DD Flashcards
1
Q
Describe Fitzpatrick skin type I
A
Hair: Red/blonde Eyes: Blue/green Skin: White Freckles: +++ Sunburn: Always Tan: 0
2
Q
Describe Fitzpatrick skin type II
A
Hair: Blonde/brown Eyes: Light to medium Skin: Fair Freckles: ++ Sunburn: Easily Tan: Minimally
3
Q
Describe Fitzpatrick skin type III
A
Hair: Brown Eyes: Medium to dark Skin: Light brown Freckles: + Sunburn: Initially Tan: Gradually
4
Q
Describe Fitzpatrick skin type IV
A
Hair: Medium to dark Eyes: Dark Skin: Moderate brown Freckles: 0 Sunburn: Minimally Tan: Tans well
5
Q
Describe Fitzpatrick skin type V
A
Hair: Dark Eyes: Dark Skin: Dark brown Freckles: 0 Sunburn: Rarely Tan: Dark tan
6
Q
Describe Fitzpatrick skin type VI
A
Hair: Dark Eyes: Darl Skin: Black Freckles:0 Sunburn: Never Tan: Always tan
7
Q
How are different skin colors produced?
A
Not due to the NUMBER of melanocytes in the skin, but rather 1) the type of melanin produced by the melanocytes:
- Eumelanin: black to brown pigment
- Pheomelanin: yellow to red-brown pigment
and 2) the distribution of melanosomes:
- Light skin: melanosomes distributed in clusters above the nucleus
- Dark skin: melanosomes distributed individually throughout cytoplasm
8
Q
What are some of the functions of skin?
A
- Decoration/beauty
- Barrier to light (melanocytes), physical stimuli (keratinocytes), and immunologic (Langerhans cells)
- Vitamin D synth (keratinocytes)
- H2O homeostasis (keratnocytes)
- Thermoreg
- Insulation/caloric reservoir
- Touch/sensation
9
Q
Describe the layers of skin
A
Epidermis - stratified squamous epithelial layer
Dermis - underlying connective tissue
- papillary layer: loose CT
- reticular layer: deeper dense CT
Subcutaneous fa
10
Q
Describe vitamin D synthesis
A
1) 7-dehydrocholesterol –> cholecalciferol (Vitamin D3) in skin by UVB
2) Cholecalciferol (Vitamin D3) and Ergocalciferol (VItamin D2) ingested/absorbed in intestines
3) Vitamin D2 and D3 converted to calcidiol (25-hydroxy Vitamin D) by liver
4) 1,25-dihydroxy-vitamin D (calcitriol) synthesized by kidneys
11
Q
What do keratinocytes do?
A
Forms a barrier layer
Synthesizes keratin, which is a major intracellular fibrous protein for the skin
12
Q
What do melanocytes do?
A
- Produce pigment
- Located in basal layer of epidermis
- Supplies/synthesizes melanin to ~30 keratinocytes
- Melanin is packaged in granules called melanosomes
13
Q
What do Langerhans cells do?
A
Dendritic cells in epidermis derived from bone marrow stem cell
Participates in cell mediated immune reactions by processing and presenting antigens (dendritic cell which goes to lymph nodes and back)
14
Q
Describe the layers of the epidermis
A
1) Stratum corneum
- outermost
- keratinocytes have lost nuclei and organelles and filled with keratin
- desmosomes still connect cells
2) Stratum lucidum
- thin and only on thick skin
- don’t have nuclei or organelles
3) Stratum granulosum
- keratohyalin granules: contain profilaggrin
- filaggrin cross links keratin and helps act as a barrier
- filaggrin is mutated in dry skin –> ichthyosis and atopic dermatitis
4) Stratum spinosum
- prickly/spiny appearance due to desmosome attachments b/w cells
- synth of involucrin and membrane coating granules
5) Stratum basalis
- single layer of columnar/cuboidal cells (keratinocytes)
- stem cells of epidermis
- hemidesmosomes attach basal cells to basal lamina (antibodies to proteins in HD can cause AI bullous pemphigoid)
- desmosomes attach keratinocytes to each other (Abs to proteins in DM can cause AI pemphigus vulgaris)
- tonofilaments: keratin filaments that insert in dense plaques of desmosomes on cytoplasmic side of PM
15
Q
Describe the layers of the dermis
A
Papillary layer
- attaches to epidermis and helps in development/differentiation
- capillary network for epidermis
- pathway for defense cells
- Meissner’s corpuscles for touch
Reticular layer
- collagen and elastic fibers for strength and flexibility
- has glands and hairs
- lots of major blood vessels
- nerves and sensory receptors
- pacinian corpuscles for vibration, pressure, and touch
16
Q
What are the difference between Meissner’s and Pacinian corpuscles?
