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Pathophysiology > Skin and Eye Disorders > Flashcards

Skin and Eye Disorders Flashcards

1
Q

Normal functions of skin

A

protection
sensation
thermoregulation
immunomodulation
production of vitamin D

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2
Q

layers of the skin

A

epidermis
dermis
hypodermis

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3
Q

epidermis

A

thinnest layer
avascular
normal skin flora here

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4
Q

Glaucoma

A

Damage to optic nerve that leads to visual field loss and blindness

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5
Q

skin flora of the epidermis

A

staph epidermidis
staph aureus
Candida albicans

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6
Q

4 layers of epidermis

A

cornified
granular
spinous
basal

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7
Q

What is glaucoma characterized by?

A

Changes in optic disc
Elevated IOP

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8
Q

dermis

A

thickest
nutrition and support
hair follicles, sebaceous glands and sweat glands

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9
Q

the type of cells in the dermis and what they do

A

fibroblasts - collagen and scar formation
macrophages - immune regulators and growth regulators

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10
Q

Types of Glaucoma

A

Open-angle glaucoma (OAG)
Closed-angle glaucoma (CAG)

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11
Q

the dermis contains multiple

A

nerve endings, lymphatics and vasculature

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12
Q

What is aqueous humor produced by?

A

Ciliary body

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13
Q

hypodermis

A

variable thickness
fat storage
provides insulation, padding, protection
mobility
protects from friction

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14
Q

Where is aqueous humor secreted?

A

Into posterior chamber

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15
Q

growths

A

cysts, raised bumps on skin

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16
Q

Pathway of aqueous humor

A

Pressure pushes aqueous humor between iris and lens, through pupil to the anterior chamber

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17
Q

rashes

A

dermatitis
inflammatory skin condition

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18
Q

macules and patches

A

flat areas of discoloration

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19
Q

papules and plaques

A

elevated palpable lesions

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20
Q

vesicles and bullae

A

fluid filled spaces within the skin

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21
Q

Aqueous humor leaves eye through

A
  1. Filtration through trabecular meshwork to Schlemm’s canal
  2. Through ciliary body - uveosceral outflow
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22
Q

pustules

A

vesicles/bulla with purulent fluid

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23
Q

nodules

A

solid, rounded skin lesion

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24
Q

common skin disorders include

A

acne
psoriasis
atopic dermatitis
dermatologic drug reactions

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25
Q

acne

A

chronic multifactorial disease
most common in urban areas
can cause scarring and hyperpigmentation
overall equal in men and women

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26
Q

Normal IOP

A

10-21 mmHg

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27
Q

IOP is regulated by

A

Production and outflow of aqueous humor

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28
Q

IOP at risk for glaucoma

A

> 22 mmHg

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29
Q

acne in adolescents is more severe in ______
acne in adults is more severe in ______

A

boys

women

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30
Q

4 major factors of acne

A

increased sebum production
alteration of keratinization process
bacterial colonization
production of inflammatory mediators

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31
Q

IOP is higher in the am or pm?

A

AM

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32
Q

environmental etiology of acne

A

exacerbated by heat/humidity
friction, clothing, hairstyles can have a negative impact
sunlight can improve acne in some

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33
Q

Classification of Gluacoma

A

Primary or Secondary

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34
Q

Risk factors for Open-angle Glaucoma

A

Older, IOP level, Myopia, African/hispanic, Type 2 DM

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35
Q

diet etiology of acne

A

dairy
high glycemic load diet
increased saturated fats

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36
Q

can smoking have an effect on acne?

A

yes

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37
Q

Risk factors for Angle-closure Glaucoma

A

Older, ocular trauma, female, Asian, hyperopia, pseudoexfoliation

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38
Q

in acne, puberty leads to

A

maturation of adrenal glands which increase androgen and sebaceous gland activity

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39
Q

when the sebaceous lipid profile is altered due to stress, irritation, etc. , it leads to

A

inflammation and formation of acne lesions

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40
Q

Open-Angle Glaucoma

A

Progressive, chronic optic neuropathy

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41
Q

sebum

A

induced by different receptors (histamine, DHT, CRH, IGF, peroxisome-proliferator activated receptors)

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42
Q

Pathophys of OAG

A

Blockage of trabecular meshwork –> changes in aqueous outflow –> High IOP

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43
Q

when linoleum acid is decreased, what happens to sebum?

