Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clin Med MSKII > Matthys > Flashcards

Matthys Flashcards

1
Q

flat spot on skin measuring <1 cm?

> 1 cm?

A

Macule

Patch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

nonpustular, nonvesicular lesion on skin <1 cm?

> 1 cm

A

papule

nodule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

small blisters < 1 cm?

> 1 cm?

A

vesicle

bulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

a collection of leukocytes in the epidermis?

A

pustule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

broad, elevated flat lesions > 1 cm

A

plaque

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Description of lesions in atopic dermatitis

A
  • erythematous popular
  • areas of scaling
  • pruritic
  • appears as patchy, dry, scaly eruptions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

location of lesions in atopic dermatitis

A
  • facial rash on cheeks, sparing perioral and perinasal areas
  • generalized erythematous popular rash on trun and extremities with sparing of diaper area
  • no eruptions noted on interdigital web areas of toes or fingers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

associated clinical findings with atopic dermatitis

A
  • xerosis and icthyosis vulgaris
  • pigmentary changes
  • eye and periorbital changes
  • hand and foot dermatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

complications with Atopic Dermatitis

A
  • infection
  • exfoliative erythroderma
  • mental and emotional anguish with growth disturbance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

pathogenesis of Atopic Dermatitis

A
  • T cell
  • food allergy
  • Aeroallergens
  • irritant contactants
  • Histology non specific with spongiosis, eos, and features consistent with LSC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Treatment of Atopic Dermatitis

A
  • Moisturize
  • Avoid irritants
  • Avoid known food allergies
  • Topical and oral antipruritic agents
  • anti inflammatory agents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

-Acute, rapidly spreading nonsuppurative infection of the skin and underlying soft tissue NOT including the muscle

A

Cellulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical finding in Cellulitis

A
  • Tender, warm poorly demarcated boggy plaque
  • commonly on extremity
  • Trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

pathogenesis of cellulitis

A
  • Trauma to an extremity either known or unknown

- concurrent ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

risk factors for cellullitis

A
  • stasis dermatitis

- Lymphedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment of Cellulitis

A
  • it is usually Staph or Strep pyogenes
  • first gen cephalosporin, macrolide or clindamycin
  • elevation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

symmetric erythematous nodules and plaques located on the anterior lower extremities

A

erythema nodosum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

age for erythema nodosum

A

peak 20-30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

clinical findings in Erythema Nodosum

A
  • Tender nodules and plaques on the bilateral knees, ankles, and shins
  • sometimes thighs and upper extremity
  • 1-15 cm in size
  • rarely ulcerate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

etiology of erythema nodosum

A

-hypersensitivity response (infection, medicine, herbs vitamins) . .can be brought on by birth control

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Treatment of erythema nodosum

A
  • anti inflammatory

- rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Psoriasis: Koebner?
Ausptitz?
Woronoff’s ring?

A
  • Recreate psoriasis based on trauma
  • Peel off scale and get pinpoint bleeding
  • Get rid of psoriasis and it leaves a sort of stain behind
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Histology of Psoriasis

A
  • Acanthotic epidermis with club shaped rete ridges and an ABSENT GRANULAR LAYER
  • tortuous vessels seen in the papillary dermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

3 common types of psoriasis

A
  • Plaque type
  • Pustular
  • Guttate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

describe Plaque type psoriasis

A
  • well demarcated scaly plaque
  • elbows, knees, belly button
  • coin shaped
  • annular pattern
  • thick
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

describe pustular type psoriasis

A
  • Sterile sheets of pustules on an erythematous base
  • Localized or generalized
  • painful with fever
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe Guttate type psoriasis

A
  • children and young adult
  • post strep infection
  • some predisposition to psoriasis
  • trunk with sparing of palms and soles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

clinical findings for Herpes Zoster

A
  • local radicular pain 2-3 days prior to the eruption
  • Disseminated Zoster
  • Herpes Zoster Ophthalmicus
  • Postherpetic neuralgia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

pathology of Herpes Zoster

A

Steel gray nuclei multinucleated giant cells with eosinophilic intranuclear inclusions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Treatment of Herpes Zoster

A
  • Antivirals
  • Contagious; can cause chickenpox
  • Pain control
  • vaccine at age 60
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what are the papulosquamous diseases

A
  • Psoriasis
  • Seborrheic dermatitis
  • Erythrasma
  • Lichenoid eruptions
  • Pityriasis rosea
  • Dermatophyte infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

environmental factors fr psoriasis vulgaris?

Genetics?