A
Meissner’s
- delicate touch
- in dermal papillae of thick skin (hands/fingers)
- Schwann cells and sensory nerve terminals surrounded by fibroblasts and collagen
Pacinian
- deep pressure/vibrations
- dermis of thin and thick skin
- look like an onion
- single sensory nerve
17
Q
What are the different types of adnexal structures
A
- Apocrine sweat glands
- Eccrine sweat glands
- Hair
- Nails
- Sebaceous glands
18
Q
What do apocrine sweat glands do?
A
In axillary, pubis, and perianal regions
- produce milky viscous secretion that is odorless
- function in puberty
- ducts which empty into hair follicles above sebaceous glands
19
Q
What do eccrine sweat glands do?
A
- over most of body
- watery, enzyme-rich, Na reabosrbed by ducts
- thermoregulates
20
Q
What does hair do?
A
- Develop in utero in a pilosebaceous unit
- Hair itself has center of sort keratin and a cortex of hard keratin
- pigment comes from melanocytes at base of hair
- arrector pili muscle can make hair stand
21
Q
What do sebaceous glands do?
A
- oil glands that secrete sebum, which is a mixture of lipids
- develop along hair follicles and lubricate hair
22
Q
What causes stasis dermatitis?
A
Venous insufficiency in the legs due to edema ; resulting exudate irritates the skin producing erythematous papules and thin plaques with scales
23
Q
What are the complicating factors of stasis dermatitis?
A
Rashes and varicose veins
Dryness, itching, ACD due to topical antibiotics
Pitting edema
24
Q
How do you treat stasis dermatitis?
A
Compression, elevation, calf exercises, topical steroids,
25
What are the differences between dermatitis and cellulitis?
Dermatitis
- Erythematous papules and plaques WITH SCALES
- Affects epidermis and dermis
Cellulitis
- Warm, tender, erythematous patches or plaques (WITHOUT SCALES)
- dermis and subcutaneous
26
What are the diagnostic criteria for atopic dermatitis?
Itchy skin and 3+ of the following:
- History of skin creases/face involvement
- Personal/family history of asthma/hay fever
- Xerosis (dry skin) within the past year
- Flexural eczema
- Started when
27
What are the potential reasons for the pathogenesis of atopic dermatitis?
- Barrier disrupted skin
- Filaggrin mutation
- Staph aureus superantigen
- Elevated IgE
- Eosinophilia
- TH2 cytokine (IL4, IL5, IL10) immune response
28
What causes irritant contact dermatitis?
Contact or exposure to an irritant: can be strong irritant and contacted once or can be a weak irritant with repeated exposure (like soap and water, perfumes, makeup, etc.)
NOT due to immune response
Presents as spongiotic dermatitis with burning as opposed to itching
29
Describe the process of allergic contact dermatitis
- exposure to an allergen
- small size penetrates skin
- Langerhans cell present allergen to T cells
- immune response
- ACD caused by TNF alpha and IL1
- development of memory T cells
- type IV delayed hypersensitivity (about 1-2 days after exposure)
30
Describe some of the most common causes of ACD
1) Nickel (sulfate)
- most frequent allergen
- in jewelry usually
2) Fragrance
- 100/2800 fragrance ingredients are known contact allergens
- regulations
3) Neomycin slfate
- topical antibotic
- more sensitive in patients with AD, SD, or otitis externa
4) Bacitracin
- occurs in patients with chronic skin ulcers
31
Wat are exanthematous eruptions?