A

sebum production increases

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44
Q

Along with high IOP, OAG must present

A

Optic disc/retinal nerve fiber structural abnormalities
Visual field abnormalities

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45
Q

C. Acne activates both the

A

innate immunity and T cell response

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46
Q

C. Acne produces _______ that hydrolyzes sebum triglycerides into ________________ which lead to _________________

A

lipase

free fatty acids

increased keratinization

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47
Q

C. Acne leads to ____________ lesions which lead to

A

inflammatory

scarring and hyperpigmentation

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48
Q

noninflammatory lesions presentation

A

closed comedones (rupture easy)

open comedones (stable)

49
Q

inflammatory lesions presentation

A

papules/pustules (raised, white with pus)

nodules (warm, tender, firm)

cysts (inflamed, double comedones)

50
Q

Acute Angle-Closure Glaucoma

A

Acute attack = medical emergency
Very high IOP may lead to complete pupillary blockage

51
Q

acne can be anywhere on the body besides for

A

palms and soles

52
Q

Pathophys of Acute Angle-Closure Glaucoma

A

Pupil dilates to where iris contracts and may adhere to lens –> blocks flow of aqueous humor –> complete blockage

53
Q

Psoriasis

A

chronic, autoimmune T lymphocyte mediated systemic disease

54
Q

Psoriasis presents as

A

sharply marginated and erythematous silvery scales with fixed plaques

55
Q

the most common type of psoriasis

A

plaque psoriasis

56
Q

plaque psoriasis

A

most common
raised red lesions covered in silvery white scales on the knees, scalp, elbows and back

57
Q

What medications can you not take with angle-closure glaucoma?

A

Ones with anticholinergic properties

58
Q

Psoriatic arthritis

A

1/3 patients
joint stiffness and pain
can lead to permanent irreversible joint damage

59
Q

other forms of psoriasis

A

guttate
inverse
pustular
erythrodermic
nail

60
Q

Non-acute closed angle glaucoma

A

IOP is usually normal

61
Q

psoriasis genetic factors

A

PSORS1 chromsome 6

62
Q

Drug-induced OAG

A

Corticosteroids

63
Q

precipitating factors that trigger abnormal immune response is psoriasis

A

injury
infection
alcohol, smoking
obesity
stress
drugs - beta blockers

64
Q

Drug-induced angle-closure glaucoma

A

Anticholinergics
Miotics
Amphetamines
Decongestants

65
Q

types of medications that can worsen preexisting psoriasis

A

NSAIDS
lithium
antimalarials
beta-blockers
fluoxetine
corticosteroid withdrawal

66
Q

Symptoms of OAG early disease

A

Asymptomatic
Slightly high IOP
Decreased outflow
Optic disc changes

67
Q

comorbidities of psoriasis due to chronic inflammation

A

CV disease
insulin resistance

68
Q

psoriasis pathophysiology

A

genetic/environmental stimuli
innate immune response –> cytokine release
adaptive immunity activates T cells –> more cytokine release
epidermal hyperplasia, dermal inflammation, silvery scales

69
Q

Symptoms of OAG advanced disease

A

Gradual vision loss
Elevated IOP
Optic nerve degeneration

70
Q

Psoriasis comorbidities

A

Psoriatic arthritis
metabolic syndrome
CV disease
Chron’s disease
MS
malignancies
psychiatric (depression)
decreased life expectancy (atherosclerosis/CV disease)

71
Q

clinical presentation of plaque psoriasis

A

lesions/plaques are red-violet color, well demarcated
silver, flaking scales, bleeding
pruritis (50%)

72
Q

Eczema is more prevalent in…

A

Young children

73
Q

plaque psoriasis is mold, moderate, severe depending on

A

BSA involvement

74
Q

Genetic predispositions to eczema include

A
  1. Skin barrier dysfunction
  2. FLG gene mutation
  3. Th2-helper cell imbalance
75
Q

skin lesions of plaque psoriasis are in

A

a specific area (knees, elbows)

76
Q

dermatologic drug interactions account for

A

15-20% of all ADRs

77
Q

risk factors of dermatologic drug interactions

A

previous drug reaction
multiple drug therapy
concurrent illness
dosage increase
comorbidities

78
Q

Th2-helper cell imbalance

A

Leads to increased IL production –> increased serum IgE –> inflammation

79
Q

Pathophys of Atopic Dermatitis

A

Dendritic cells meet allergens and enhance Th2 cells –> increased IgE and ILs
Reduced AMPs –> increased susceptibility to infections

80
Q

irritant drug reactions

A

topical route
localized irritation

81
Q

allergic drug reactions

A

topical/systemic
induces an immune reaction, may first present as a skin reaction and become systemic

82
Q

type 1 allergic reaction

A

immediate (IgE)
allergen binds to IgE –> release inflammatory mediators

83
Q

type 2 allergic reaction

A

delayed
cytotoxic cell destruction

84
Q

Atopic Dermatitis Predisposing Factors

A

Climate, infections, genetics
Allergens

85
Q

type 3 allergic reaction

A

delayed (immune complex)
antigen antibody complexes form and deposit on blood vessel walls

86
Q

Clinical presentation of Atopic Dermatitis

A

Atopic pleat
Headlight sign
Hyperpigmented eyelids
Keratosis pilaris
Lichenification

87
Q

type 4 allergic reaction

A

delayed (T cell mediated)
antigen cause activation of T lymphocytes which release cytokines

88
Q

type 1 allergic reaction signs

A

urticaria/angioderma

89
Q

type 3 allergic reaction signs

A

serum sickness
vasculitis
drug induced lupus

90
Q

type 4 allergic reaction signs

A

contact dermatitis
maculopapular rashes
exanthems

91
Q

Essential features of Atopic Dermatitis

A

Pruritus
Eczema

92
Q

Minor features of Atopic Dermatitis

A

Early onset
Atopy
Xerosis

93
Q

type 1 allergic reaction drug causes

A

penicillin (anaphylaxis)

94
Q

type 3 allergic reaction drug causes

A

penicillin - serum sickness
minocycline - vasculitis

95
Q

type 4 allergic reaction drug causes

A

sulfonamide antibiotics
penicillins
TB PPD test

96
Q

Vasculitis

A

Inflammation and blood vessel wall necrosis

97
Q

exanthems

A

rash without fever, most common
urticaria and angioedema
blistering
pustular

98
Q

Vasculitis involves

A

papules, nodules, ulcerations, vesiculobullous lesions

99
Q

exanthems includes

A

Severe cutaneous adverse reactions to drugs (SCARs)
SJS/TEN
DRESS

100
Q

Anaphylaxis - Type 1 hypersensitivity

A

life threatening
usually immune mediated
acute onset and can have a late phase

101
Q

Drugs that can cause vasculitis

A

Allopurinol
Penicillins
Sulfonamides
Thiazides
Phenytoin
Vancomycin

102
Q

acute onset of anaphylaxis includes

A

skin, respiratory tract and decrease in blood pressure

103
Q

DRESS

A

Drug Rash with Eosinophilia and Systemic Symptoms

104
Q

most common medications causing anaphylaxis

A

penicillins, aspirin, NSAIDs and insulin

105
Q

1st skin symptoms of anaphylaxis

A

flushing, pruritus, urticaria and angioedema

106
Q

Triad for DRESS

A
  1. Rash
  2. Eosinophilia
  3. Internal organ involvement
107
Q

2nd respiratory symptoms of anaphylaxis

A

throat and chest tightness, dysphagia, dysphonia, hoarseness, cough, stridor, SOB

108
Q

Drugs associated with DRESS

A

Anticonvulsants
Allopurinol
Sulfonamides

109
Q

3rd symptoms of anaphylaxis include

A

dizziness, hypotension and GI symptoms

110
Q

most fatal symptoms of anaphylaxis

A

respiratory symptoms

111
Q

Erythema multiforme (EM)

A

Round ‘bull’s eye’ rings
Not always associated with drug reactions –> herpes simplex

112
Q

Stevens-Johnson Syndrome (SJS)

A

Severe EM
Flu-like symptoms
Rash and exfoliation of skin

113
Q

Toxic Epidermal Necrolysis (TEN)

A

Severe SJS
Cytotoxic T-cells –> proteases cleave keratinocyte proteins –> apoptosis

114
Q

Dermatologic Emergencies

A

SJS and TEN

115
Q

SCARs

A

SJS
TEN
EM

116
Q

Progression of SCARs

A

Include mucous membrane erosion and epidermal detachment

117
Q

Complications of SCARs

A

Permanent visual impairment
Nail loss, scarring
Irregular pigmentation

118
Q

Drugs that cause SCARs

A

Sulfonamides (TMP-SMX)
Allopurinol
Penicillins
Carbamazepine
Cephalosporins

119
Q

SJS and TEN Pathophys

A

Type IV Hypersensitivity Reactions
Cytotoxic T cells attack epithelial cells in mucosa and epidermis

Pathophysiology (15 decks)

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