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CLASS 22005 DERM > YOU MIGHT WANNA KNOW THIS > Flashcards

YOU MIGHT WANNA KNOW THIS Flashcards

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Dermatology Board Prep flashcards
1
Q

What type of tissue:

(a) Covers external surfaces of the body and some internal organs
(b) Lines body cavities, blood vessels, and ducts

A

Epithelium

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2
Q

Most superficial layer of cells

A

apical layer

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3
Q

deepest layer of the cell

A

basal layer

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4
Q

(a) Thin extracellular structure composed mostly of protein fibers
(b) Located between the epithelium and underlying connective tissue layer
(c) Helps to bind and support the epithelium

A

Basement membrane

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5
Q

What type of epithelial tissue:

(1) Thin, flat shape allows rapid passage of substances through them

A

Squamous Epithelium

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6
Q

What type of epithelial tissue:

(1) Tall as they are wide and shaped like cubes or hexagons

A

Cuboidal Epithelium

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7
Q

What type of epithelial tissue:

Taller than they are wide

A

Columnar epithelium

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8
Q

What type of epithelial tissue:

A single layer of cells that functions in a diffusion, osmosis, filtration, secretion and absorption.

A

Simple Epithelium

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9
Q

production and release of substances

A

Secretion

Simple Epithelium

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10
Q

intake of fluids or other substances

A

Absorption

Simple Epithelium

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11
Q

movement of water across a semipermeable membrane from an area of lower solute concentration to an area of higher solute concentration.

A

Osmosis

Simple Epithelium

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12
Q

movement of particles from an area of high concentration to an area of low concentration

A

Diffusion

Simple Epithelium

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13
Q

(1) Most common cells in connective tissue
(2) Produce & maintain most of the tissue’s extracellular components
(3) Synthesizes & secretes collagen and elastin
(4) Major component of the reparative capacity of connective tissue

A

CT Cells – Fibroblasts

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14
Q

What kind of connective tissue:

Function in localized release of compounds important to inflammatory response, innate immunity, and tissue repair.

A

CT Cells – Mast Cells

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15
Q

What kind of connective tissue:

(1) Abundant (25% of all protein in body)
(2) Very strong and resistant to shear forces
(3) Key element of all connective tissues, as well as epithelial basement membranes

A

CT Fibers – Collagen Fibers

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16
Q

Types of cell membranes

A
  1. Mucous
  2. Serous
  3. Synovial
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17
Q

What type of cell membrane:

(1) Line entire GI, respiratory, reproductive, and much of the urinary system.
(2) Epithelial layer secretes mucous (mucin) via goblet cells.

A

Mucous Membranes

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18
Q

What type of cell membrane:

(1) Lines body cavity that doesn’t open directly to exterior & covers organs that lie within the
cavity.
(a) Parietal: Attached to cavity wall
(b) Visceral: Part that covers and attaches to the organs
(c) Mesothelium: Secretes serous fluid and provides lubrication for organ movement
(2) Pleura: Lining thoracic cavity and covering the lungs.
(3) Pericardium: Lining the heart cavity and covering the heart.
(4) Peritoneum: Lining abdominal cavity and abdominal organs

A

Serous Membranes

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19
Q

What type of cell membrane:

(2) Pleura: Lining thoracic cavity and covering the lungs.
(3) Pericardium: Lining the heart cavity and covering the heart.
(4) Peritoneum: Lining abdominal cavity and abdominal organs

A

Serous Membranes

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20
Q

layers of the skin

A
  1. Epidermis
  2. Dermis
  3. Subcutaneous
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21
Q

Which layer of the skin is alive

epidermis or dermis

A

dermis

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22
Q

Layers of the epidermis

A 
Stratum Corneum
Stratum Lucidum
Stratum Granulosum
Stratum Spinosum
Stratum Basale

(Come, Lets, Get, Sun, Burnt)

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23
Q

What Layer:

(a) Cells consist mostly of keratin
(b) Cells are shed & replaced from below

A

Stratum Corneum

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24
Q

What Layer:

(a) Found only in palms & soles of hands & feet

A

Stratum Lucidum

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25
Q

What Layer:

(a) Losing cell organelles and nuclei
(b) Infusion of waterproofing lipids

A

Stratum Granulosum

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26
Q

What Layer:

(a) Cells beginning to flatten

A

Stratum Spinosum

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27
Q

What Layer:

Stem cell layer; new cells arise here

A

Stratum Basale

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28
Q

T/F:
Melanocyte numbers are similar in individuals of different racial backgrounds; differences of pigmentation result from the amount & quality of melanin in the skin

A

T

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29
Q

(1) Typically found within the stratum spinosum
(2) Form a mobile and dense network of cells that samples any antigens that attempt to pass through the epidermis
(3) These monocyte-derived cells represent a large part of the skin’s adaptive immunity

A

Dendritic Cells

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30
Q

Release secretions directly into the bloodstream

A

Endocrine glands:

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31
Q

Release secretions onto an epithelial surface via a duct

A

Exocrine glands:

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32
Q

An exocrine gland in the skin that opens into a hair follicle and secretes an oily/waxy sebum

A

Sebaceous Glands

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33
Q

(1) Cover nearly the entire body surface; especially dense on the palms, soles, forehead, and upper limbs (500/cm2)
(2) Empty directly onto the skin surface, not from hair follicles
(3) Serves as major thermoregulation component of the integumentary system
(4) Sweat is a dilute electrolyte solution comprised of H2O, NaCl, and minimal waste products
(5) Minimal Odor from sweat

A

Sudoriferous – Eccrine Glands

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34
Q

(1) Largely confined to the axillae, perineum, and concentrated in hairy areas
(2) Attached to the hair follicle; apocrine sweat empties onto the skin via the follicle opening
(3) sweat is cloudy, viscous, and initially odorless. However, serves as a nutrient source for microbes and attains its characteristic odor upon being degraded by bacteria.
(4) these glands do not become functional until puberty and have a hormonal activation pattern

A

Sudoriferous – Apocrine Glands

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35
Q

There are three main pigments that influence skin pigmentation:

A

(a) Melanin (epidermis)
(b) Carotene (dermis)
(c) Hemoglobin (red blood cells within capillaries of dermis)

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36
Q

Primary determinant of skin color, hair color and eye color

A

Melanin

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37
Q

(1) ___ exposure stimulates melanin production; increasing both the amount and darkness of the melanin pigment imparted into the epidermis
(2) Increasing melanin amount and darkness serves an adaptive protective function since melanin protects the skin against damage
(3) overexposure is a predisposing factor for skin cancer

A

Ultraviolet (UV) Light & Skin Color

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38
Q

(1) Acquired depigmentation the skin characterized by loss of melanocytes
(2) Thought to be a systemic autoimmune disorder in which antibodies attack the melanocytes

A

Vitiligo

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39
Q

functions of the skin

A

a. Temperature Regulation
b. Protection
c. Cutaneous Sensation
d. Excretion/Absorption/Synth

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40
Q

What does the skin synthesize

A

Vitamin D

Vitamin D is converted to calcitriol which aids in the absorption of calcium and phosphorus

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41
Q

(1) The inevitable physiologic changes of the skin that occur with time and are influenced by genetic and hormonal factors
(2) This form of aging is not preventable and happens to everyone

A

Intrinsic Aging

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42
Q

(1) The preventable structural & functional changes of the skin that occur with exposure to:
(a) Environmental factors
(b) Lifestyle (tobacco, ETOH, illicit drugs, etc.)
(c) Social determinants
(d) Elective cosmetic surgeries
(2) Most important source of preventable extrinsic aging is ultraviolet radiation exposure
(a) Termed “photo-aging”

A

Extrinsic Aging

43
Q

What kind of tissue has the poorest capacity for renewal because it does not undergo mitosis to replace damaged neurons

A

Nervous tissue

44
Q

(1) Serves mainly to clear bacteria & debris from the wound and to prepare wound environment for repair
(2) Platelet & fibrin clot forms in the injured space, providing hemostasis and inducing both cellular and chemical inflammatory responses. Severed nerves also provide signals that increase inflammation in the injured area.
(3) Mast Cells release chemical mediators causing local capillary vasodilation, increasing permeability and augmenting local blood flow and migration of inflammatory cells to the injured area
(4) Neutrophils phagocytose cellular debris, bacteria, and foreign material, and release multiple factors that further the inflammatory reaction. After neutrophils are done, they are removed via physical sloughing or are phagocytosed themselves by macrophages.

A

Healing – Inflammation Phase

(1) Inflammatory phase (1-3 days post injury):

45
Q

(1) Purpose is to construct granulation tissue to fill the defect caused by the wound
(2) Fibroblasts are the major cellular agent in this phase and produce Type III collagen to provide structural integrity to the new tissue
(3) Collagen provides contractile force to minimize wound surface area during healing. Once enough extracellular matrix has been laid down most fibroblasts undergo apoptosis.
(4) Keratinocytes from wound edges migrate onto wound surface and advance across the wound, leaving proliferating keratinocytes behind until they reach the keratinocytes on opposite wound edge

A

Healing – Proliferative Phase

(1) Proliferative phase (2 to 10 days post injury):

46
Q

(1) 2–3 weeks post-injury: tissue defects have been replaced with granulation tissue & covered
by new epithelial cells
(2) Wound tissue now consists of disorganized collagen and extracellular matrix proteins without dermal appendages (hair follicles/sweat glands) and is covered with epithelium
(3) Surface of the wound contracts, causing base of the wound to be wider than the surface
(4) Fibroblasts, macrophages, and endothelial cells in wound space begin to apoptosis or exit wound

A

Healing – Early Remodeling Phase

47
Q

(1) Remodeling Phase (months to > 1 year):
(2) The type III collagen laid down by the fibroblasts are replaced with type I collagen and collagen fibrils become more organized
(3) As collagen rearranges, the tensile strength of the wound increases from 20% at 3 weeks after injury, to 70–80% at 6 weeks, but never reaches the full strength of uninjured tissue
(4) Over time, collagen fiber rearrangement makes the scar become less thick & firm
(5) The initial capillaries formed in the inflammatory phase regress and the scar becomes and less erythematous

A

Healing – Late Remodeling Phase

48
Q

What kind of healing

Relies on dermal edges that are close together and easily approximated

A

Primary Intention

49
Q

What kind of healing

Relies on formation of granulation tissue to fill the space between the wound opening or edges

A

Secondary Intention

50
Q

How do you measure skin lesions

A

Always in mm or cm

51
Q

Calluses or Corns

well circumscribed areas of thickened epidermal keratin that develop at locations of repeated pressure or friction

A

Calluses

52
Q

Calluses or Corns

develop similarly, but have a central hyperkeratotic core that is often painful.

A

Corns

53
Q

1) Accumulation of melanocytes/nevus cells in dermis
2) Symmetric brown macule or papule with smooth, regular borders
3) Typically have homogeneous beige, pink, or brown
4) Usually < 6 mm
5) Number associated with sun exposure

A

Nevus

54
Q

Inflammation of a hair follicle that can occur anywhere on the body where hair is found.

A

Folliculitis

55
Q

Folliculitis

Most frequent bacterial infection etiology

A

S. Aureus

56
Q

Folliculitis

Risk Factors

A

(1) Hair removal (shaving, plucking, waxing, epilating agents)
(3) Occlusive dressing or clothing
(5) Diabetes mellitus
(7) Use of hot tubs or saunas
(8) Chronic antibiotic use (gram-negative folliculitis)

57
Q

Folliculitis

Tx for Staph folliculitis

A

(a) Mupirocin ointment applied TID for 10 days
(b) Cephalexin: 250-500 mg PO QID (7-10 days)
(c) Dicloxacillin: 250-500 mg PO QID (7-10 days)

58
Q

Folliculitis

Tx for MRSA folliculitis

A

(a) Bactrim DS: 1-2 tablets BID PO (5-10 days)
(b) Clindamycin: 300 mg PO TID (10 to 14 days)
(c) Doxycycline: 50-100 mg PO BID (5-10 days)

  • PCN Allergy approved
59
Q

Most common form of impetigo. Formation of
vesiculopustules that rupture, leading to crusting with a characteristic golden appearance; local lymphadenopathy may occur.

A

Nonbullous impetigo

60
Q

staphylococcal impetigo that progresses from small to large flaccid bullae(newborns/young children) caused by epidermolytic toxin release; ruptured bullae leaving brown crust; less lymphadenopathy; trunk more often affected; <30% of patients

A

Bullous impetigo

61
Q

Impetigo Risk Factors

A

(1) Warm, humid environment
(5) Poor hygiene, poverty, crowding, epidemics, wartime
(6) Familial spread

62
Q

a cutaneous pyoderma characterized by thickly crusted erosions or ulcerations.
Usually a consequence of neglected impetigo and classically evolves in impetigo occluded by footwear and clothing.

A

Ecthyma

63
Q

Impetigo

Diagnostic Tests and Interpretation

A

Woods lamp and KOH prep to rule out fungal infection in areas of high fungal likelihood

64
Q

Impetigo Treatment

A

(1) Avoidance of infection spread is the key; hand washing is vital, especially for reducing spread in children.
(2) Prevent with mupirocin ointment TID to sites of minor skin trauma.
(3) Remove crusts; clean with gentle washing 2 to 3 times daily; and clean with antibacterial soap, chlorhexidine, or Betadine.
(4) Washing of entire body may prevent recurrence at distant sites

65
Q

Most common portal of entry for lower leg cellulitis

A

toe web intertrigo with fissuring, 2/2 interdigital tinea pedis.

66
Q

cellulitis

Diagnostic Tests to r/o

A

US to r/o Deep Vein Thrombosis (DVT)

67
Q

Cellulitis Treatment

Purulent cellulitis (probable CA-MRSA)

A

*

68
Q

Cellulitis Treatment

Human/animal Bites

A

Amoxicillin + clavulanic acid (Augmentin)

69
Q

Cellulitis

When to consider a MEDADVICE

A

(a) Elevated white blood cell count with marked left shift.
(b) Failure to respond to oral antibiotics.
(c) Severe infection, suspicion of deeper or rapidly spreading infection, tissue necrosis, or severe pain.
(d) Worsening symptoms that do not resolve/improve after 24 to 48 hours of therapy.
(e) Cellulitis of the hand and face may require hospitalization.

70
Q

Which MDT

The pain is progressive, relentless, and severe and is often out of proportion to the severity of the physical findings

A

Necrotizing Fasciitis

71
Q

Necrotizing Fasciitis

Treatment

A

Prompt and wide surgical debridement is the cornerstone of treatment.

72
Q

Necrotizing Fasciitis

Disposition

A

Immediate medevac is required for this patient

73
Q

Necrotizing Fasciitis

Complications

A

Toxic shock syndrome (acute toxin-mediated febrile illness caused by the production and release of exotoxins by S. aureus.

74
Q

A well-circumscribed, painful, inflammatory nodule at any site that contains hair follicles. May extend into the dermis and subcutaneous tissues.

A

Furuncle

75
Q

A coalescence of several inflamed follicles into a single inflammatory mass with purulent drainage from multiple follicles

A

Carbuncle

76
Q

mainstay of treatment for an abscess, furuncle, or

carbuncle

A

Incision and Drainage

77
Q

s an acute inflammatory process, with or without abscess formation, that involves the proximal and lateral nail folds and that has been present for less than six weeks

A

Paronychia

78
Q

Paronychia is Most commonly caused by

A

Staphylococcus aureus, Streptococcus pyogenes infection in the periungual tissues by minor mechanical or chemical traumas that disrupt the nail
fold barrier.

79
Q

the most common infection of the hand, representing 35% of all hand infections in the United States.

A

Paronychia

80
Q

Paronychia Treatment where MRSA is common

A

Bactrim/Septra DS

81
Q

Felon Treatment

A

(1) Prompt incision, with division of the fibrous septa to ensure adequate drainage.
(2) Should be performed by Dermatologist if available.
(3) IDC should treat with antibiotics.

82
Q

Labs for Fungal Infections

A

(a) Typically not required as clinical diagnosis is sufficient.
(b) Lab diagnosis based on identification of yeast and pseudohyphae in potassium hydroxide wet mounts of scrapings from a lesion.
(c) Positive culture alone is usually meaningless because Candida is omnipresent.

83
Q

Which Tinea:

Infection of crural fold and gluteal cleft.

A

Tinea Cruris

84
Q

Which Tinea:

Infection involving the face, trunk, and/or extremities;
often presents with ring-shaped lesions, hence the misnomer ringworm.

A

Tinea Corporis

85
Q

Which Tinea:

Infection of the scalp and hair; affected areas of the scalp can show characteristic black dots resulting from broken hairs.

A

Tinea Capitis:

86
Q

Tx for Fungal Infections

A

(a) Topical

1) Clotrimazole, Miconazole or Terbinafine applied BID for a minimum of 2 weeks

87
Q

T/F:

Dermatophytes are fungal

A

T

88
Q

T/F:

Tinea Versicolor is a yeast

A

T
*Caused by Pityrosporum orbiculare, which is part of the normal skin flora

Organism is nourished by sebum; converts from yeast form to mycelial form and causes the disorder

89
Q

Tinea Versicolor tx

A

Selenium Sulfide 2.5% applied from neck to waist wash off after 515 minutes, repeat daily x 7 days. Repeat weekly x 1 month, then monthly for maintenance

90
Q

Onychomycosis Pretreatment diagnostic testing

A

(c) Treatment is not done on deployment due to inability to perform LFT testing.
(d) Oral antifungal therapy is considered the gold standard for onychomycosis; higher complete cure rates & shorter course of treatment compared with topical therapy

91
Q

A contagious parasitic infection of the skin caused by the mite Sarcoptes scabiei, var. hominis

A

Scabies

92
Q

How are scabies primarily transmitted

A

human-to-human direct skin contact

93
Q

scabies Presentation

A

Intense pruritus that worsens at night is a cardinal feature.

94
Q

Labs/Studies/Imaging for scabies

A

Ink test: Rub a black felt-tip marker across an affected area. Remove excess ink is wiped away with an alcohol pad, burrow appears darker than the surrounding skin because of ink accumulation in the burrow

95
Q

scabies tx

A

Permethrin 5% or Lindane 1% applied to entire skin surface from the neck down, including under the fingernails and toenails an in the umbilicus

Treatment regimen should be repeated in 1 week.

All clothes and bedding must be washed in hot water or put in a hot dryer
at the time of application.

Can also be set aside wrapped in plastic bags for 14 days

96
Q

Pediculus Humanus Capitis tx

A

Permethrin rinse 1% (Nix); Permethrin 5% (Elimite); Lindane % (Kwell)

97
Q

Pityriasis Rosea Presentation

A

(1) Prodromal symptoms are reported in as much as 69% of patients and typically include some variation of the following:
(a) Malaise, mild fever, headache, sore throat, cough, or mild URI or GI symptoms.
(b) Classic PR begins with a solitary herald patch that appears on the trunk or proximal limbs that precedes secondary eruption by 7-14 days.
(c) Herald patch: a 2-5 cm round or oval, sharply delimited, pink or salmon-colored lesion on the chest, neck, or back
(d) Lesions are distributed with long axes along cleavage (Langer’s) lines:
1) “Christmas tree pattern” on back

98
Q

Pityriasis Rosea tx

A

(g) Symptomatic treatment of pruritus:
1) Non-sedating oral antihistamines (centrizine, loratidine, fexofenadine)
2) Sedating antihistamines if sleep interrupted
(benedryl/atarax).
3) Topical corticosteroids commonly used, however, drains AMAL meds due to size or eruption (logistically dumb).

99
Q

HSV-1 tx

A

(3) Antiviral treatment is typically not required by many patients due to selflimited nature of disease
(5) Antiviral medications reduce duration by about 1 day (range 0.5 days-2 days) but cannot cure infection (lifelong latency).
(a) Acyclovir 400 mg PO 5x / day for 5 days

100
Q

Diffuse pox-like eruption complicating atopic dermatitis; sudden appearance of lesions in typical atopic areas (upper trunk, neck, head); high fever, localized edema, adenopathy

A

Eczema herpeticum

101
Q 
Herpes Zoster (Shingles)
Common findings
A

(1) Acute Neuritis with Prodrome:
(a) Characteristic prodrome may precede rash by 1-5 days; paresthesias with allodynia or hyperesthesia described by Pt as a deep “burning,” “throbbing,” or “stabbing” sensation
(2) Derm Manifestations:
(a) Typically unilateral dermatomal rash without midline crossing that favors the thoracic, cranial (particularly trigeminal), lumbar, and cervical dermatomes.

102
Q

Herpes Zoster (Shingles) tx

A

(1) Goal is to limit the extent/duration/severity of pain & rash in the primary dermatome & to prevent disease elsewhere.
(2) <72 hours after onset
(a) Antiviral therapy should be initiated to maximize benefits of treatment.
(b) Valacyclovir: 1000 mg three times daily for seven days.
(c) Acyclovir: 800 mg five times daily for seven days.

103
Q

(1) frequently involves the ophthalmic division of the trigeminal nerve.
(2) Presents with malaise, fever, headache, and periorbital burning/itching.
(3) Approximately 50 percent of patients with this experience direct ocular involvement if antiviral therapy is not used.
(4) Hutchinson’s Sign: Vesicles on the tip/side of the nose precedes the development.
(a) The nasociliary branch of the trigeminal nerve innervates both the cornea and the lateral dorsum of the nose as well as the tip of the nose

A

(1) HZO frequently involves the ophthalmic division of the trigeminal nerve.
(2) Presents with malaise, fever, headache, and periorbital burning/itching.
(3) Approximately 50 percent of patients with HZO experience direct ocular involvement if antiviral therapy is not used.
(4) Hutchinson’s Sign: Vesicles on the tip/side of the nose precedes the development of HZO.
(a) The nasociliary branch of the trigeminal nerve innervates both the cornea and the lateral dorsum of the nose as well as the tip of the nose

CLASS 22005 DERM (25 decks)

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