Drug-induced rashes
Common drugs:
- Aminopenicillins
- Sulfonamides
- Cephalosporins
- Anticonvulsants
- Allopurinol
DDx is viral exanthem which enhances the risk of drug eruption
32
How do you treat drug eruptions?
Stop meds
Topical steroids for inflammation and anti-histamines
Should resolve after 1-2wks but can take up to 3mos
33
What is urticaria?
Hives; dermal edema with eosinophils and/or neutrophils;
Type I hypersensitivity reaction mediated by IgE antibodies; reexposure --> antibody binds to IgE on mast cells causing release of histamine
Inflammation of dermis
34
What are the differences between acute and chronic urticaria?
Acute:
- coming and going 6wks
- can be autoimmune
35
What is nummular dermatitis?
Appearance of red, scaly, crusty patches
Treated by less soap, more moisturizer, and topical steroids
36
What is seborrheic dermatitis?
Dandruff of the scalp
- thin plaques/patches of white, yellow flaky scales
- occurs in areas with a lot of sebaceous glands (scalp, face, ears, chest)
In adults over medial eyebrows, nasolabial folds, and ears; chronic relapsing; seen in HIV and Parkinson's patients
In infants, have a sort of "cradle cap" on head and may spread
37
What is the pathogenesis of seborrheic dermatitis?
Overproductions of oil and irritation due to yeast called Malassezia furfur
Maybe more of an imbalance of normal flora (P. acnes decreases in areas of seb derm)
38
How do you treat seb derm?
Mild shampoos, hydrocortizne cream, dandruff shampoos, ketoconazole cream/shampoo, low potency topical steroids
39
What is psoriasis?
Hyperproliferation of epidermis; neutrophils and dilated capillary loops in dermal papillae resulting in scaly patches
Occurs on extensor surfaces (knees, elbows, belly button)
Commonly a genetic predisposition
Guttate can be triggered by strep throat
40
What are the subtypes of psoriasis?
```
Chronic plaque disease
Guttate
Erythroderma
Pustular
Psoriatic Arthritis
```
41
What comorbidities present with psoriasis?
Psoriasis causes a low grade systemic inflammation, which leads to heart disease, obesity, insulin resistance, metabolic syndrome
Arthritis
Crohn's disease
42
How do you treat psoriasis?
If localized:
- Calcipotriol
- Corticosteroids
- Topical reinoids
- Phototherapy
If widespread:
- Methotrexate
- Cyclosporin
- Systemic retinoids
- Biologics
43
```
LOCATION?
Stasis Dermatitis --> ?
Seborrheic Dermatitis --> ?
Atopic Dermatitis --> ?
Psoriasis --> ?
```
```
LOCATION
Stasis Dermatitis --> Lower legs
Seborrheic Dermatitis --> Scalp
Atopic Dermatitis --> Flexor surfaces
Psoriasis --> Extensor surfaces (w/ arthritis)
```
44
```
ETIOLOGY?
Stasis Dermatitis --> ?
Seborrheic Dermatitis --> ?
Atopic Dermatitis --> ?
Irritant Dermatitis --> ?
Allergic contact dermatitis --> ?
```
ETIOLOGY?
Stasis Dermatitis --> Lowe extremity edema
Seborrheic Dermatitis --> Malassezia furfur
Atopic Dermatitis --> Filaggrin
Irritant Dermatitis --> Common irritants
Allergic contact dermatitis --> Common allergens
45
MISC.
Atopic dermatitis
- associated with?
Allergic contact dermatitis
- how does it manifest?
- how do you confirm?
Psoriasis
- associated with?
MISC.
Atopic dermatitis
- associated with asthma and allergic rhinitis
Allergic contact dermatitis
- how does it manifest? delayed type IV hypersensitivity reaction
- how do you confirm? diagnosed with patch testing
Psoriasis
- associated with? CV disease
46
Which type of collagen is >85% of adult dermis and major component of bone?