A
  • Smoking, sun, alcohol

- HLA-B13 autosomal dominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

drugs that can lead to psoriasis

A
  • lithium
  • B-blockers
  • NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

pregnancy and psoriasis

A

can make it better

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

highlights for Seborrheic dermatitis

A
  • Scalp/face/chest
  • P. ovale
  • Humidity, trauma, seasons
  • HIV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

pathophysiology of Seborrheic Dermatitis

A
  • Abnormal immune response to P. Ovale with normal amount of the yeast
  • Free Fatty acid release
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

describe the lesions of Seborrheic Dermatitis

A
  • Branny greasy red scale on face/chest/penis

- mild flaking in hair baring areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

highlight of Erythrasma

A
  • Corynebacterium minutissimum: gram + rod, part of normal skin flora
  • CHRONIC
  • Diabetes
  • warm humid places
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

pathophysiology of erythrasma

A
  • Bacterial infection affecting the intertriginous areas (toes/groin/axilla)
  • red/brown scaly macules with on erosive collarette like scale
  • WOOD’s LAMP
40
Q

Highlights for Lichen Planus

A
  • Hep C
  • painful/burning
  • Wrists/nails/oral cavity/genitalia . . SCC of the oral mucosa
  • Wickham’s stria
  • puruitic, purple, papules, and plaques
41
Q

Highlights for Pityriasis Rosea

A
  • rose or pink colored scaly patches or thin plaques
  • spring and fall
  • Herald patch
  • pruritic eruption
  • “Christmas tree” pattern
  • if around pregnant woman they can have miscarriages at a higher rate
42
Q

pathophysiology of pityriasis rosea

A
  • viral exanthema
  • increase in CD4 and Langerhan’s cells in the dermis
  • unknown
43
Q

Reddish-orange scaling plaques of unknown etiology with palmoplantar keratoderma and follicular keratotic papules

A

Pityriasis Rubra pilaris

44
Q

highlights for pityriasis Rubra Pilaris

A
  • Autosomal dominant inheritance

- Disease has many features of a vitamin A deficiency

45
Q

Describe Griffith’s classification of Pityriasis Rubra Pilaris

A
  • Type 1: classic adult type, most common, red brown plaques with “islands of sparing”
  • Type 2: adult atypical, icthyosiform
  • Type 3: classic juvenile, similar to 1 but before age 2
  • Type 4: CIRCUMSCRIBED JUVENILE, well demarcated follicular hyperkeratosis along elbows and knees
  • type 5: ATYPICAL JUVENILE, prominent follicular hyperkeratosis with scleroderma type changes on palms and soles
  • Type 6: HIV, orange red plaques with follicular hyperkeratosis and islands of sparing, skin, mucous membranes, nails, eyes
46
Q

Highlights of cutaneous T cell lymphoma

A
  • T cell lymphoma affecting the CD4 helper cells
  • lymph nodes and organs become involved during the disease process
  • > 50 years of age
  • 27:1 M:F
47
Q

Pathophysiology of cutaneous T cell lymphoma

A
  • HTLV
  • unknown
  • CD8
  • B cells
48
Q

Clinical features of cutaneous T cell lymphoma

A
  • Scalin plaques which mimic eczema
  • itchy
  • multiple different shades of red-brown
  • round, oval annular or bizarre shape
  • CHECK FOR LAD
49
Q

Diagnosis and treatment of cutaneous T cell lymphoma

A
  • Biopsy, chest X ray, CBC with buffy coat

- topical steroids, PUVA, topical nitrogen mustard

50
Q

highlights for Discoid Lupus Erythematosus

A
  • scarring atrophic photosensitizing dermatosis

- 20-40

51
Q

pathophysiology of discoid lupus erythematosus

A
  • not well understood
  • genetic predisposition
  • Heat shock protein induced by UV light
52
Q

Clinical features of discoid lupus erythematosus

A
  • mild itching of lesions; most asymptomatic
  • be aware of SLE symptoms; pericarditis, neurologic sx
  • malignant transformations (SCC) can occur in chronic lesions
  • Psoriasis, LP, PCT
  • Erythematous papule or plaque with modest amount of scale
  • hypo or hyperpigmented
  • SCARRED
  • mucosal, palms and soles
53
Q

Diagnosis and treatment of discoid lupus erythematosus

A
  • ANA and biopsy
  • sunscreen
  • topical steroid
  • IL steroids
  • surgery
  • antimalarials
54
Q

pathophysiology and different drugs for Drug eruption

A
  • over dosage: purpura with Coumadin
  • Accumulation: Argyria with silver nitrate
  • phototoxic: doxycycline
  • Imbalance of normal flora: candidiasis with antibiotics
  • Jarisch-Herxheimer: reaction to killing of bacterial or fungal by appropriate agent
55
Q

who is at 10x risk of getting drug eruption

A

immunocompromised

56
Q

Clinical features of drug eruption

A
  • morbilliform, erythematous macular popular eruption with minimal scale until progressed or cleared
  • 2 weeks after new meds
  • Review all meds of prior 2 months
57
Q

