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Skin > Examination > Flashcards

Examination Flashcards

1
Q

Macule

A

Corcumscribed
Flat lesion
Visible coz of change in color( hyper / hypopigmented/ erythematous)

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2
Q

Patch

A

Macule >0.5cm

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3
Q

Colour change in epidermal and dermal pigmentation

A

epidermal pigmentation is brown

upper dermal pigmentation is purple
lower dermal pigmentation is blue/grey

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4
Q

Papule

A

Small <0.5 cm
Elevated

Due to - hyperplasia of cells of epi/dermis , metabolic deposits in dermis , cellular infilterate in dermis

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5
Q

Nodule

A

Paule >0.5 cm

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6
Q

Plaque

A

Called plaque whether < or> 0.5 cm

ALTERED CONSISTENCY OF SKIN
May be raised/ depressed but surface area larger than height

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7
Q

Blisters

A

Fluid filled
2 types
1. Vesicle- < 0.5 cm
2.bulla -> 0.5 cm

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8
Q

Pustule

A

Pus filled whether 0.5 cm

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9
Q

Wheal

A

Evanescent elevated lesion due to edema of dermis/sc tissue

URTICARIA- white elevated lesion surrounded by erythema
Subsides in 24 hrs
Linear- dermatographic urticaria

ANGIOEDEMA
Extends into Sc tissue
Lasts 24- 48 hrs
Mc at mucocutaneous jxn

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10
Q

Pathognomic lesion of scabies

A

Burrow:

Serpentine
Thread like
Open end marked by papule

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11
Q

Comedones

A

Inspissated plugs of keratin and sebum in pilosebacious orifices

Open: black head- keratin plug is black
Closed: white head - covered by skin

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12
Q

Diff bw crust and scale

A

Scale- collection of cells of horny layer
Dry surface on removal

Crust- collection of epi cells, dried serum and sometimes blood.
Moist surface on removal

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13
Q

Silvery removable scale seen in

A

Psoriasis

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14
Q

Skin manifestations of tuberous sclerosis

A
  1. angiofibroma/adenoma sebaceum-nose , nasolabial folds and cheeck
  2. ask leaf macule-hypopigmented , trunk
  3. shagreen patch-leathery, lumbosacral region
  4. periungal fibromas/koenen tumor
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15
Q

X linked icthyoses

A 
Only males
Deficiecy in steroid sulfate
Large dark , tightly adherent
Sites: generalised, flexures encroached
Ass: corneal opacities , cryptorchidism
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16
Q

Icthyosis vulgaris

A

AD
Deficiency in filagggrin
Both males and females
Small, branny , except on shins where large.
Pasted in centre with upturned edge.
Extensors of limbs, lower back.
Associated with- hyperlinear palms and soles, keratosis pilaris , atopic diathesis

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17
Q

NF1

A

SKIN
Cafe au lait macules(CALM)- uniformly pigmented, oval

Cutanoues neurofibroma-3 types
Dermal(button hole sign)
Plexiform(diffuse plaques ,wormy/knotty)
Subcutaneous

Intertiginous frekling/ crowe s sign( axillary and inguinal frekling)

EYES - optic glioma , lisch nodules

BONE-thining of cortex , sphenoidal dysplasia, pseudoarthrosis

PHEOCHROMOCYTOMA

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18
Q

NF2

A

Bilateral acoustic neuroma
Meningioma/gliomas
Mimimal cut manifestatiin
No lisch nodules

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19
Q

Acanthosis nigricans causes

A 
BENIGN
Obesity
Hereditary
Hair- an syn(hyperandrogenic, insulin resistance, cushing)
Acral
Endocrine(hyper androg, cushing, DM)
Drugs(corticosteroids, OCPs)

MALIGNANT
Mc gastric adenoca , genitourinary

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20
Q

Lesion in acanthosis nigricans

A

Hyperpigmentation
Dirty look
Thickening
Velvety

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21
Q

Molecular defect in XP xeroderma pigmentosa

A

Defective repair of UV damaged DNA

Leading to development of skin cancers

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22
Q

Molecular defect in XP xeroderma pigmentosa

A

Defective repair of UV damaged DNA

Leading to development of skin cancers

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23
Q

XP lesion

A 
Photosensitivity
Multiple frekles
Eventually actinic keratosi
Keratoacanthoma
BCC
SCC 
Melanoma
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24
Q

Prototype lesion of Chronic plaque psoriasis

A 
Mildly itchy papule /plaque
Well demarcated
Erthymatous base
Surmounted by scales
Indurated
Discoid
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25
Q

Koebner s phenomenon

A

When lesion develop at the site of trauma(scratch, surgical incisiin, tatoo, injury)