Collagen type I
47
Where is collagen III found most readily?
in in fetal dermis, but not adult dermis
48
Where is collagen IV found?
basement membrane in dermoepidermal junction; in vessels
49
Where is collagen VII found?
in anchoring fibrils to attach epidermis to dermis
50
Describe collagen formation
- procollagen synthesized within fibroblasts; secreted and then assembled into alpha helical three separate chains together outside of cell
- vitamin C is important
- if lack of vitamin c: failure of wounds to heal, hair abnormally grows, blood vessels are fragile, teeth will fall out
51
What kind of strength do collagen fibers provide?
tensile strength
52
What kind of strength do elastic fibers provide?
resiliency (ability of skin to be distorted and return to original shape
53
What is solar elastosis?
- degeneration of elastic fibers due to sunlight exposure making collagen bundles dystrophic and clump and aggregate
54
Describe ground substance
- made up of GAGs
- pie filling between collagen and elastic fibers and appendageal structures
- sponge-like and can take it and expel water
55
Blood vessels in dermis?
- none in epidermis
- have a deep plexus and superficial plexus
- activation of immune complexes can lead to vasculitis and damage to vessels and extravasation of RBCs
56
Nerves in dermis?
- inform and protect
| - nerve endings go to dermoepidermal junction
57
What are Pacinian corpuscles?
- resemble an onion
- pressure and vibration
- genital area
58
What are Meissner's corpuscles?
- pinecone shape
- fine touch and tactile discrimination
- in distal pulps of fingers
59
Describe the two types of hair follicles
- Terminal hairs: start in dermis and are large and coarse
| - Vellus hairs: small and apigmented and diffusely over body
60
What do sebaceous glands do?
- secrete oil along hair and lubricate follicle
61
What do eccrine glands do?
- thermoregulation
| - watery and not much odor
62
What do apocrine gland do?
- more viscous and have an odor
| - same thermoregulatory function as eccrine glands
63
What are signs of Seborrheic Dermatitis?
- dandruff
| - hand tremor due to association with parkinson's
64
What causes acanthosis nigricans?
- dark areas in skin folds, hands, and neck
- related to diabetes
- endocrinopathies
-
65
What can cause fever of unknown origin?
- infective endocarditis
| - splinter hemorrhage in nails
66
What happens in systemic scleroderma?
- thickened skin on hands and fingers
| - tightened skin around mouth
67
What happens in Licehn Planus?
- pruritic papules on skin and lesions in mouth
68
What happens in Lupus?
- MDSOAPBRAIN
- Malar rash, discoid rash, serositis, oral ulcers, photosensitivity, blood disorders, renal involvement, arthritis, immunologic, neurologic
69
Cherry Hemangiomas
- middle age
- most common vascular tumor
- generally no underlying disease
- treat with electrodessication, liquid nitrogen
70
Infantile Hemangioma
- most common soft tissue of infancy
- benign endothelial neoplasm
- dermal proliferation of capillary sized endothelial cell lined vessels
- more common in girls
- can ulcerate, can interrupt visual feild, trouble if near lip, nose, anogenital area
- treat with observation, local wound care, steroids, beta blockers, usually involute by themselves
71
Port wine stain
- vascular malformation
- at birth and continues into adulthood
- varicose veins, venous stasis, edema, ulcers
- follow trigeminal nerve
- treat with pulsed dye laser
72
Nevus Sebaceus
- yellow linear plaque on face or scalp
- assoc w alopecia
- can have neurologic abnormalities and epithelial neoplasms
- treat with observation or surgery
73
Sebaceous Hyperplasia
- benign tumor of oil gland
- face, trunk, ext
- treat with nothing, excision, electrodessication, liquid nitrogen, TCA acid, laser
74
Acrochordon
- soft flesh colored papule
- neck, axilla, infra mammary
- recurrent trauma, torsion
- treat with nothing, snip excision, cryotherapy, electrodessication
75
Lipoma
- benign tumor of adipose tissue
| - no treatment, or excise surgically
76
Dermatofibroma
- usually on legs alone
- brown firm papules
- pain and pruritis
- no treatment, surgically excise
77
Keloid scar
- overgrowth of granulation tissue at site of a healed skin injury (collagen type 3 being replaced by type 1)
- grows beyond area of original wound
- treat with topical steroids, surgical excision, surgery with radiation
78
Seborrheic Keratosis
- "stuck on" appearance (exophytic papule)
- small pits and light brownish
- on chest and back usually
- treat with alpha hydroxy acids, lactic acid, cryosurgery, surgery
79
Intradermal Nevi
- moles
- head and neck most common
-
80
Junctional Nevus
- plantar and palmar surfaces
- 1-5mm
- macule, smooth, tan to brown to black
81
Compound Nevus
- trunk and proximal ext
| -
82
Blue Nevus
- proliferation of melanocytes that produce lots of melanin
- tyndall effect produces blue color
- blue papule or nodule 1-2mm
- treat with surgical removal or nothing
83
Congenital Nevus
- vary in size
| - treat with surgical excision, but not recommended
84
Dysplastic Nevus
- acquired: epidermal or dermal proliferation of nevomelanocytes; abnormal growth pattern
- sporadic/familial
- before 20yo
- especially trunk
- round to oval to irregular
- variation in color
- indistinct border
- varying in size
- melanomas are contiguous with dysplastic nevi
85
FAMM syndrome
Familial Atypical Moles and Melanoma
- malignant melanoma in 1st or 2nd degree relatives
- lots of melanocytic nevi
- certain histo features
- 3 genes mapped to melanomas
- treat with mole mapping, photography, removal of atypical nevi,
86
Cafe au lait macules
- inc in melanocytes with inc melanin prod
- trunk and prox ext
- multiple --> NF
87
Neurofibromas
- flesh colored papules with "button hole" (goes inwards when pushed)
- proliferation of neural tissue in dermis
88
Neurofibromatosis
- AD inheritance
- 50% spontaneous
- defect in TS gene on ch17 for NF-1
- diagnosis: needs 2+ of either 6+ CAL spots, 2+ neurofibromas/1 plexiform neurofibroma, axillary or inguinal freckling, optic glioma, 2+ lisch nodules, osseous lesions, first degree relative with NF
89
Impetigo
- most common superficial bacterial infection in kids
- person to person
- high humidity, poor hygiene
- s pyrogenes, s aureus
- treat with soaking and removal of crusts, topical Abx, systemic Abx
90
Streptococcal Non-Bullous Impetigo
- face in children
- single lesion to multiple
- yellow crust
- LAD
- glomerulonephritis in 5%
91
Staphylococcal Non-Bullous Impetigo
- face, any age group
- secondary lesion from injury or dermatitis
- yellow colored crust
92
Bullous Impetigo
- anywhere in body
- single lesion to multiple
- initially flaccid blister; become collapsed
- scalded skin syndrome
93
Cellulitis Epidemiology
- very young and elderly
- immunocompromised
- IV drug users
94
Cellulitis bacteriology
- Erysipelas (facial); assoc w. beta hemolytic streptococci (s pyrogenes)
- Cellulitis; s pyrogenes, s aureus, h influenzae;
95
Erysipela features
- confined to face
- 2-5day incubation period
- fever, chills, malaise
- sharply demarcated erythema w/ non pitting edema
- LAD
96
Cellulitis features
- extremities
- 2-5day incubation
- ill defined non palpable area of painful erythema and is warm
- may hemorrhage
- LAD
97
Cellulitis diagnosis
- features
- CBC - leukocytosis
- biopsy
98
Cellulitis treatment
- antibiotics against streptococall or staphylococcal organisms
99
Dermatophyte infections epi
- some fungi geographically restr
| - superficial fungi really common
100
Dermatophyte infections mycology
- 30 species
| - require keratin (skin, hair, nails)
101
Dermatophye infections features
- tinea capitis: scalp/hair (kerion w/ abscess)
- tinea faciei: face
- tinea barbae: beard
- tinea corporis: non-hair skin (majocchi's granuloma w/ pustules and granulomas)
- tinea cruris: genital
- tinea manuum: hands
- tinea pedis: feet
- tinea unuquium: nail
102
Dermatophyte Infection diagnosis
- KOH positive
| - culture, biopsy
103
Dermatophyte Infection treatment
- topical antifungal
| - systemic antifungal
104
Candidiasis epi
- mucous membranes and skin
- more common in patients w/ diabetes, corticosteroids use, or broad Abx
- Candida are normal flora in GI tract
105
Candidiasis mycology
- feed off of glucose or serum
106
Candidiasis features
- mucocutaneous infections
- oral thrush
- angular cheilitis
- cutaneous candidiasis
107
Candidiasis diagnosis
- KOH exam
- culture
- biopsy
108
Candidiasis treatment
- topical antifungal
| - systemic antifungal
109
Tinea versicolor epi
- humid and warm areas
| - post pubertal patients
110
Tinea versicolor mycology
- feed off of follicular lipids
| - malassezia furfur
111
Tinea versicolor features
- trunk
- tan colored, scaly macules --> patches
- hypopigmented
- follicular papules in pustules on trunk and arms
112
Tinea versicolor diagnosis
- KOH exam
| - culture
113
Tinea versicolor treatment
- selenium sulfide shampoo
- topical imidazoles
- oral meds
114
Scabies epi
- more often in children and sexually active people
| - mites spread by person to person contact
115
Scabies parasitology
- confined to humans
| - 30day lifecycle in epidermis --> 60-90 eggs that hatch in 10 days
116
Scabies features
- symmetric webspace, flexures, axilla, genital, buttocks
| - erythematous papules and burrows
117
Scabies diagnosis
- characteristic burrows or genital nodules
- mineral oil on skin and examined for infestation
- skin biopsy
118
Scabies treatment
- permethrin 5% cream
- lindane 1% lotion
- crotamiton 10%
- sulfur 5-10%
- ivermectin
119
Lice epi
- worldwide
- head lice: 12mil new per year in US
- crab lice: homosexuals and young men 15-40
120
Lice parasitology
Pediculus humanus var capitis: scalp
" var corporis: trunk
Phthirus pubis: genital
121
Lice features
Head lice: scalp, intense pruritis, erythema, scale, secondary infection, eggs attached to hair shafts; white when hatch
Body lice: intense pruritis and erythematous papules
Crab lice: hair of genital area; pruritis; base of hairs
122
Lice diagnosis
- finding nit or louse
123
Lice treatment
Head lice: pyrethrin, permethrin, lindane, malathion, ivermectin
Body lice: disinfect clothing w/ fumigation; topical treatments
Crab lice: permethrin, pyrethrin, lindane, ivermectin
124
How can topical medication get through to dermis/epidermis?
1) passive diffusion
2) transported through channels or pores within a lacunar system
3) via appendageal structures like sweat glands or hair follicles
125
What are drug factors affecting percutaneous absorption?
- active drug concentration (directly proportional to cutaneous absorption)
- composition of vehicle
- molecular size of drug/prodrug
- lipophilicity of drug
126
What are patient factors affecting percutaneous absorption?
- barrier disruption
- anatomic location
- skin hydration
- occlusion
127
What are the most common vehicles for topical meds?
- ointment: water in oil emulsion
- creams: oil in water emulsion
- gels: semisolid emulsion in alcohol base
- lotions/solutions: powder in water (some oil in water)
- foam: pressurized collection of gas in liquid film
128
Ointments
- strong potency
- hydrating, low irritation
- greasiness
- may stain clothing
- avoid face, hands, groin
129
Creams
- moderate potency
- some hydration
- large allergy risk, but low irritation risk
130
Gels
- strong potency
- drying
- high allergy and irritation risk
- oral mucosal surfaces and scalp
- avoid fissures
131
Lotions/solutions
- low potency
- variable drying
- large allergy and moderate irritation risk
- scalp and intertriginous areas
- avoid fissures
132
Foams
- stable at room temp, but melts at body temp
- supersaturated active ingredients
- strong potency
133
What factors to consider when choosing a vehicle?
1) anatomic location
2) contact allergy/sensitization
3) irritancy
134
Explain how corticosteroids are anti-inflammatory
- GCS binds to receptors
- release of HSP
- translocation of GC receptor into nucleus
- GCR forms a dimer and binds to GC response element of promoter region of steroid-responsive genes
- alter production of inflammatory pathways
- inhibit NF-kB pathway --> red of genes that are involved in inflam (cytokines, adhesion molecules,etc.)
- GCR interacts with AP1 --> dec transcription of growth factor and cytokine genes
- GCS inhibit TNFalpha, GCSF, and lots of interleukins
135
Hydrocortisone
- the gentle touch
- good for mild eczema
- treats inflammatory dermatoses in face, intertriginous area, groin
- lowest class
136
Triamcinolone acetonide
- affordable
- class 4
- most moderate spongiotic dermatoses
- not rec for long term use
137
Clobetasol propionate
- class 1
- most potent
- acute eruptions that need rapid help
- avoid face and groin
138
What effects does UVR damage to the skin have?
1) damage to DNA, RNA, lipids, and proteins
2) pro-inflammatory effects
3) immunosuppressive effects
4) induction of innate defenses
5) induction of apoptosis
6) vitamin d synth
139
UVB rays cause
- eye problems
- sunburns
- dna damage
140
UVA rays cause
- dna damage
- premature aging
- loose skin
- wrinkles
- dark patches
141
Skin architecture
- UVB wavelenghts are shorter and cannot penetrate as deeply, so affect keratinocytes, melanocytes, and langerhans cells
- UVA can penetrate deeper since its wavelength is longer and affects fibroblasts and connective tissue
142
vitamin d synthesis
- UVR induces synthesis of cholecalciferol (VD3) and ergocalciferol (VD2);
- both convert to active form in liver and kidney (dihydroxy VD3)
143
main types of DNA damage from UVR
- thymine dimers (UVB)
- pyrimidine 6 4 pyrimidone (UVB)
- hydroxyguanosine (UVA)
144
photocarcinogenic cascade
- UV exposure
- DNA Damage
- formation of mutations
- multistage carcinogenesis (init, promot, transform)
- melanoma, NMSC (basal cell carcinoma, squamous cell carcinoma)
145
skin defense against UVR
- dna repair
- apoptosis of dna damaged cells
- defenses against ROS
- melanin
146
Melanin production
- melanocytes in basal layer of skin
| - melanin deposited into keratinocytes
147
Basal Cell Carcinoma features
- nodular is most common
- don't cause symptoms until large
- flat, firm, pale or small, raised, pink, translucent, shiny, waxy
- may bleed or hurt
148
BCC pathophysiology
- starts in lowest layer of epidermis (basal cell layer)
| - arise from pluripotent cells
149
BCC clinical course
- begin on areas exposed to sun
- grows slowly
- rare to metastasize
150
Actinic Keratosis clinical course
- can develop in SCC
- typically in fair skinned
- produced by UVR
- distributed in areas of sun exposure
- hyperkeratosis
- erythematous papules
151
AK treatment
cryotherapy
| - topical meds
152
Squamous cell carcinoma clinical appearance
- growing lumps, rough surface
| - flat red patches
153
SCC clinical course
- starts in upper part of epidermis
- sun exposed skin
- risk factors: UVR, thermal injury, HPV, burn, scars, ulcers, other chronic injury (Marjolin's ulcer)
- invade fatty tissue and spread through LNs more than BCC
154
Non melanoma skin cancer risk factors
- UVR damage of keratinocytes
- Fair skin
- men
- chemicals
- radiation
-
155
Melanoma
- breslow measurement of thickness is the most important factor in determining prognosis of melanoma
- treat with excision or radiation therapy
156
Kaposi Sarcoma
- from cells that line lymph or blood vessels
- tumors on skin or mucosal surfaces
- purple red or brown tumors on skin
157
What ways can bacteria gain access to the body?
- mouth
- respiratory tract
- anus
- urogenital tract
- conjunctiva
- scratch/injury
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What are Koch's Postulates?
1) Specific microbes are present regularly in characteristic lesions of the disease
2) The specific microbes can be isolated and grown in vitro
3) Injection of the cultured microbes into animals reproduces the disease seen in humans
4) Specific microbes can be re-isolated from the lesions of the disease in animals
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What is the difference between frank and opportunistic pathogens?
- frank: can readily cause disease in normal hosts
| - opportunistic: host needs to be compromised and less often in normal hosts
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What are the stages of infection?