Diagnosis and treatment of drug eruption

A
  • Blood work
  • Biopsy
  • HISTORY!!!
  • Clincal exam
  • antihistamines
  • Steroids
58
Q

highlights for Impetigo

A
  • highly contagious gram + bacterial infection of superficial layers of skin . . staph
  • bullous/nonbullous
  • <6 most common
59
Q

pathophysiology of impetigo

A
  • S. Aureus
  • 30% nares small % groin, hand, rectum, pharynx
  • normal flora
  • exfoliative endotoxins A and B
  • Neonates and infants most common for bullous
60
Q

Clinical features of impetigo

A
  • rapid blister, asymptomatic
  • hot weather
  • Crowded conditions
  • poor immune function
  • Atopic dermatitis, herpes infection, trauma
  • honey colored crust
  • Flaccid <1 cm bulla, usually ruptured
  • collarete of scale
  • no sore throat or LAD
  • Face most common but can be anywhere
61
Q

Treatment of Impetigo?

A
  • Antibiotics

- Glomerulonephritis

62
Q

highlights for staph scalded skin syndrome

A
  • Toxin mediated exfoliative dermatitis
  • severe impetigo to widespread skin denudation
  • exfoliation followed by painful erythema
  • Infants and young children
  • Nurseries and daycare
63
Q

pathophysiology of staph scalded skin syndrome

A
  • S. Aureus
  • Exotoxins (ET-1 and ET-2)
  • Blister at the GRANULAR LAYER OF THE EPIDERMIS SPLITTING THE DESMOSOMES
64
Q

Clinical features of staph scalded skin syndrome

A
  • Focus of infection
  • Fever, faint orange red macules
    • nikolsky sign (skin is sloughed off by rubbing)
  • Paper like wrinkling of the epidermis
  • cultures are sterile
  • Dramatic . . heals in 5-7 days
65
Q

Treatment of staph scalded skin syndrome

A
  • Antibiotics
  • Fluids
  • culture/biopsy . . frozen section
66
Q

highlights for pemphigus vulgaris

A
  • Autoimmune blistering disease of the skin and oral mucosa

- circulating immunoglobulin G antibody against the intraepidermal keratinocytes

67
Q

pathophysiology of Pemphigus vulgaris

A
  • Binding of IGG autoantibodies causes loss of adhesion b/t keratinocytes
  • Desmoglein 3
  • Circulating IGG1 and IGG4
  • Disease activity correlated with circulating antibodies
68
Q

clinical features of pemphigus vulgaris

A
  • All races
  • 50-70% oral mucosa involvement
  • mucosa more than skin
  • flaccid bulla on the skin with an erosion in the oral
    • Nikolsky’s sign
    • Asboe-Hansen sign- Lateral pressure on the bulla will spread the bulla to uninvolved skin
69
Q

Causes of pemphigus vulgaris

A
  • Genetic
  • Age
  • Disease Association . . MYASTHENIA GRAVIS AND THYMOMA
70
Q

Diagnosis and treatment of pemphigus vulgaris

A
  • Biopsy (DIF and HE)
  • IDIF
  • Prednisone, Imuran
  • Ophthalmologist
71
Q

highlights of Herpes Simplex

A
  • 2 types; HSV 1 and 2
  • M>W
  • HSV 1 encephalitis 60-80% mortality
  • Primary infection, latency, recurrence
72
Q

pathophysiology of Herpes Simplex

A
  • HSV 1 respiratory droplets
  • HSV 2 genital contact
  • cytolytic infection with fluid filled vesicles
  • 70-90% of population has HSV1 and 22% has HSV2
73
Q

Clinical features of Herpes simplex

A
  • Asymptomatic to painful; prodrome of itching and burning
  • Herpetic whitlow and herpes gladiatorum
  • recurrent lesions common
  • immune status
  • encephalitis
  • Vesicular or ulcerative on an erythematous base
  • oral, genital, body, keratoconjunctival, encephalitis, anal
  • Seizures, headaches
74
Q

Diagnosis and treatment of Herpes simplex

A
  • Culture or biopsy

- antivirals

75
Q

pathophysiology of Chicken pox

A
  • Primary varicella virus; herpes family type 3
  • Respiratory and direct contact with skin
  • 10-21 day incubation
  • Infectious 1-2 days prior to the rash and until the lesion crust
76
Q

clinical features of chicken pox

A
  • history of recent outbreak
  • Itchy rash
  • “oval teardrop on a erythematous base”
  • “dew drop on a rose pedal”
  • Face, trunk
  • Fever, shallow aphthous ulcers on oral mucosa
  • Spares the distal extremity
77
Q