Aka isomorphic phenomenon

Seen in:: Little Plans Kan Make Win Very Descent 
Lichen planus
Psoriasis(characteristic)
kaposi sarcoma 
molluscum contagiosum 
warts 
Vitiligo
DLE

true koebner
psoriasis
lichen

false
wart
molluscum

rare 
darier
hailey hailey ds
erythema  multtiforme 
lichen sclerosi
lichen nitidus
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26
Q

Grattage test

A

Scales in the psoroatic plaque can be accentuated by grating with glass slide

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27
Q

Auspitz test

A

3 steps
Grattage test

As u continue to scrape ,glistening white membrane appears(berkleys membrane)

On removing memb punctate points becone visible

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28
Q

Sites of predilictiin for psoriasis

A 
Usually bilateral symm
Pressure points(knees and elbow)
Extensors more
face uncommon(refractory)
Scalp(spillage to forehead and nape of neck)
Lumbosacral
Periumblical
Palms and soles
Flexual
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29
Q

Reiters syndrome

A

Antecedant inf(genital, enteric)
Arthritis
Iridocyclitis, conjuctivitis
Mucocutaneous(rupoid psoriasis- heaped up scales , keratoderma blennorrhagica , circinate balanitis)

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30
Q

Types of psoriasis

A

Chronic plaque
Guttat
Pustular

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31
Q

Guttate psoriasis

A

Childn and adoloscent
may be ppted by streptococcus infection
Lesions in shower
Trunk

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32
Q

Dactylitis seen in

A

Psoriasis

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33
Q

Nail changes in psoriasis

A 
Pitting
Plate thickening
Subungual hyperkeratosis
Discolouration
Onycholysis
Oil spots
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34
Q

Histopathological findings in psoriasis

A

EPIDERMAL
Parakeratosis

Hyperkeratosis ( stratum corneum)

Acanthosis (diffuseepidermalhyperplasia:basale , spinosum)

Thin/no granular layer

Suprapapillary thinning- berkeley memb

Collection of neutrophils to form munro microabcess , spongiform pustule of kogoj

Club shaped elongated rete ridges

DERMAL
Dilation amd tortusity of capillaries

Lymphocytes

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35
Q

Tazarotene

A

Vit a derivative

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36
Q

Moa of macrolides

A

.

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37
Q

Onychomycosis

A

Fungal infection of nail

Tinea unguim is fungal infection of nail plate due to dermetophyte

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38
Q

Interactions of Macrolides with CYP450

A

All are enz inhibitors(cla/erythro/telith) except AZITHROMYCIN

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39
Q

SE of macrolides

A

Git-epigastric pain

+motilin R -promotes int motility without affecting colon

Used in diabetic gastroparesis and postop ileus

But tolerance develops and flora eff :not used as prokinetic

Ototoxic:high dose

Hypersenstivity

Hepatitis:estolate

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40
Q

Excretion of macrolides

A

All in bile(azith/eryth/telithro) except clarithromycin

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41
Q

Macrolides spectrum

A 
Gpc (not MRSA)
Clamydia
Mycoplasma
Mycobacteria
Spirochete
h.pylori
C. Jejuni
Legionella
H.influenza
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42
Q

Nail changes in tinea unguim

A

Thichened nail
Subungal hyperkeratosis which is friable
Onycholysis
Tunneling

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43
Q

Hidradenitis suppurativa

A

Apocrine glands

Occlusion - rupture - inflammation and infection

Axilla, perineum and genitalia

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44
Q

Chlamydial infection Rx

A

Axithromycin or doxycline

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45
Q

Role of minoxidil in alopecia

A

.vasodilation and angiogenic potential

Reduces miniaturization of terminal hair and also converts miniaturized hair into terminal hair

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46
Q

Spagetti amd meat ball appearance seen in

A

Malssazia furfur

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47
Q

CSF penetration of macrolides

A

Do not penetrate

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48
Q

KOH mount findings of candida

A

Budding yeast and pseudohyphae

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49
Q

Piyriasis versicolor caused by

A

Malassezia furfur

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50
Q

Lesion of pityriais versicolor

A

Distint Perifollicular macules (mostly hypopigmented , can be hyperpig )

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51
Q

KOH finding of pityriasis versicolor

A

Spaghetti and meat ball appearance (spores and short branched hyphae)

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52
Q

Typical lesion of dermatophytes

A

Annular/arcuate spreads centrigugally

Margin is active showing papules, vesicles , scaling , pustules

Centre is relatively clear though in chronic cases there is lichenification

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53
Q

What is ringworm

A

Tinea/ dermatophyte infection

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54
Q

Types of alopecia

A

Cicatracial and non cicatracial

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55
Q

Alopecia aereta

A

Non cicatracial with no inflammation( erythema , inflammation , paules)
Skin specific autoimmune
Exclamation marks
Commonly at scalp, beard , mostache , eyebrows , eyelashes
Regrowth with gey hair
Nail changes(pitting and thinning)

