- for special new born ocular bacterial infections such as neisseria gonnorhea and chalmydia trachmatis, use SYSTEMIC TREATMENT.
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:
- Vasocontrictor/ antihistamine combo
* NAphazoline/ Pheniramine (Naphcon-A, Opcon-A)
* 1-2 gtt bid - 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 - Counseling points
*symptons get worse b4 they get better
3 days or so, and may persist
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)
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:
- eye lubricant drops: 1-2 gtts up to 6x per day
- eye lubricant ung.: 1/2 inch qid pen or hs.
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
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
21
Q
Bed bug bite
Treatments
A
- avoid scratching
- low or medium potency topical steroid
- systemic antihistamine
22
Q
Pediculosis humanus captious (head lice)
transmission:
manifestation:
Treatment:
A
transmission: head ot head. hand to head
vectors. hats, pillows
manifestation: itching
Treatment:
- Permethrin 1%
- Pyrethrins and piperonyl butoxide
- Wet combing
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
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
25
Wet combing
what is it used for:
how to do it:
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
26
Body Lice (pediculosis corporis)
general treatment:
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
27
Pubic Lice (phthirus pubs)
transmission:
SS:
treatment: (including household contacts)
also what is ciliaris, and what is the pharm treatment
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
28
Scabies
```
what is it:
manifestations :
Dx:
treatment:
Counseling:
control of transmission
```
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
29
Chiggers
What is it:
Treatments:
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
30
Mosquitos
transmission:
treatment:
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
31
Ticks
what is it:
disease transmission:
How to remove tick:
Treatment:
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
32
DEET
indication:
available dosage forms and strength:
how to use:
age indication
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
33
Exclusions for self-treatment for bites
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
4. SS of secondary infection of bite area
34
Exclusions for self-treatment for stings
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
35
Patho of acne
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
36
pH of health skin
~4.7-5.7
37
types of acne lesions
1. white head (close comedones
2. black head (open comedones)
3. papules (pinhead)
4. cysts
5. nodules
6. pustules (pimple)
38
Acne Treatment:
Mild:
Moderate:
Severe:
Mild:
a. first line: Benzoyl peroxide (BP) OR topical retinoid
Moderate:
1st line: Topical combo therapy
ex: BP+ retinoid
Severe: Oral isotretinoin
39
acne classifications
mild:
moderate:
severe:
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
40
Home care of acne
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
41
vehicles used for skin types
```
dry skin:
oily skin:
hairy areas:
also...
solutions:
pledgets:
```
dry skin: lotions or creams
oily skin: gels or foams
hairy areas: foams
also. ..
solutions: drying but cover large areas
pledgets: cover large areas
42
Targeted treatment Factors for acne
Follicular/ hyperpoliferation
oral/ topical retinoids
azalea acid
salicylic acid
hormonal therapies
43
Targeted treatment Factors for acne
Increased sebum production
oral retinoids
hormonal therapies
clascoterone cream
44
Targeted treatment Factors for acne
C. acnes proliferation
benzoyl peroxide
ABX
azaleic acid
dapsone topical
45
Targeted treatment Factors for acne
inflammation
oral/opical retinoids
oral tetracyclines
azalea acid
clascoterone cream
dapsone topical
46
Targeted treatment Factors for acne
androgen receptor inhibitor
clascoterone cream
47
Topical Retinoids
ex:
effects:
side effects:
notes:
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
48
Clascoterone cream
class:
ADVERSE EFFECTS
class: androgen receptor inhibitor
Adverse effects: HPA suppression has been reported (concern w. occlusive dressings)
49
topical antimicrobials for treatment of acne
action:
adverse effects:
how to use;
product:
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)
50
oral abx for acne
ex:
adverse effects
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
51
Salicylic acid
Moa:
moa: BHA: desquaming agent. lipophylic
synergistic effect with BP
52
other acne meds
sulfur
AHA's
tea tree oil
Azaleic acid
53
Hormonal acne agents
moa:
ex:
adverse effects:
notes:
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
Oral isotretinoin
```
ex:
indication:
moa:
ci:
DDI:
```
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
Oral isotretinoin
daily dose calculation
cumulative dose calculation
micronized dose calculation
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
Oral isotretinoin
adverse effects
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
GOAL OF IPLedge program
prevent pregnancies in pts. taking isotretinoin
prevent pregnant patient from taking isotretinoin
58
equation for # of pregnancy tests over course of therapy
N+4.
| N= # of months on oral isotretinoin
59
ipledge program
do not dispense oral isotretinoin to pt after
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
non allowable forms of BC for ipledge
progesterone only mini pills
female condoms
natural family planning (rhythm method or fertility awareness)
breastfeeding
withdrawal
cervicle shield
61
oral isotretinonin monitoring
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
oral isotretinoin warnings
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
4 main Categories of Allergic Dermatologic drug reactions
exanthematous
urticarial
blistering
pustular
64
cutaneous drug eruptions
exanthematous
if no fever: simple maculopapular rash
if fever: hypersensitivity syndrome reaction (aka DRESS)
65
cutaneous drug eruptions
Urticartial
if no fever: urticaria/ angioedema
if fever: serum sickness-like
66
cutaneous drug eruptions
blistering
if no fever: fixed drug eruption
fever: SJS, TEN
67
cutaneous drug eruptions
pustular
if no fever: acneiform
fever:AGEP
68
what is the first thing you ask a pt when they present with a drug induced dermatologic problem? why?
"do you have a fever?"
fever is a hallmark sign of a severe drug reaction
69
Maculopapular Rash
```
Onset time:
Offending agents:
SS:
Risk factors: --
Treatment:
```
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
Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)
Onset time:
Offending agents:
SS:
Risk factors:
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
Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)
Treatment
1. main
2. specific treatments
3. notes
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
topical steroids potency
I. Super high
II. high
III. high
```
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
Urticartia
```
Onset time:
Offending agents:
SS: (including type of reaction)
Risk factors: --
Treatment:
```
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
Serum Sickness-Like reactions
```
Onset time:
Offending agents:
SS:
Risk factors: --
Treatment:--
```
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
Fixed Drug Eruptions
```
Onset time:
Offending agents:
SS:
Risk factors: --
Treatment: --
```
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
Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)
```
Onset time:
Offending agents:
SS: (also diff btw, SJS & TEN)
Risk factors:
Sequelae:
```
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
acute phase SJS/TEN complications that require pharmacotherapy
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
Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)
General Treatment
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
Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)
Summary of Treatments for SJS/TEN
1. systemic corticosteroids
2. IVIG
3. Cyclosporine
4. Thalidomide
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
Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)
Summary of Treatments for SJS/TEN
IVIG
1. BENEFITS:
2. RISKS
3. TAKE HOME:
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
Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)
Summary of Treatments for SJS/TEN
Cyclosporine
1. BENEFITS:
2. RISKS
3. TAKE HOME:
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
Steven -Johnson Syndrome (SJS) and Toxic Eipdermal Necrolysis (TEN)
Summary of Treatments for SJS/TEN
Thalidomide
1. BENEFITS:
2. RISKS
3. TAKE HOME:
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
Hyperpigmentation
```
Onset time:--
Offending agents:
SS:--
Risk factors: --
Treatment: --
```
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
Acute Generalized Exanthematous Pustulosis
```
Onset time:
Offending agents:--
SS:
Risk factors: --
Treatment: --
```
Onset time: < 3 days
Offending agents: --
SS: widespread erythema, pustules (small numerous), high fever, leukocytosis with neutrophilic
Risk factors: --
Treatment: --
85
Photosensitivity
```
Onset time: --
Offending agents:
SS:--
Risk factors: --
Treatment:
```
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
General management of drug induced dermatologic disorders
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
Cross reactivity of sulfa drugs and ex: of sulfa non ABX
cross reactivity btw sulfa ABX and sulfa non ABX are minimal.
ex:
* loop diuretics
* thiazide diuretics
* sulfonylureas
* sulfasalazine
* dapsone
88
Cross reactivity btw PCNs and Cephalosporins.
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
Pharmacists role in drug-induced dermatologic disorders
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
Primary Open Angle Glaucoma (POAG)
PAtho:
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
IOP as a risk factor
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
1. IOP glaucoma continuum pressure classifications
2. normal cups to disk ratio
3. Visual acuity
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
2. normal cup to disk ratio: 0.3
3. visual acuity: if acuity < 20/20, myopia (nearsightedness could be developing)
93
POAG risk factors for developing
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
Who should be treated for glaucoma
1. all patients with elevated IOP ANDDDD glaucomatous changes
95
Goals of treatment for Glaucoma
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
Main drug classes used in POAG
1. Prostalglandin analogs
2. Beta Blockers
3. Alpha Agonists
4. Carbonic anhydrase inhibitors
5. Rho kinase inhibitors
97
Drug classes used in POAG
Prostalglandin Analogs
```
examples:
MOA:
effectiveness:
adverse effects:
CI:
```
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
Drug classes used in POAG
class comparison of prostaglandin analogs
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
Drug classes used in POAG
Beta Blockers
```
examples:
MOA:
effectiveness:
adverse effects:
CI:
```
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
Drug classes used in POAG
BEta Blocker Class comparison
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
Drug classes used in POAG
Alpha-2 adrenergic agonists
```
examples:
MOA:
effectiveness:
adverse effects:
Precautions:
```
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
Brimonidine-timolol combo vs latanoprost
iop reduction:, no difference
diurnal control similar
latanoprost cheaper at this time
103
Drug classes used in POAG
Carbonic anhydrase inhibitors
```
examples:
MOA:
effectiveness:
adverse effects:
Precautions:
```
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
Drug classes used in POAG
Rho Kinase Inhibotor
```
examples:
MOA:
effectiveness:
adverse effects:
Precautions:--
```
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
First, second line options for POAG
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
Treatment Suggestions for POAG
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
time to follow up with pt in POAG
1.glaucomatous progression : follow up in 1-2 months
2. 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
Early Manifest Glaucoma Trial (EMGT) talking points
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
Risk factors for progression of POAG
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
Ocular hypertension
definition
definition: elevated IOP (>21 mmHg) and no glaucomatous changes
111
In considering treatment for pt with Ocular hypertension, who should be treated
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
Normal Tension Glaucoma definition
normal intraoccular pressure (13-21 mmHg) with signs of glaucomatous changes
113
In considering treatment for pt with Normal tension glaucoma, who should be treated
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
Primary Angle Closure Glaucoma
patho:
pupillary block (len contacts iris at pupillary margin, preventing outflow of aqueous humor
115
types of angle closure glaucoma
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
risk factors for developing angle closure glaucoma
shallow anterior chamber depth (including eastern asian ancestry), family hx, hyperopia (far sightedness), age
117
types of attacks for acute angle closure glaucoma
1. subacute: self limiting
2. Acute angle closure crisis (AACC)
* typically signaled by prodrome..
* opthalmic emergency
118
Goals of treatment for Acute Angle Closure Crisis (AACC)
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
AACC pharm treatments
IOP
1. carbonic anhydrase inhibitor
2. beta blocker
3. alpha agonist
4. hyper osmotic (last line)
120
AACC pharm treatments
angle
Pilocarpine
121
AACC pharm treatments
inflammation
ophthalmic steroid (used only after first lines used or could make it worse)
122
first lines used for AACC
1. carbonic anhydrase inhibitors
2. beta blockers
3. alpha agonist
4. pilocarpine
123
Specific AACC treatment
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
what is the Problem with pressure induced ischemia in AACC
what do we do about it ?
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
Hyperosmotics in AACC
effects:
examples:
* 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
AACC Treatment confirmation (How to know meds are working )
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
Chronic Primary AngleClosure Glaucoma (PACG)
goal of treatment:
treatment:
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
