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Specialty Medicine > Skin Terminology and exam > Flashcards

Skin Terminology and exam Flashcards

1
Q

What are some aspects of the history taking that are specific to derm complaints?

A
  • How has it spread

- How have lesions changed

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2
Q

What are the components of the atopic triad?

A
  • Asthma
  • Allergies
  • Atopic Dermatitis
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3
Q

What are the family history bits that should be obtained with derm complaints?

A

Skin CA

Autoimmune conditions

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4
Q

What are the major indications for a total body skin exam?

A
  • personal h/o skin CA
  • Increased risk for malignancy
  • new rash
  • f/u for extensive skin lesions
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5
Q

What should be done besides just inspecting a skin lesion?

A

Palpate it

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6
Q

What are the five major characteristics that should be used to describe a skin lesion?

A
  • Palpability
  • Color
  • texture
  • Size
  • Location
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7
Q

Are scratches or trauma skin lesions primary or secondary?

A

secondary

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8
Q

What is the definition of a macule?

A

Flat, Less than or equal to 1 cm

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9
Q

What is the definition of a patch?

A

flat, More than 1 cm

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10
Q

What is a papule?

A

raised solid lesion measuring less than or equal to 1 cm

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11
Q

What is a nodule?

A

raised solid lesion measuring more than 1 cm

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12
Q

What is a tumor?

A

raised solid lesion measuring more than 2 cm

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13
Q

What is a plaque?

A

Flat topped area measuring more than 1 cm

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14
Q

What are vesicles?

A

Raised, clear fluid filled lesion, measuring less than or equal to 1 cm

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15
Q

What is a bullae?

A

Raised, clear fluid filled lesion, measuring more than 1 cm

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16
Q

What is a pustule?

A

Raised lesion filled with white fluid or pus

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17
Q

What are wheals? how long do they usually last for?

A

Round or flat topped edematous and erythematous lesions that last less than 48 hours

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18
Q

What are telangiectasias?

A

Enlarged, superficial blood vessels

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19
Q

Are telangiectasias blanchable? Why or why not?

A

Yes–blood is still in vessels, so can move about

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20
Q

Are purpura blanchable? Why or why not?

A

No–blood is sequestered

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21
Q

What is the difference between an erosion and a ulcer?

A
  • Erosion = loss of epidermis in skin and heals without a scar
  • Ulcers = epidermis and dermis is involved
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22
Q

What are scales?

A

flakes or plates of skin come off

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23
Q

What are crusts?

A

Dried plasma or exudate

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24
Q

What are excoriations?

A

Traumatized or abraded areas d/t rubbing

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25
Q

What is atrophy of the skin?

A

Thinning or absence of epidermis or SQ fat

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26
Q

What are scars?

A

Fibrosis of skin

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27
Q

What are keloids?

A

Exaggerated scars beyond wound edges

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28
Q

What are eschars?

A

Plaque covering ulcer–implies extensive damage and necrosis

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29
Q

What is the difference between a hypertrophic scar and a keloid?

A

Keloid goes beyond wound edges

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30
Q

What are petechiae?

A

1-2 mm purplish/ reddish macules that are NOT blanchable

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31
Q

What are purpura?

A

3mm - 1 cm urplish/ reddish macules that are NOT blanchable

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32
Q

What are ecchymoses?

A

Purplish or reddish area greater than 1 cm

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33
Q

Areas of hypopigmented macules and patches after sunlight exposure = ?

A

Tinea versicolor by malassezia furfur

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34
Q

How do you diagnose tinea versicolor?

A
  • Wood light will show an orange-yellow hue

- KOH prep will show spaghetti and meatballs appearance

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35
Q

KOH prep showing a spaghetti and meatballs appearance = ?

A

Malassezia furfur

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36
Q

What is the treatment for tinea versicolor?

A

Ketoconazole or topical antifungals

37
Q

What is the MOA of topical steroids?

A

inhibits NF-kappaB, which suppresses both B and T cell function
-Lowers cytokine transcription

38
Q

What are the side effects of topical administration of steroids?

A
  • skin atrophy
  • Telangiectasias
  • Striae
  • Acne
39
Q

What hematological abnormality can steroids produce?

A

demargination of PMNs

40
Q

What is the use of class I steroids?

A
  • Severe dermatoses

- NON facial and NON intertriginous areas

41
Q

What is the length of treatment for class I, classes II-V, and classes Vi-VII?

A 
I = less than 3 weeks
II-V = less than 8 weeks
VI-VII = 1-2 week intervals
42
Q

What are the areas that you should NOT apply class I steroids to?

A

Face or intertriginous areas

43
Q

What is the use of class II-V steroids?

A

Mild to moderate non facial and non intertriginous areas

44
Q

What is the use for classes VI-VII steroids?

A

large areas, including intertriginous areas and face

45
Q

What class of steroid is: clobetasol propionate?

A

Super high (class I)

46
Q

What class of steroid is: Fluocinonide?

A

II

47
Q

What class of steroid is: Triamcinolone?

