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INTEG > FINAL > Flashcards

FINAL Flashcards

1
Q

“the itch that rashes”

A

Atopic Dermatitis

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2
Q

Charactersitics

puritic, superficial, chronic, scaly

A

Atopic Dermatitis

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3
Q

Atopic Triad

A

Atopic dermatitis
Asthma
Allergic Rhinoconjunctivitis

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4
Q

What causes the faulty epidermal barrier in atopic dermatitis patients?

A

Deficiency in filaggrin
Decrease in ceramides
Transdermal water loss

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5
Q

Atopic Dermatitis Manifestation

superficial scaly macules (slightly yellowish - hypopigmentation), patches over the cheeks, symmetrical distribution

A

Pityriasis Alba

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6
Q

Atopic Dermatitis Manifestation

darkened mildly erythematous or tanned perioribtal areas, bilaterally and symmetrically

A

Allergic Shiners

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7
Q

Atopic Dermatitis Manifestation

sparse or confluent distrubtion of follicular papules, symmetric on dorsal upper arms or trunk

A

Keratosis Pilaris

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8
Q

Atopic Dermatitis Manifestation

skin thickening, seen at popliteal fossa and antecubital fossa symmetrically
consequence of the itch scratch cycle
Hyperpigmentation

leathery patches

A

Lichenification

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9
Q

Atopic Dermatitis Manifestation

dry “coin-lack” patches, sparsely distributed on extremities and trunk, itchy

A

Nunmular Eczema

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10
Q

Atopic Dermatitis Manifestation

periorbital eczema
infraorbital folds in the skin below the eyelids

A

Dennie-Morgan folds
Dennies Pleats

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11
Q

Atopic Dermatitis Manifestation

lip-smacking eczema – perioral

A

Atopic Cheilitis

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12
Q

What is the most common complication of Atopic dermatitis?

A

Secondary Bacterial Infection
IMPETIGO

Staph aureus = MC cause of secondary bac infection

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13
Q

Secondary Viral Infection of Atopic Dermatitis

caused by HSV
– lesions (vesicles, ulcers and crusts) on face

A

Eczema Herpeticum
= Kaposi Varicelliform Eruption

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14
Q

dermatological sign that consists of fine telangiectasias around the nail

A

Braverman’s Sign

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15
Q

a change observed after stroking lesions on the skin of a person with systemic mastocytosis or urticaria pigmentosa
skin biopsy shows INC number of dermal mast cells

A

Darier’s Sign

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16
Q

is the appearance of new skin lesions on previously unaffected skin secondary to trauma

A

Koebner phenomenon

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17
Q

TEN or SJS

greater than 30% of the body vs. less than 10% of the body surface

A

30 = TEN
10 = SJS

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18
Q

When you do a skin biopsy of a patient with SJS/TEN overlap what do you see?

A

Necrotic Epithelium

No T-Cell destruction of the dermo-epidermal junction

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19
Q

What are the mortality rates of TEN, SJS and the overlap?

A

SJS = 5-12%
TEN = 40%
Overlap = 10-30%

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20
Q

What pathogen could cause an infection –> SJS or TEN?

A

mycoplasma pneumonia

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21
Q

What could lead to toxic shock syndrome: TEN or SJS?

A

TEN

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22
Q

What hallmark is seen a part of 1-14 day prodrome of SJS?

A

nonspecific upper respiratory tract infection

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23
Q

What factors can cause a poor prognosis of SJS?

A

Old Age > 70
Intestinal involvement
Pulmonary Involvement

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24
Q

What complications can arise from SJS/TEN overlap?

A

Blindness, pigmentary scritures/scarring

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25
Q

Most common drugs which cause SJS/TEN?

A

Sulfa: sulfasalazine
Antibiotics: Ampicillin/Amoxicillin
Antiepileptics: phenytoin, carbmazepine, phenobarbital, lamotrigine

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26
Q

Controversial Tx Option – SJS

inhibits CD8 cells – slow progression of active disease and DEC mortality potentially

A

Cyclosporine

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27
Q

A patient with Urticaria asks how long it will take for her skin to return to normal?

A

Fleeting Time Course
30 min – 24 hours

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28
Q

What makes uritcaria CHRONIC vs. ACUTE?

A

Chronic = > 6 weeks

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29
Q

What is reponsible for the immune-mediated activation in Urticaria?

A

MAST CELLS

Type 1 hypersensitivity

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30
Q

What treatment is prefered in the treatment of Uritcaria?

A

Second Generation H-1 Blockers:
Cetrizine, levocetrizine, loratadine, desloratadine, fexofenadine

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31
Q

Whats linked to more severe CSU: Eosinophelia or Eosinopenia ?

A

Eosinopenia

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32
Q

Eosinopenia was linked to poor response of treatment with standard histamine blockers and what monoclonal antibody?

A

Omalizumabb

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33
Q

hyperpigmented mucous membranes, palmar creases, perineum, nipples and nevi
Adrenal insufficency

A

Addison Disease

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34
Q

Periorbital ecchymoses = racccoon eyes
Macroglossia with dental impression on tongue
waxy/translucent facial papules

A

Primary Amyloidosis

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35
Q

Skin disorders associated to HEP C

history of alcholol abuse

A

PCT = porphyria cutanea tarda
Lichen Planus

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36
Q

What is this associated to?

Hereditary Hemorrhagic Telangiectasia = multiple small bright red macules and papules on the tongue and lips

A

GASTRIC Disease

also blue rubber bled nevus syndrome

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37
Q

What is this associated to?

Dermatitis Herpetiformis
Erythematous papules on elbows/knees

GLUTEN SENSITIVE

A

Gastric Disease

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38
Q

What is the most common skin manifestation of diabetes?

A

Diabetic Dermopathy
skin hyperpigmentation on tibia

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39
Q

What is this associated to?

Acanthosis nigricans of the neck in a patient with insulin resistance and obseity

A

Diabetes

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40
Q

eruptive xanthomas are frequently associated with poorly controlled what?

A

diabetes mellitus

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41
Q

Patient has erythema gyratum repens … what do you suspect

A

BREAST CANCER

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42
Q

Patient has kaposi’s sarcoma
red-violet papules on the palate in addition to oral candidiasis … what do you suspect?

A

HIV

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43
Q

Pemphigus vulgaris and pemphigus foliaceus are autoimmune diseases caused by what type of hypersensitivity reactions?

A

TYPE 2 = Antibody Mediated

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44
Q

IgG autoantibodies in pemphigus vulgaris and pemphigus foilaceus bind to what?

A

Intracellular desmosomal proteins (desmoglein type 1/3)

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45
Q

lysis of the intracellular adhesive junctions between neighboring squamous epithelial cells that results in the rounding up detached cells =

A

Acantholysis

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46
Q

suprabasal acantholytic blister

erosion

A

Pemphigus Vulgaris

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47
Q

subcorneal blister
– superficial epidermis at the level of stratum granulosum

more superficial

A

Pemphigus foilaceus

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48
Q

bullous phemphigoid – target antigen is located at

A

HEMIdesmosomes

desomosomes – pemphigus

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49
Q

What is a key distinction factor regarding the blisters between pemphigus and pemphigoid?

A

Pemphigus – acantholysis
Pemphigoid – blister roof consists of full thickness epidermis with intact intracellular junctions – lacks acantholysis

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50
Q

In bullous pemphigoid blisters, the supepidermal vesicle is rich with what type of inflammatory infiltrate?

A

EOSINIOPHILIC

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51
Q

gestational pemphigoid/herpes gestationis usually occurs during what trimester of pregnancy?

A

2nd or 3rd

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52
Q

autoimmune blistering disorder associated with gluten sensitivity that is characterized by extremely pruritic grouped vesicles and papules =

A

Dermatitis herpetiformis

affects mainly males – 3rd/4th decades of life

53
Q

in dermatitis herpetiformis; IgA antibodies bind to what
?

A

Gluten – gliadin

54
Q

Morphology of what disease?

IgA autoanitbody at the tips of dermal papillae
Microabscesses – vacuolization and focal dermoepidermal seperation that ultimately coalese to form a true subepidermal blister

A

Dermatitis Herpetiformis

55
Q

What disease?

microscopic and ultrastrutural studies have revealed vacuolar degeneration of basal and parabasal keratinocytes and dermal lymphohistiocytic infiltrates

A

VITILIGO

56
Q

Vitiligo patients have an increased freq. of other autoimmune disorders such as:

A

Hashimoto thyroiditis
Graves
Pernicious Anemia
Addison disease

57
Q

Subclass of scleroderma

A

MORPHEA

58
Q

Heterogeneous spectrum of disorders is a key feature of ….

A

Systemic Lupus

59
Q

+ANA titer is indicative of …

A

American College of Rheumatology classification of SLE

60
Q

Autoimmune CT disease of uncertain etiology demonstrating bimodal aged distribution of juvenile and adult forms is a key feature of …

A

Dermatomyositis

61
Q

Varaince of scleroderma consists of

A

CREST

62
Q

Genetic component (endogenous) and enviroment (Exogenous)

A

SLE

63
Q

immunosuppresion by DEC mast cells can be treated primarily with?

A

Gluccorticoids

64
Q

Osteoporosis is a complication of?

A

Systemic gluccorticoid (too much of it)

65
Q

Irritation syndrome results from

A

Adverse reactions to cosmetics

66
Q

Bacterial/Fungal/Viral infections are a complication of?

A

Chemical Peels

67
Q

Lateral venous system varicoses can be treated by?

A

Sclerotherapy

68
Q

Mohs surgery is best indicated for:

A

Basal Cell Carcinomas that have ill defined borders on the face

69
Q

This oral drug is used to treat psoriasis
MOA = binds retoind X receptors – antiinflam/antiproliferative actions
Keratinocyte differentiation is normalized

AE = liver problems TERATOGEN

A

Acitretin

70
Q

this oral drug treats psoriasis
MOA = phosphodieterase-4 inhibitor

A

Apremilast

71
Q

Thiw TNF-alpha inhibitor decoys a TNF-alpha receptor and are not a monoclonal antibody
Binds selectively to TNF-alpha

A

Etanercept

72
Q

This TNF-alpha inhibitor is a chimeric monoclonal ab
Binds to soluble and transmembrane forms of TNF-alpha

A

Infliximab

73
Q

this TNF-alpha inhibitor is fully humanized anti-TNF-a IgG1
binds specifically to TNF-alpha

A

Adalimumab

74
Q

This TNF-alpha inhibitor binds selectively and neutralizes human TNF-alpha activity
not a complete ab – lacks Fc region
* does not indue complement activation
* no ADDC or apoptosis

treats plaque psoriarisis

A

Certolizumab

75
Q

thia drug is a human IgGK monoclonal ab
binds to p40 protein subunit shared by IL-12 and IL23 inhibiting TH1/TH17 cell mediated responses
inhibits the release of proinflam. cytokines

A

Ustekinumab

76
Q

these drugs bind selectively to p19 subunit of IL-23 cytokine – inhbits the release of pronflam cytokine

A

Guselkumab, Tildrakizumab, Risankizumab

23 Forillas Tasted Rasins

77
Q

these drugs bind selectively with IL-17A cytokine – inhibits the release of proinflam cytokines

A

Secukinumab and Ixekizumab

78
Q

this drug is an anti-IL-17A RECEPTOR comp. inhibitor

A

Broadalumab

79
Q

this topical treatment blocks calcineurin and is used to treat atopic dermatitis

A

Pimecrolimus

80
Q

This topical is used in the treatment of scalp plaque psoriasis

A

Flucinolone

81
Q

this topical drug binds to vit. D receptors – inhibits keratinocyte proliferation, enhances keratinocyte differentation/inhibits inflammation

A

Calcipotriene

82
Q

This topical, non-steroidal is a phosphodiesterase-4 inhibitor

A

Roflumilast

83
Q

This topical; non-steroidal is an aryl hydrocarbon receptor agonist

A

Tapinarof

84
Q

Diphenydramine, Hydroxyzine and Doxepin can be used in treatment for

A

Pruritis

Doxepin can proling QT interval

85
Q

this topical, weak hypopigmenting agent inhibits the enzyme tyrosinase

A

Hydroquinone

86
Q

This topical is a monobenzyl ether which can cause irreversible depigmentation – vitiligo

A

Monobenzone

87
Q

this topical stimualtes hair growth is secondary to vasodilation
treatment of androgenetic alopecia

A

Minoxidil

88
Q

ORAL
5alpha-reducatse enzyme inhibitor
Blocks conversion of testosterone
tx: Androgenetic alopecia

A

FINASTERIDE

preg. women should not be exposed

89
Q

this opthalmic solution = synthetic prostraglandin analog
increase the percent and duration of hairs in the growth phase
TX: Hypotrichosis of eyelashes

A

Bimatoprost

90
Q

topical cream – irreversible inhibitor of ornithine decarboxylase
Tx: Facial hirsutism

A

Eflornithine

91
Q

These drugs are used in tx. of acne vulgaris – block peptide transfer at 50S ribosomal subunit – protein synthesis

A

Erythomycin/Clindamycin

92
Q

these antibiotic agents bind to 16S rRNA of the 30S subunit
pRevents the binding of aminoacyl -tRNA to mRNA ribosome complex
inhibits bacterial protein synthesis

A

Doxycycline, Minocycline and Tetracycline

93
Q

this topical is an ethyl ester produrg
binds to RAR-Beta/gamma
Tx: Acne /psoriasis

preg catergory X

A

Tazarotene

94
Q

these drugs inhibit fungal squalene epoxidase –> DEC synthesis of ergosterol –> accumulation of squalene –> INC membrane permeability – cell death

FUNGICIDAL

A

Allyamine: Terbinafine/Naftifine
Butenafine

95
Q

What is the first treatment that is most effective for onychomycosis

A

Terbinafine

96
Q

this oral drug binds to keratin precursor cells – interferes with microtubule function – disrupts fungal mitosis

A

Griseofulvin

tinea captitis

97
Q

topical treatment of tinea pedic, cruris/coporis, onychymcosis, cut. candidiasis/seborrheic dermatitis
DISRUPTS The synthesis of DNA, RNA and protein

A

CICLOPIROX

98
Q

this topical is reversible and noncomp. inhibitor of fungal squalene epoxidase

tinea pedis, cruris and corporis

A

Tolnaftate

99
Q

antiviral agent binds toll like receptor 7

tx: anogenital warts/molluscum contagiousm, HSV

A

Imiquinmod

100
Q

oral anitivral – immunomodulatory effects by blocking histamine induced stimulation of T-suppressor cell activity

Tx: Warts/molluscum contagiosum

A

Cimetidine

101
Q

anti-parastitic agent = topical
directly absorbed – stimulates nervous system – seizures/death of parasitic arthropods

Tx: Scabies/head lice

A

Lindane

102
Q

This drug can be used to treat scabies and head lice by blocking the deactivation of Na+ channels – uncontrabble depolarization of neuronal membranes – seizures and ultimately paralusis and death of parasite

A

Permethrin

103
Q

treatment for riverblindness

A

IVERMECTIN

104
Q

treatment of schistosomiasis

A

Praziquantel

105
Q

this drug is a humanized monoclonal IgG4 kappa ab – binds to programmed death receptor and blocks interaction of PD-1 with its ligands – preventing T-cell interaction

tx for unresectable or metastatic melanoma

A

Pembrolizumab/Nivolumab

106
Q

drug = anti-CTLA -4 antibody

A

ipilimumab

107
Q

drug interacts with the high affinity-IL2 receptor – stimulates a cytokine cascade – prolifertes/induces B/T cells

A

Aldesleukin

Aldeseleakin 2

108
Q

this drug is a kinase inhibitor that targers BRAF V600E
reversible inhibitor of mitogen activated extracellular signal regulated kinase 1

A

Encorafenib

Dabrafenib

109
Q

reversible inhibitor of MEK1/MEK2
inhibitor of some mutated forms of BRAF serine threonine kinase

A

Cobimetinib

110
Q

hedgehog pathway inhibitors
block PTCH1 genetic mutation

A

Vismodegib and Sonidegib

111
Q

What is the most commonly used agent for prophylaxis pre op surg?

A

Cephalosporins

112
Q

Examples of antiseptics which can be used to inhibit or kill bacteria on mucous membranes, body tissues or skin:

A

Chlorhexidine
Mupirocin
Povidone Iodine Gel

113
Q

What is the major pathogen in surgical wound infections?

A

S. Aureus

114
Q

this incisional infection occurs 30-90 days post op, involves fascial and muscle layers

A

Deep Incisional SSI

115
Q

this incisional infection occurs 30 days post op, involved skin and subcutaneous tissues

A

Superficial Incisional SSI

116
Q

What cardiac changes do we see after a burn?

A

Loss of plasma volume
INC PVR
DEC CO

117
Q

What pulmonary changes do we see after a burn?

A

DEC Compliance

118
Q

What renal changes do we see due to a burn?

A

GFR Dec = dec renal blood flow

119
Q

What degree of burn?

nerve endings still intact; only epidermis is burnt so no scarring

A

FIRST DEGREE

120
Q

What degree burn?

extend to the dermis but doesnt penetrate it

A

SECOND Degree

121
Q

What degreee burn?

burns are full thickness burns that are not painful since the nerve endings are destroyed

A

3rd degree

122
Q

what degree burn

burns are also painless are full thickness plus Subcutaneous, muscle, and bone are destroyed

A

Fourth Degree

123
Q

Treatment steps of burn patients

A
  1. Stop the burn
  2. Primary Survery
  3. Resusitation
  4. Secondary survey
  5. burn center if need
124
Q

During the resuscitation phase in a burn treatment, what is the most important part?

A

Fluid resuscitation since systemic capillary leak syndrome occurs after a serious burn

125
Q

What are the four stages of wound healing?

A

Hemorrhagic
Substrate
Proliferative
Remodeling/Maturation

126
Q

What is the primary factor of the Hemmorhagic phase?

A

platelet derived growth factor

127
Q

During healing by secondary intention, granulation tissue forms during what phase?

A

Inflammatory/Substrate Phase

128
Q

Due to the loss of the epidermis, abrasions injury may be susceptible to:

A

Clostridium tetni and staph aureus

INTEG (2 decks)

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