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56
Q

Androgenetic alopecia

A

Miniatrization of hair follicles(terminal into
vellus hair)

Males:Androgen dependant
Typical presentation -frontoparietal and frontal recession , thinning of vertx

Females - no typical presentation , diffuse hair loss , initially as widening of central parting

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57
Q

Telogen effluvium

A

All hair enter telogen phase and are shed simultaneously

Cause
Infections
Childbirth
Surgical trauma
Haemorrhage
Emotional stress
Drugs
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58
Q

Splinter haemorrhages seen in

A

Trauma
Psoriasis
Bacterial endocarditis

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59
Q

Paronychia

A

Inflammation of nail fold

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60
Q

Koilonychia

A

Spoon shaped nails seen in iron deficiency

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61
Q

Pitting in
psoriasis
alopecia aereta
Eczema

A

Coarse with other changes

Fine and thinning of nail plate

Coarse, deep irregular cross ridging

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62
Q

Beau ‘s line

A

Transverse grooves

After severe, acute illness

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63
Q

Aa for melanin synthesis

A

Tyrosine

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64
Q

Frekles

A

Fair skinned

Each lesion has color variation within and from others

Photoexposed parts(face, dorsolateral forearms , hands , neck)

Darken on sun exposure
AD

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65
Q

Melasma site

A 
Symmetrically on 
cheeks
Nose
Forehead 
chin
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66
Q

Type of skin color change with clofazamine

A

Orange

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67
Q

Lentigenes

A

In any skin color

Well defined, uniform color

Any part of body including mucosa

No change in color after sunexposure

Seen in
PEUTZ JEGHERS
CRONKHITE CANADA SYNDROME

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68
Q

Minocyline skin pigment changes

A

Blue black

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69
Q

Vitiligo is due to anatomical/ functional defect in melanocytes

A

Anatomical

Absent

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70
Q

Koebners phenomenon seen in

A

Psoriasis
Vitiligo
Lichen planus

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71
Q

Site of predeliction for vitiligo

A

Any part

But areas prone to repeated friction and trauma( dorsae hand and feet , elbows and knees)

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72
Q

Characteristic lesion of LP

A

Itchy violaceous polygonal flat topped papules with wicham stria

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73
Q

5 Ps of LP

A

P pruritic

P purple

P polygonal

P plane topped

P papules

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74
Q

Pterygium of nail is diagnostic of

A

LP

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75
Q

Sites of prediliction of LP

A

Flexors of wrist

Ankles

Shins

Lower back

Associated changes:
Nail- thinning, trachyonychia , tenting, pterygium

Scalp: violaceous perifollicular , cicatracial alopecia

Palmoplantar : keratotic papule with central dull

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76
Q

Hostopathological changes in LP

A

No parakeratosis

Hyperkeratosis

Thickened granular layer

Basal cell degeneration ( max joseph spaces ,coloid bodies)

Saw toothed dermoepidermal jxn
Irregular saw toothed appearance due to basal cell loss
Lymphocytes lead to indistint DE jxn

Band like upper dermal infilterate

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77
Q

Dermatitis herpetiformis

A

Itchy(excoriation) ,grouped(herpetiformis ) , edematous paupules and small vesicles on normal/erythematous skin.

Sites: extensors and pressure points

Dermoepidermal split
Granular IgA deposits at tips of dermal papilla
Dermal papillary tip neutrophilic abcesses

Associated: gluten sensitive enteropathy

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78
Q

Bullous pemphigoid

A

AI

Linear deposits of IgG Abs and C3 at dermoepidermal jxn (against hemidesmosomes)

Lesion: itchy , large , tense bulla , rupture less readily , roof of bulla just settles down as the contents are absorbed , heal with milia( small pearly paules ) ,

Bulla spread sign and nikolsky sign negative

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79
Q

Pemphigous

A

Intraepidermal bullous disorder
AI
Acantholysis
IgG auto Abs against DESMOGLEINS

Types:2 main
Pemphigous vulgaris
Pemphigous foilaceous

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80
Q

Pemphigous vulgaris

A

Lesion: flaccid bullae- rapidly rupture - painful erosions - heal slowly

Bedside test:
NIKOLSKY SIGN- tangential pressure on normal skin results in new bulla formation

BULLA SPREAD SIGN/ ASBOE HANSEN SIGN : spread of bulla on applying pressure on prexisting bulla