1) Encounter - how agent meets host
2) Entry - how the agent enters the host
3) Spread - how the agent spreads from the site of entry
4) Multiplication - how the agent multiples in the host
5) Damage - how tissue damage is caused by the agent and/or the host response/any virulence factors
6) Outcome - does the microbial agent or host win battle?
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Encounter
- agent exogenous or endogenous?
- contact from where?
- route of infection
- infectious dose?
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Entry
- cross an epithelial barrier?
- invasion or passive?
- colonization of body surfaces
- adherence
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Spread
- spreading factors: hyaluronidase, elastase, collagenase
| - coagulase inhibits spread by depositing fibrin
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Multiplication
- must replicate faster than clearance by defense
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Damage
- microbial toxins to tissue
| - blocking defense mechs
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Outcome
- survival of obligate parasites requires a portal of exit as well as a portal of entry
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What is a virus?
- submicroscopic
- obligate intracellular parasites (need to infect a host first)
- invades a host cell, replicates genome, and directs synthesis of viral components
- house DNA/RNA in capsids
- viral genome contains all info for an infectious cycle
- relationship with host
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How are viruses categorized?
1) classical: through physical prop (DNA/RNA, helical/icosahedral capsid, nake or enveloped)
2) how they produce mRNA
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What are two key principles of viral genomes?
1) genomes serve as the template for synthesis of progeny genomes; small, finite number of nucleic acid copying strategies
2) function of viral genomes inside the cell is to make mRNA
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What are the 6 classes of viral genome configuration?
1) dsDNA (gapped circular dsDNA)
2) ssDNA
3) dsRNA
4) ss+RNA
5) ss-RNA
6) ss+RNA w/ DNA intermediate
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How do DNA viruses express?
- if gapped, then need to be filled
- if ssDNA then need to be replicated before transcription
- RNA polymerase II transcribes mRNA using -strand of DNA
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How do RNA viruses express?
- use RNA-dep RNA polymerase, which is not found in host cells
- for +RNA: can be translated directly with ribosomes
- for -RNA and dsRNA: +sense RNA must be transcribed; RdRp helps with that
- for +RNA with DNA intermediate: retroviruses; copy ssRNA into dsDNA using reverse transcriptase; dsDNA integrates into host cells DNA
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What does viral disease depend on?
- effects that viral replication has on host cells
- host response to the infection
- ability of virus to spread
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What are the factors that influence disease induction and outcome?
1) route of infection
2) initial site of replication
3) virus spread from initial site
4) mechanisms of virus-indued symptoms and signs of infections
5) tropism
6) transmission and shedding
7) host factors in susceptibility
8) immune-mediated pathology
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What are the main routes of infection for viruses?
- respiratory, alimentary, and genitourinary
| - lots of mucosal surfaces and immune responses that viruses must overcome
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What is needed for a successful initial infection?
- sufficient virus
- susceptible cells at site of entry
- host defenses absent
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Compare acute local and systemic viral infections
- acute local: short incubation times, short lived immunity due to rapidly mutating viruses, IgA
- acute systemic: secondary replication at other sites, lifelong immunity, IgA and IgG
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What are the 3 outcomes of viral infection of a cell?
- abortive infection or failed infection (no virus produced)
- lytic/acute infection resulting in production of virus and death of host cell
- persistent infection which can be chronic w/ production of virus, latent w/ no virus produced, or transforming which may produce virus
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Interferon activity
- IFNalpha and beta from infected cells
- IFNgamma from T cell and NK cells
- IFNs cause anti-viral state through blocking of transcription of cell proliferation and other stuff and induce inflammation
- can induce synth of gene products that arrest cell cycle or induce an apoptotic state or induce synth of proteins that are involved in presentation of virus proteins by cytotoxic T lymphocytes (MHC class I)
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HSV1 and HSV2 features
- painful vesicles on skin at site of inoculation
- HSV1: oral herpes
- HSV2: genital herpes
- transmission through contact; genital or oral secretions or from mucosal surface
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HSV1 clinical patterns
- most primary infections are asymptomatic and occur during childhood