Diagnosis and treatment of Chicken pox

A
  • clinical, culture, biopsy
  • NO ASPIRIN
  • VZIG
  • antivirals
  • antihistamines
78
Q

highlights for Bullous Pemphigoid

A
  • Chronic, AUTOIMMUNE, subepidermal blistering disease that RARELY involves the oral mucosa
  • Autoantibodies of IgG
  • uncommon
79
Q

Pathophysiology of bullous pemphigoid

A
  • IgG binds to skin antibodies activating complement and inflammatory mediators
  • Inflammatory cells release proteases causing bulla formation
  • Serum levels of BP Ag 2 may correlate with disease activities in some pts
80
Q

Clinical features of bullous pemphigoid

A
  • subacute or acute formation of tense bulla
  • UV radiation or drug induced
  • Bullous, vesicular, urticarial, acral in children
  • Causes include genetic, age, epitope spreading
81
Q

Diagnosis and treatment of bullous pemphigoid

A
  • Biopsy (HE and DIF)
  • IDIF
  • Prednisone and other immunosuppressive
82
Q

Highlights for polymorphous light eruption

A
  • idiopathic photodermatoses relating to sun exposure
  • papules, vesicles, and plaques
  • 75% American indian
  • F 2-3X >M
83
Q

Pathophysiology of polymorphous light eruption

A
  • UNKNOWN
  • type IV delayed hypersensitivity
  • UV-A induced ICAM-1
84
Q

Clinical features of Polymorphous light eruption

A
  • sunlight is etiologic factor most of time
  • Spring, lessens thoughout summer
  • about 30 min after sun exposure
  • papules, vesicles, urticarial or EM type features
  • UV-A or UV-B
85
Q

Diagnosis and Treatmet of polymorphous light eruption

A
  • R/O porphyria, lupus
  • Photopatch testing
  • Photo testing MED
  • topical steroid, oral or IM steroids, antimalarials
86
Q

highlights for Dermatitis herpetiformis

A
  • Immune mediated skin disease with a gluten sensitive enteropathy
  • rare in African american
87
Q

pathophysiology of dermatitis herpetiformis

A
  • Skin and GI
  • Circulating immune complexes are found
  • IgA binds antigen in the bowel and skin
  • Increased expression of HLA-B1, B8, DR8, DRQ
  • Patient have uniform gluten sensitivity
88
Q

Clinical features of Dermatitis herpetiformis

A
  • Pruritic, burning skin blisters distributed in a symmetric fashion; grouped
  • Last days to weeks
  • Urticarial wheal to vesicle to bulla
89
Q

Diagnosis and treatment of Dermatitis herpetiformis

A
  • HE and DIF biopsy
  • Clinical exam
  • Be aware of associated diseases
  • Dapsone and gluten free diet
90
Q

highlights for Erythema multiforme

A
  • Benign self-limited eruption classically seen as targetoid or iris shaped macules or vesiculopapules on the palms or soles
  • 50% under age 20
91
Q

pathophysiology of erythema multiforme

A
  • not understood/HSV cell mediated immune response
  • infection major cause
  • Drug . . sulfa/phenytoin/PCN/allopurinol
  • Foods, sunlight, contactants
92
Q

Clinical features of erythema multiforme

A
  • Dull red macules or papules with vesicles on palms or soles with little mucosa involvement
  • iris or target like
  • Bilateral and often symmetric
  • Polycyclic or arcuate
  • Koebner phenomenon
  • Mucosal involvement in up to 70%
  • Lips, anus, eyes, oropharynx
93
Q

Diagnosis and treatment of erythema multiforme

A
  • Biopsy
  • antivirals
  • steroids
94
Q

Highlight of Toxic Epidermal Necrolysis (TEN)

A
  • Extensive FULL THICKNESS skin detachment
  • Erythema multiforme spectrum
  • Early symptoms non specific
95
Q

pathophysiology of TEN

A
  • HLA-B12
  • SLE
  • HIV
  • Medicines, infection: cell mediated cytotoxic reaction against epidermal cells, CD8 cells macrophages cytokines
96
Q

Clinical features of TEN

A
  • 1-3 week prodrome
  • Fever, skin tenderness
  • skin pain, burning
  • newly added drugs most common
  • Morbilliform, EM type eruption
  • skin with crinkled surface
  • Sheet like epidermal loss
    • Nikolsky’s sign
  • Mucosal membrane involvement
97
Q

Diagnose and treatment of TEN

A
  • D/C drug suspected
  • IV fluids
  • Burn unit
  • Steroids as last resort
  • IVIG
  • Prevent infection

Clin Med MSKII (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions