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BL and DD Unit 3 > DD > Flashcards

DD Flashcards

1
Q

Describe Fitzpatrick skin type I

A 
Hair: Red/blonde
Eyes: Blue/green
Skin: White
Freckles: +++
Sunburn: Always
Tan: 0
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2
Q

Describe Fitzpatrick skin type II

A 
Hair: Blonde/brown
Eyes: Light to medium
Skin: Fair
Freckles: ++
Sunburn: Easily
Tan: Minimally
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3
Q

Describe Fitzpatrick skin type III

A 
Hair: Brown
Eyes: Medium to dark
Skin: Light brown
Freckles: +
Sunburn: Initially
Tan: Gradually
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4
Q

Describe Fitzpatrick skin type IV

A 
Hair: Medium to dark
Eyes: Dark
Skin: Moderate brown
Freckles: 0
Sunburn: Minimally
Tan: Tans well
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5
Q

Describe Fitzpatrick skin type V

A 
Hair: Dark
Eyes: Dark
Skin: Dark brown
Freckles: 0
Sunburn: Rarely
Tan: Dark tan
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6
Q

Describe Fitzpatrick skin type VI

A 
Hair: Dark
Eyes: Darl
Skin: Black
Freckles:0
Sunburn: Never
Tan: Always tan
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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
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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
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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

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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

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11
Q

What do keratinocytes do?

A

Forms a barrier layer

Synthesizes keratin, which is a major intracellular fibrous protein for the skin

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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
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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)

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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

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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
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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
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17
Q

What are the different types of adnexal structures

A
  • Apocrine sweat glands
  • Eccrine sweat glands
  • Hair
  • Nails
  • Sebaceous glands
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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
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19
Q

What do eccrine sweat glands do?

A
  • over most of body
  • watery, enzyme-rich, Na reabosrbed by ducts
  • thermoregulates
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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
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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
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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

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23
Q

What are the complicating factors of stasis dermatitis?

A

Rashes and varicose veins

Dryness, itching, ACD due to topical antibiotics

Pitting edema

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24
Q

How do you treat stasis dermatitis?

A

Compression, elevation, calf exercises, topical steroids,

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25
Q

What are the differences between dermatitis and cellulitis?

A

Dermatitis

  • Erythematous papules and plaques WITH SCALES
  • Affects epidermis and dermis

Cellulitis

  • Warm, tender, erythematous patches or plaques (WITHOUT SCALES)
  • dermis and subcutaneous
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26
Q

What are the diagnostic criteria for atopic dermatitis?

A

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
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27
Q

What are the potential reasons for the pathogenesis of atopic dermatitis?

A
  • Barrier disrupted skin
  • Filaggrin mutation
  • Staph aureus superantigen
  • Elevated IgE
  • Eosinophilia
  • TH2 cytokine (IL4, IL5, IL10) immune response
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28
Q

What causes irritant contact dermatitis?

A

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

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29
Q

Describe the process of allergic contact dermatitis

A
  • 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)
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30
Q

Describe some of the most common causes of ACD

A

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

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31
Q

Wat are exanthematous eruptions?

A

Drug-induced rashes

Common drugs:

  • Aminopenicillins
  • Sulfonamides
  • Cephalosporins
  • Anticonvulsants
  • Allopurinol

DDx is viral exanthem which enhances the risk of drug eruption

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32
Q

How do you treat drug eruptions?

A

Stop meds
Topical steroids for inflammation and anti-histamines

Should resolve after 1-2wks but can take up to 3mos

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33
Q

What is urticaria?

A

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

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34
Q

What are the differences between acute and chronic urticaria?

A

Acute:

  • coming and going 6wks
  • can be autoimmune
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35
Q

What is nummular dermatitis?

A

Appearance of red, scaly, crusty patches

Treated by less soap, more moisturizer, and topical steroids

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36
Q

What is seborrheic dermatitis?

A

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

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37
Q

What is the pathogenesis of seborrheic dermatitis?

A

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)

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38
Q

How do you treat seb derm?

A

Mild shampoos, hydrocortizne cream, dandruff shampoos, ketoconazole cream/shampoo, low potency topical steroids

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39
Q

What is psoriasis?

A

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

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40
Q

What are the subtypes of psoriasis?

A 
Chronic plaque disease
Guttate
Erythroderma
Pustular
Psoriatic Arthritis
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41
Q

What comorbidities present with psoriasis?

A

Psoriasis causes a low grade systemic inflammation, which leads to heart disease, obesity, insulin resistance, metabolic syndrome

Arthritis

Crohn’s disease

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42
Q

How do you treat psoriasis?

A

If localized:

  • Calcipotriol
  • Corticosteroids
  • Topical reinoids
  • Phototherapy

If widespread:

  • Methotrexate
  • Cyclosporin
  • Systemic retinoids
  • Biologics
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43
Q 
LOCATION?
Stasis Dermatitis --> ?
Seborrheic Dermatitis --> ?
Atopic Dermatitis --> ?
Psoriasis --> ?
A 
LOCATION
Stasis Dermatitis --> Lower legs
Seborrheic Dermatitis --> Scalp
Atopic Dermatitis --> Flexor surfaces
Psoriasis --> Extensor surfaces (w/ arthritis)
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44
Q 
ETIOLOGY?
Stasis Dermatitis --> ?
Seborrheic Dermatitis --> ?
Atopic Dermatitis --> ?
Irritant Dermatitis --> ?
Allergic contact dermatitis --> ?
A

ETIOLOGY?
Stasis Dermatitis –> Lowe extremity edema
Seborrheic Dermatitis –> Malassezia furfur
Atopic Dermatitis –> Filaggrin
Irritant Dermatitis –> Common irritants
Allergic contact dermatitis –> Common allergens

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45
Q

MISC.
Atopic dermatitis
- associated with?

Allergic contact dermatitis

  • how does it manifest?
  • how do you confirm?

Psoriasis
- associated with?

A

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

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46
Q

Which type of collagen is >85% of adult dermis and major component of bone?

A

Collagen type I

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47
Q

Where is collagen III found most readily?

A

in in fetal dermis, but not adult dermis

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48
Q

Where is collagen IV found?

A

basement membrane in dermoepidermal junction; in vessels

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49
Q

Where is collagen VII found?

A

in anchoring fibrils to attach epidermis to dermis

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50
Q

Describe collagen formation

A
  • 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
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51
Q

What kind of strength do collagen fibers provide?

A

tensile strength

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52
Q

What kind of strength do elastic fibers provide?

A

resiliency (ability of skin to be distorted and return to original shape

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53
Q

What is solar elastosis?

A
  • degeneration of elastic fibers due to sunlight exposure making collagen bundles dystrophic and clump and aggregate
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54
Q

Describe ground substance

A
  • made up of GAGs
  • pie filling between collagen and elastic fibers and appendageal structures
  • sponge-like and can take it and expel water
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55
Q

Blood vessels in dermis?

A
  • 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
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56
Q

Nerves in dermis?

A
  • inform and protect

- nerve endings go to dermoepidermal junction

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57
Q

What are Pacinian corpuscles?

A
  • resemble an onion
  • pressure and vibration
  • genital area
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58
Q

What are Meissner’s corpuscles?

A
  • pinecone shape
  • fine touch and tactile discrimination
  • in distal pulps of fingers
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59
Q

Describe the two types of hair follicles

A
  • Terminal hairs: start in dermis and are large and coarse

- Vellus hairs: small and apigmented and diffusely over body

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60
Q

What do sebaceous glands do?

A
  • secrete oil along hair and lubricate follicle
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61
Q

What do eccrine glands do?

A
  • thermoregulation

- watery and not much odor

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62
Q

What do apocrine gland do?

A
  • more viscous and have an odor

- same thermoregulatory function as eccrine glands

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63
Q

What are signs of Seborrheic Dermatitis?

A
  • dandruff

- hand tremor due to association with parkinson’s

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64
Q

What causes acanthosis nigricans?

A
  • dark areas in skin folds, hands, and neck
  • related to diabetes
  • ## endocrinopathies
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65
Q

What can cause fever of unknown origin?

A
  • infective endocarditis

- splinter hemorrhage in nails

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66
Q

What happens in systemic scleroderma?

A
  • thickened skin on hands and fingers

- tightened skin around mouth

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67
Q

What happens in Licehn Planus?

A
  • pruritic papules on skin and lesions in mouth
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68
Q

What happens in Lupus?

A
  • MDSOAPBRAIN
  • Malar rash, discoid rash, serositis, oral ulcers, photosensitivity, blood disorders, renal involvement, arthritis, immunologic, neurologic
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69
Q

Cherry Hemangiomas

A
  • middle age
  • most common vascular tumor
  • generally no underlying disease
  • treat with electrodessication, liquid nitrogen
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70
Q

Infantile Hemangioma

A
  • 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
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71
Q

Port wine stain

A
  • vascular malformation
  • at birth and continues into adulthood
  • varicose veins, venous stasis, edema, ulcers
  • follow trigeminal nerve
  • treat with pulsed dye laser
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72
Q

Nevus Sebaceus

A
  • yellow linear plaque on face or scalp
  • assoc w alopecia
  • can have neurologic abnormalities and epithelial neoplasms
  • treat with observation or surgery
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73
Q

Sebaceous Hyperplasia

A
  • benign tumor of oil gland
  • face, trunk, ext
  • treat with nothing, excision, electrodessication, liquid nitrogen, TCA acid, laser
74
Q

Acrochordon

A
  • soft flesh colored papule
  • neck, axilla, infra mammary
  • recurrent trauma, torsion
  • treat with nothing, snip excision, cryotherapy, electrodessication
75
Q

Lipoma

A
  • benign tumor of adipose tissue

- no treatment, or excise surgically

76
Q

Dermatofibroma

A
  • usually on legs alone
  • brown firm papules
  • pain and pruritis
  • no treatment, surgically excise
77
Q

Keloid scar

A
  • 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
Q

Seborrheic Keratosis

A
  • “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
Q

Intradermal Nevi

A
  • moles
  • ## head and neck most common
80
Q

Junctional Nevus

A
  • plantar and palmar surfaces
  • 1-5mm
  • macule, smooth, tan to brown to black
81
Q

Compound Nevus

A
  • trunk and proximal ext

-

82
Q

Blue Nevus

A
  • 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
Q

Congenital Nevus

A
  • vary in size

- treat with surgical excision, but not recommended

84
Q

Dysplastic Nevus

A
  • 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
Q

FAMM syndrome

A

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
Q

Cafe au lait macules

A
  • inc in melanocytes with inc melanin prod
  • trunk and prox ext
  • multiple –> NF
87
Q

Neurofibromas

A
  • flesh colored papules with “button hole” (goes inwards when pushed)
  • proliferation of neural tissue in dermis
88
Q

Neurofibromatosis

A
  • 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
Q

Impetigo

A
  • 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
Q

Streptococcal Non-Bullous Impetigo

A
  • face in children
  • single lesion to multiple
  • yellow crust
  • LAD
  • glomerulonephritis in 5%
91
Q

Staphylococcal Non-Bullous Impetigo

A
  • face, any age group
  • secondary lesion from injury or dermatitis
  • yellow colored crust
92
Q

Bullous Impetigo

A
  • anywhere in body
  • single lesion to multiple
  • initially flaccid blister; become collapsed
  • scalded skin syndrome
93
Q

Cellulitis Epidemiology

A
  • very young and elderly
  • immunocompromised
  • IV drug users
94
Q

Cellulitis bacteriology

A
  • Erysipelas (facial); assoc w. beta hemolytic streptococci (s pyrogenes)
  • Cellulitis; s pyrogenes, s aureus, h influenzae;
95
Q

Erysipela features

A
  • confined to face
  • 2-5day incubation period
  • fever, chills, malaise
  • sharply demarcated erythema w/ non pitting edema
  • LAD
96
Q

Cellulitis features

A
  • extremities
  • 2-5day incubation
  • ill defined non palpable area of painful erythema and is warm
  • may hemorrhage
  • LAD
97
Q

Cellulitis diagnosis

A
  • features
  • CBC - leukocytosis
  • biopsy
98
Q

Cellulitis treatment

A
  • antibiotics against streptococall or staphylococcal organisms
99
Q

Dermatophyte infections epi

A
  • some fungi geographically restr

- superficial fungi really common

100
Q

Dermatophyte infections mycology

A
  • 30 species

- require keratin (skin, hair, nails)

101
Q

Dermatophye infections features

A
  • 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
Q

Dermatophyte Infection diagnosis

A
  • KOH positive

- culture, biopsy

103
Q

Dermatophyte Infection treatment

A
  • topical antifungal

- systemic antifungal

104
Q

Candidiasis epi

A
  • mucous membranes and skin
  • more common in patients w/ diabetes, corticosteroids use, or broad Abx
  • Candida are normal flora in GI tract
105
Q

Candidiasis mycology

A
  • feed off of glucose or serum
106
Q

Candidiasis features

A
  • mucocutaneous infections
  • oral thrush
  • angular cheilitis
  • cutaneous candidiasis
107
Q

Candidiasis diagnosis

A
  • KOH exam
  • culture
  • biopsy
108
Q

Candidiasis treatment

A
  • topical antifungal

- systemic antifungal

109
Q

Tinea versicolor epi

A
  • humid and warm areas

- post pubertal patients

110
Q

Tinea versicolor mycology

A
  • feed off of follicular lipids

- malassezia furfur

111
Q

Tinea versicolor features

A
  • trunk
  • tan colored, scaly macules –> patches
  • hypopigmented
  • follicular papules in pustules on trunk and arms
112
Q

Tinea versicolor diagnosis

A
  • KOH exam

- culture

113
Q

Tinea versicolor treatment

A
  • selenium sulfide shampoo
  • topical imidazoles
  • oral meds
114
Q

Scabies epi

A
  • more often in children and sexually active people

- mites spread by person to person contact

115
Q

Scabies parasitology

A
  • confined to humans

- 30day lifecycle in epidermis –> 60-90 eggs that hatch in 10 days

116
Q

Scabies features

A
  • symmetric webspace, flexures, axilla, genital, buttocks

- erythematous papules and burrows

117
Q

Scabies diagnosis

A
  • characteristic burrows or genital nodules
  • mineral oil on skin and examined for infestation
  • skin biopsy
118
Q

Scabies treatment

A
  • permethrin 5% cream
  • lindane 1% lotion
  • crotamiton 10%
  • sulfur 5-10%
  • ivermectin
119
Q

Lice epi

A
  • worldwide
  • head lice: 12mil new per year in US
  • crab lice: homosexuals and young men 15-40
120
Q

Lice parasitology

A

Pediculus humanus var capitis: scalp
“ var corporis: trunk
Phthirus pubis: genital

121
Q

Lice features

A

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
Q

Lice diagnosis

A
  • finding nit or louse
123
Q

Lice treatment

A

Head lice: pyrethrin, permethrin, lindane, malathion, ivermectin

Body lice: disinfect clothing w/ fumigation; topical treatments

Crab lice: permethrin, pyrethrin, lindane, ivermectin

124
Q

How can topical medication get through to dermis/epidermis?

A

1) passive diffusion
2) transported through channels or pores within a lacunar system
3) via appendageal structures like sweat glands or hair follicles

125
Q

What are drug factors affecting percutaneous absorption?

A
  • active drug concentration (directly proportional to cutaneous absorption)
  • composition of vehicle
  • molecular size of drug/prodrug
  • lipophilicity of drug
126
Q

What are patient factors affecting percutaneous absorption?

A
  • barrier disruption
  • anatomic location
  • skin hydration
  • occlusion
127
Q

What are the most common vehicles for topical meds?

A
  • 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
Q

Ointments

A
  • strong potency
  • hydrating, low irritation
  • greasiness
  • may stain clothing
  • avoid face, hands, groin
129
Q

Creams

A
  • moderate potency
  • some hydration
  • large allergy risk, but low irritation risk
130
Q

Gels

A
  • strong potency
  • drying
  • high allergy and irritation risk
  • oral mucosal surfaces and scalp
  • avoid fissures
131
Q

Lotions/solutions

A
  • low potency
  • variable drying
  • large allergy and moderate irritation risk
  • scalp and intertriginous areas
  • avoid fissures
132
Q

Foams

A
  • stable at room temp, but melts at body temp
  • supersaturated active ingredients
  • strong potency
133
Q

What factors to consider when choosing a vehicle?

A

1) anatomic location
2) contact allergy/sensitization
3) irritancy

134
Q

Explain how corticosteroids are anti-inflammatory

A
  • 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
Q

Hydrocortisone

A
  • the gentle touch
  • good for mild eczema
  • treats inflammatory dermatoses in face, intertriginous area, groin
  • lowest class
136
Q

Triamcinolone acetonide

A
  • affordable
  • class 4
  • most moderate spongiotic dermatoses
  • not rec for long term use
137
Q

Clobetasol propionate

A
  • class 1
  • most potent
  • acute eruptions that need rapid help
  • avoid face and groin
138
Q

What effects does UVR damage to the skin have?

A

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
Q

UVB rays cause

A
  • eye problems
  • sunburns
  • dna damage
140
Q

UVA rays cause

A
  • dna damage
  • premature aging
  • loose skin
  • wrinkles
  • dark patches
141
Q

Skin architecture

A
  • 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
Q

vitamin d synthesis

A
  • UVR induces synthesis of cholecalciferol (VD3) and ergocalciferol (VD2);
  • both convert to active form in liver and kidney (dihydroxy VD3)
143
Q

main types of DNA damage from UVR

A
  • thymine dimers (UVB)
  • pyrimidine 6 4 pyrimidone (UVB)
  • hydroxyguanosine (UVA)
144
Q

photocarcinogenic cascade

A
  • UV exposure
  • DNA Damage
  • formation of mutations
  • multistage carcinogenesis (init, promot, transform)
  • melanoma, NMSC (basal cell carcinoma, squamous cell carcinoma)
145
Q

skin defense against UVR

A
  • dna repair
  • apoptosis of dna damaged cells
  • defenses against ROS
  • melanin
146
Q

Melanin production

A
  • melanocytes in basal layer of skin

- melanin deposited into keratinocytes

147
Q

Basal Cell Carcinoma features

A
  • 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
Q

BCC pathophysiology

A
  • starts in lowest layer of epidermis (basal cell layer)

- arise from pluripotent cells

149
Q

BCC clinical course

A
  • begin on areas exposed to sun
  • grows slowly
  • rare to metastasize
150
Q

Actinic Keratosis clinical course

A
  • can develop in SCC
  • typically in fair skinned
  • produced by UVR
  • distributed in areas of sun exposure
  • hyperkeratosis
  • erythematous papules
151
Q

AK treatment

A

cryotherapy

- topical meds

152
Q

Squamous cell carcinoma clinical appearance

A
  • growing lumps, rough surface

- flat red patches

153
Q

SCC clinical course

A
  • 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
Q

Non melanoma skin cancer risk factors

A
  • UVR damage of keratinocytes
  • Fair skin
  • men
  • chemicals
  • ## radiation
155
Q

Melanoma

A
  • breslow measurement of thickness is the most important factor in determining prognosis of melanoma
  • treat with excision or radiation therapy
156
Q

Kaposi Sarcoma

A
  • from cells that line lymph or blood vessels
  • tumors on skin or mucosal surfaces
  • purple red or brown tumors on skin
157
Q

What ways can bacteria gain access to the body?

A
  • mouth
  • respiratory tract
  • anus
  • urogenital tract
  • conjunctiva
  • scratch/injury
158
Q

What are Koch’s Postulates?

A

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

159
Q

What is the difference between frank and opportunistic pathogens?

A
  • frank: can readily cause disease in normal hosts

- opportunistic: host needs to be compromised and less often in normal hosts

160
Q

What are the stages of infection?

A

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?

161
Q

Encounter

A
  • agent exogenous or endogenous?
  • contact from where?
  • route of infection
  • infectious dose?
162
Q

Entry

A
  • cross an epithelial barrier?
  • invasion or passive?
  • colonization of body surfaces
  • adherence
163
Q

Spread

A
  • spreading factors: hyaluronidase, elastase, collagenase

- coagulase inhibits spread by depositing fibrin

164
Q

Multiplication

A
  • must replicate faster than clearance by defense
165
Q

Damage

A
  • microbial toxins to tissue

- blocking defense mechs

166
Q

Outcome

A
  • survival of obligate parasites requires a portal of exit as well as a portal of entry
167
Q

What is a virus?

A
  • 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
168
Q

How are viruses categorized?

A

1) classical: through physical prop (DNA/RNA, helical/icosahedral capsid, nake or enveloped)
2) how they produce mRNA

169
Q

What are two key principles of viral genomes?

A

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

170
Q

What are the 6 classes of viral genome configuration?

A

1) dsDNA (gapped circular dsDNA)
2) ssDNA
3) dsRNA
4) ss+RNA
5) ss-RNA
6) ss+RNA w/ DNA intermediate

171
Q

How do DNA viruses express?

A
  • 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
172
Q

How do RNA viruses express?

A
  • 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
173
Q

What does viral disease depend on?

A
  • effects that viral replication has on host cells
  • host response to the infection
  • ability of virus to spread
174
Q

What are the factors that influence disease induction and outcome?

A

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

175
Q

What are the main routes of infection for viruses?

A
  • respiratory, alimentary, and genitourinary

- lots of mucosal surfaces and immune responses that viruses must overcome

176
Q

What is needed for a successful initial infection?

A
  • sufficient virus
  • susceptible cells at site of entry
  • host defenses absent
177
Q

Compare acute local and systemic viral infections

A
  • 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
178
Q

What are the 3 outcomes of viral infection of a cell?

A
  • 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
179
Q

Interferon activity

A
  • 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)
180
Q

HSV1 and HSV2 features

A
  • 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
181
Q

HSV1 clinical patterns

A
  • most primary infections are asymptomatic and occur during childhood

BL and DD Unit 3 (11 decks)

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