A

III - V

48
Q

What class of steroid is: hydrocortisone

A

VI-VII

49
Q

What class of steroid is: desonide

A

VI - VII

50
Q

What class of steroid is: Fluocinolone acetonide?

A

VI-VII

51
Q

True or false: no matter the vehicle, the same medication will have the same potency

A

False

52
Q

What is the major upside and downside to the use of gels as a vehicle?

A 
\+ = Stays where you put it
- = EtOH is irritating
53
Q

What is the major upside and downside to the use of foams as a vehicle?

A

+ = Easy to apply and spread rapidly

  • = expensive
54
Q

What is the major upside and downside to the use of oils as a vehicle?

A 
\+ = Less stinging
- = Messy
55
Q

What is the major benefit to ointments as a vehicle?

A

Protective barrier

56
Q

What is the use of benzoyl peroxide? Downsides?

A

Acne

Stain pillows

57
Q

What is the major benefit of retinoids?

A

keratinolytic

58
Q

What is the classic side effect of isotretinoin?

A

Teratogenic

59
Q

What is the MOA of azoles? Are these fungistatic or fungicidal?

A

Inhibits 14-alpha demethylase to prevent the conversion of lanosterol to ergosterol–an essential component of the fungal membrane

Fungistatic

60
Q

What is the MOA of allylamines? Suffix?

A
  • Inhibit squalene epoxidase

- terbinafine, naftifine etc

61
Q

What type of fungal infections are allylamines better suited for?

A

Dermatophytes more than candida

62
Q

What type of fungal infections are polyenes better suited for?

A

candida

63
Q

What is the MOA of polyenes? Examples?

A
  • bind to ergosterol in the fungal cell membrane and thus weakens it, causing leakage of K+ and Na+ ions, which may contribute to fungal cell death
  • Amp B and nystatin
64
Q

What are the major side effects of imidazoles?

A

Antiandrogen

-Hepatotoxic

65
Q

What are the major side effects of allylamines?

A

hepatotoxic
HA
GI effects

66
Q

What is the MOA of echinocandins? Names?

A

Inhibit the synthesis of glucan in the cell wall, via noncompetitive inhibition of the enzyme 1,3-β glucan synthase[1][2] and are thus called “penicillin of antifungals

-caspofungin

67
Q

What is the effect of azoles on p450 system?

A

Inhibits

68
Q

What are the histamine receptors that are inhibited to cause sleepiness? Suppress HCl production?

A 
H1 = sleep
H2 = antacid
69
Q

What are the major side effects of first generation antihistamines?

A

Dry and wobbly

70
Q

“Some drugs create awesome knockers” = ?

A
  • Spironolactone
  • Digitalis
  • Cimetidine
  • Alcohol
  • Ketoconazole
71
Q

First of second generation antihistamine: diphenhydramine

A

First

72
Q

First of second generation antihistamine: cetirizine

A

Second

73
Q

First of second generation antihistamine: hydroxyzine

A

First

74
Q

First of second generation antihistamine: chlorpheniramine

A

First

75
Q

First of second generation antihistamine: loratidine

A

Second

76
Q

First of second generation antihistamine: Fexofenadine

A

Second

77
Q

What are the two major H2 antagonists used in the treatment of GERD?

A

Ranitidine

Cimetidine

78
Q

What are the three major medications that can be used for psoriasis?

A

Coal tar
Tazarotene
Vit D analogues

79
Q

What is calcitriol (D2 or D3)?

A

D3

80
Q

What are the three major antibodies that are found with SLE?

A

Smith
dsDNA
ANA

81
Q

What is the antibody that is found with drug induced SLE?

A

Antihistone

82
Q

What is antiphospholipid antibody syndrome?

A

an autoimmune, hypercoagulable state caused by antiphospholipid antibodies. APS provokes blood clots (thrombosis) in both arteries and veins as well as pregnancy-related complications such as miscarriage, stillbirth, preterm delivery, and severe preeclampsia.

83
Q

What are the top three causes of death in SLE pts?

A
  1. CV
  2. Infection
  3. Renal disease
84
Q

What are the three general drugs used to treat SLE?

A

NSAIDS
Immunosuppressants
Steroids

85
Q

What are the complement levels that are low in SLE?

A

C3
C4
CH50

86
Q

What are the components of the RASH OR PAIN mnemonic for the signs of SLE?

A
  • Rash
  • Arthritis
  • Soft tissue/serositis
  • Heme disorders
  • Oral/nasopharyngeal ulcers
  • Renal disease / Raynaud’s
  • Photosensitivity
  • ANA abs
  • Immunosuppressants
  • Neuro disorders
87
Q

What are the drugs that cause SLE? (SHIPPE)

A
  • Sulfa
  • Hydralazine
  • INH
  • Phenytoin
  • Procainamide
  • Etanercept
88
Q

What are the sulfa drugs? (“poplar FACTSSS”)?

A 
Probenecid
Furosemide
Acetazolamide
Celecoxib
Thiazide
Sulfonamides
Sulfasalazine
Sulfonylureas

Specialty Medicine (36 decks)

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