Skin and Eye Disorders Flashcards
Normal functions of skin
protection
sensation
thermoregulation
immunomodulation
production of vitamin D
layers of the skin
epidermis
dermis
hypodermis
epidermis
thinnest layer
avascular
normal skin flora here
Glaucoma
Damage to optic nerve that leads to visual field loss and blindness
skin flora of the epidermis
staph epidermidis
staph aureus
Candida albicans
4 layers of epidermis
cornified
granular
spinous
basal
What is glaucoma characterized by?
Changes in optic disc
Elevated IOP
dermis
thickest
nutrition and support
hair follicles, sebaceous glands and sweat glands
the type of cells in the dermis and what they do
fibroblasts - collagen and scar formation
macrophages - immune regulators and growth regulators
Types of Glaucoma
Open-angle glaucoma (OAG)
Closed-angle glaucoma (CAG)
the dermis contains multiple
nerve endings, lymphatics and vasculature
What is aqueous humor produced by?
Ciliary body
hypodermis
variable thickness
fat storage
provides insulation, padding, protection
mobility
protects from friction
Where is aqueous humor secreted?
Into posterior chamber
growths
cysts, raised bumps on skin
Pathway of aqueous humor
Pressure pushes aqueous humor between iris and lens, through pupil to the anterior chamber
rashes
dermatitis
inflammatory skin condition
macules and patches
flat areas of discoloration
papules and plaques
elevated palpable lesions
vesicles and bullae
fluid filled spaces within the skin
Aqueous humor leaves eye through
- Filtration through trabecular meshwork to Schlemm’s canal
- Through ciliary body - uveosceral outflow
pustules
vesicles/bulla with purulent fluid
nodules
solid, rounded skin lesion
common skin disorders include
acne
psoriasis
atopic dermatitis
dermatologic drug reactions
acne
chronic multifactorial disease
most common in urban areas
can cause scarring and hyperpigmentation
overall equal in men and women
Normal IOP
10-21 mmHg
IOP is regulated by
Production and outflow of aqueous humor
IOP at risk for glaucoma
> 22 mmHg
acne in adolescents is more severe in ______
acne in adults is more severe in ______
boys
women
4 major factors of acne
increased sebum production
alteration of keratinization process
bacterial colonization
production of inflammatory mediators
IOP is higher in the am or pm?
AM
environmental etiology of acne
exacerbated by heat/humidity
friction, clothing, hairstyles can have a negative impact
sunlight can improve acne in some
Classification of Gluacoma
Primary or Secondary
Risk factors for Open-angle Glaucoma
Older, IOP level, Myopia, African/hispanic, Type 2 DM
diet etiology of acne
dairy
high glycemic load diet
increased saturated fats
can smoking have an effect on acne?
yes
Risk factors for Angle-closure Glaucoma
Older, ocular trauma, female, Asian, hyperopia, pseudoexfoliation
in acne, puberty leads to
maturation of adrenal glands which increase androgen and sebaceous gland activity
when the sebaceous lipid profile is altered due to stress, irritation, etc. , it leads to
inflammation and formation of acne lesions
Open-Angle Glaucoma
Progressive, chronic optic neuropathy
sebum
induced by different receptors (histamine, DHT, CRH, IGF, peroxisome-proliferator activated receptors)
Pathophys of OAG
Blockage of trabecular meshwork –> changes in aqueous outflow –> High IOP
when linoleum acid is decreased, what happens to sebum?
sebum production increases
Along with high IOP, OAG must present
Optic disc/retinal nerve fiber structural abnormalities
Visual field abnormalities
C. Acne activates both the
innate immunity and T cell response
C. Acne produces _______ that hydrolyzes sebum triglycerides into ________________ which lead to _________________
lipase
free fatty acids
increased keratinization
C. Acne leads to ____________ lesions which lead to
inflammatory
scarring and hyperpigmentation
noninflammatory lesions presentation
closed comedones (rupture easy)
open comedones (stable)
inflammatory lesions presentation
papules/pustules (raised, white with pus)
nodules (warm, tender, firm)
cysts (inflamed, double comedones)
Acute Angle-Closure Glaucoma
Acute attack = medical emergency
Very high IOP may lead to complete pupillary blockage
acne can be anywhere on the body besides for
palms and soles
Pathophys of Acute Angle-Closure Glaucoma
Pupil dilates to where iris contracts and may adhere to lens –> blocks flow of aqueous humor –> complete blockage
Psoriasis
chronic, autoimmune T lymphocyte mediated systemic disease
Psoriasis presents as
sharply marginated and erythematous silvery scales with fixed plaques
the most common type of psoriasis
plaque psoriasis
plaque psoriasis
most common
raised red lesions covered in silvery white scales on the knees, scalp, elbows and back
What medications can you not take with angle-closure glaucoma?
Ones with anticholinergic properties
Psoriatic arthritis
1/3 patients
joint stiffness and pain
can lead to permanent irreversible joint damage
other forms of psoriasis
guttate
inverse
pustular
erythrodermic
nail
Non-acute closed angle glaucoma
IOP is usually normal
psoriasis genetic factors
PSORS1 chromsome 6
Drug-induced OAG
Corticosteroids
precipitating factors that trigger abnormal immune response is psoriasis
injury
infection
alcohol, smoking
obesity
stress
drugs - beta blockers
Drug-induced angle-closure glaucoma
Anticholinergics
Miotics
Amphetamines
Decongestants
types of medications that can worsen preexisting psoriasis
NSAIDS
lithium
antimalarials
beta-blockers
fluoxetine
corticosteroid withdrawal
Symptoms of OAG early disease
Asymptomatic
Slightly high IOP
Decreased outflow
Optic disc changes
comorbidities of psoriasis due to chronic inflammation
CV disease
insulin resistance
psoriasis pathophysiology
genetic/environmental stimuli
innate immune response –> cytokine release
adaptive immunity activates T cells –> more cytokine release
epidermal hyperplasia, dermal inflammation, silvery scales
Symptoms of OAG advanced disease
Gradual vision loss
Elevated IOP
Optic nerve degeneration
Psoriasis comorbidities
Psoriatic arthritis
metabolic syndrome
CV disease
Chron’s disease
MS
malignancies
psychiatric (depression)
decreased life expectancy (atherosclerosis/CV disease)
clinical presentation of plaque psoriasis
lesions/plaques are red-violet color, well demarcated
silver, flaking scales, bleeding
pruritis (50%)
Eczema is more prevalent in…
Young children
plaque psoriasis is mold, moderate, severe depending on
BSA involvement
Genetic predispositions to eczema include
- Skin barrier dysfunction
- FLG gene mutation
- Th2-helper cell imbalance
skin lesions of plaque psoriasis are in
a specific area (knees, elbows)
dermatologic drug interactions account for
15-20% of all ADRs
risk factors of dermatologic drug interactions
previous drug reaction
multiple drug therapy
concurrent illness
dosage increase
comorbidities
Th2-helper cell imbalance
Leads to increased IL production –> increased serum IgE –> inflammation
Pathophys of Atopic Dermatitis
Dendritic cells meet allergens and enhance Th2 cells –> increased IgE and ILs
Reduced AMPs –> increased susceptibility to infections
irritant drug reactions
topical route
localized irritation
allergic drug reactions
topical/systemic
induces an immune reaction, may first present as a skin reaction and become systemic
type 1 allergic reaction
immediate (IgE)
allergen binds to IgE –> release inflammatory mediators
type 2 allergic reaction
delayed
cytotoxic cell destruction
Atopic Dermatitis Predisposing Factors
Climate, infections, genetics
Allergens
type 3 allergic reaction
delayed (immune complex)
antigen antibody complexes form and deposit on blood vessel walls
Clinical presentation of Atopic Dermatitis
Atopic pleat
Headlight sign
Hyperpigmented eyelids
Keratosis pilaris
Lichenification
type 4 allergic reaction
delayed (T cell mediated)
antigen cause activation of T lymphocytes which release cytokines
type 1 allergic reaction signs
urticaria/angioderma
type 3 allergic reaction signs
serum sickness
vasculitis
drug induced lupus
type 4 allergic reaction signs
contact dermatitis
maculopapular rashes
exanthems
Essential features of Atopic Dermatitis
Pruritus
Eczema
Minor features of Atopic Dermatitis
Early onset
Atopy
Xerosis
type 1 allergic reaction drug causes
penicillin (anaphylaxis)
type 3 allergic reaction drug causes
penicillin - serum sickness
minocycline - vasculitis
type 4 allergic reaction drug causes
sulfonamide antibiotics
penicillins
TB PPD test
Vasculitis
Inflammation and blood vessel wall necrosis
exanthems
rash without fever, most common
urticaria and angioedema
blistering
pustular
Vasculitis involves
papules, nodules, ulcerations, vesiculobullous lesions
exanthems includes
Severe cutaneous adverse reactions to drugs (SCARs)
SJS/TEN
DRESS
Anaphylaxis - Type 1 hypersensitivity
life threatening
usually immune mediated
acute onset and can have a late phase
Drugs that can cause vasculitis
Allopurinol
Penicillins
Sulfonamides
Thiazides
Phenytoin
Vancomycin
acute onset of anaphylaxis includes
skin, respiratory tract and decrease in blood pressure
DRESS
Drug Rash with Eosinophilia and Systemic Symptoms
most common medications causing anaphylaxis
penicillins, aspirin, NSAIDs and insulin
1st skin symptoms of anaphylaxis
flushing, pruritus, urticaria and angioedema
Triad for DRESS
- Rash
- Eosinophilia
- Internal organ involvement
2nd respiratory symptoms of anaphylaxis
throat and chest tightness, dysphagia, dysphonia, hoarseness, cough, stridor, SOB
Drugs associated with DRESS
Anticonvulsants
Allopurinol
Sulfonamides
3rd symptoms of anaphylaxis include
dizziness, hypotension and GI symptoms
most fatal symptoms of anaphylaxis
respiratory symptoms
Erythema multiforme (EM)
Round ‘bull’s eye’ rings
Not always associated with drug reactions –> herpes simplex
Stevens-Johnson Syndrome (SJS)
Severe EM
Flu-like symptoms
Rash and exfoliation of skin
Toxic Epidermal Necrolysis (TEN)
Severe SJS
Cytotoxic T-cells –> proteases cleave keratinocyte proteins –> apoptosis
Dermatologic Emergencies
SJS and TEN
SCARs
SJS
TEN
EM
Progression of SCARs
Include mucous membrane erosion and epidermal detachment
Complications of SCARs
Permanent visual impairment
Nail loss, scarring
Irregular pigmentation
Drugs that cause SCARs
Sulfonamides (TMP-SMX)
Allopurinol
Penicillins
Carbamazepine
Cephalosporins
SJS and TEN Pathophys
Type IV Hypersensitivity Reactions
Cytotoxic T cells attack epithelial cells in mucosa and epidermis