MUCOSAL LESION: universal

Site: scalp, face , flexures , trunk

SPLIT: Intraepidermal
Suprabasal

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81
Q

Pemphigous foilaceous

A

Lesion: superficial bulla - rupture rapidly - so only scale crust seen

MUCOSAL LESION : rare

Site: initially seborrhic distribution , becomes generalised

SPLIT: intreepidermal
Subcorneal / granular layer

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82
Q

Epidermal necrolysis

A

Cause: drugs-anticonvulsants , antibacterials , NSAIDS, allopurinol

Lesion: deeply erythematous(purpuric), may develop bulla , peel off in sheets , denuded area
Mucosal : eyes and mouth frequently

Site: face , trunk and proximal extremities

Depending on BSA

  1. SJS :<10 %
  2. SJS-TEN : 10 - 30 %
  3. TEN : >30 %
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83
Q

Psedohyphae

A

Pseudohyphae” are distinguished from true hyphae by their method of growth, relative frailty and lack ofcytoplasmicconnection between the cells.

They are the result of a sort of incompletebuddingwhere the cells elongate but remain attached after division

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84
Q

Isotretinoin

A

Moa: (all causes)

  1. inhibit sebum production
  2. Normalizing follicular epidermal hyperproliferation
  3. dec P.acne
  4. reducing inflammation

Use: severe acne

Side effects:
Dry skin, cheiltis, hair loss,dryness of eyes , nose bleeds

Teratogenic , contraception using 2 diff methods during and 1 mth after Rx

Not to donate blood

Pseudotumor cerebrii

Liver fxn test

Hypertriglycerides

Myalgia, bertebral hyperostosis, altered night vision

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85
Q

Retinoids

A 
RITA
Retinoic acid
Isotretinoin
Tazarotene
Adapalene

Moa:
Especially for comedones
Increasing epidermal cell turnover
Increasing dehiscence of atratum corneum

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86
Q

layers of epidermidis from below upward are

A

basal cell layer (stratum basale )
prickle cell layer (stratum spinosum)
granular cell layer(stratum granulosum )
horny cell layer ( stratum corneum )

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87
Q

skin is thickest at

A

palms ,soles,back ie 3mm

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88
Q

skin is thinnest at

A

eyelids

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89
Q

dermis is divided into

A
  • papillary dermis

* reticular dermis

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90
Q

stratum lucidum is found in

A

palms and soles

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91
Q

subcutaneous tissue is absent in

A

eyelids and male genitalia

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92
Q

basement membrane zone is made up of

A

•lamina lucida
•lamina densa
•sublamina
densa

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93
Q

keratinocytes r derived from

A

ectodermally derived

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94
Q

melanocytes are derived from

A

neural crest cells

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95
Q

melanocytes r found in

A

hair follicles
choroid
iris
skin

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96
Q

epidermal melanin unit is formed from

A

36 keratinocytes/melanocyts

melanocytes give their melanosomes to the keratinocytes

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97
Q

where r merkel cells found

A

clustered near unmylinated sensory nerve ending to form touch spots or hair discs or iggo discs at the bottom of rete ridges

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98
Q

epithelium of skin is

A

stratified squamous epithelium

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99
Q

melanocytes are present in

A

stratum basale

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100
Q

normal turnover time of epidermis is

A

28 days ie 4 weeks

but turnover time in psoriasis 4days

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101
Q

lines of blaschko represent

A

developmental growth pattern of skin

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102
Q

stratum lucidum is present in bw

A

stratum granulosum and stratum corneum

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103
Q

which layer of epidermis is underdeveloped in very low birth weight infants in initial 7 days

A

stratum corneum

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104
Q

odland bodies are present in

A

upper spinous layer

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105
Q

malpighian

layer includes

A

basal and spinous layer

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106
Q

langerhans cells are seen in

A

malpighian layer

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107
Q

birbeck granules are present in

A

langerhans cells they possess characteristic rod or racquet

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108
Q

wht is rosacea

A

chronic conditions characterized by diffuse inflammation of centrofacial area with seborrhea,telangiectasia, papules,pustules, nodules

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109
Q

etiology of rosea

A

anything that is too hot too cold too spicy
role of mite demodex and bacteria h pylori
there is pronounced flushing in response to heat ,emotional stimulation alcohal,hot drink ,spicy food

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110
Q

topical DOC for roscea

A

metronidazole

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111
Q

oral DOC for rosacea

A

doxycycline

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112
Q

types of roscea

A
  • erythematotelangiectatic
  • papulopustular
  • rhinophymatous
  • ocular rosacea
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113
Q

sites of predilection for acne roscea

A

convexity of face involved

characteristic sparing of periorbital and perioral region and flexural region

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114
Q

treatment of grade 1 acne

A

benzoyl peroxide +topical retinoids

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115
Q

treatment of grade 2

acne

A

grade 1+topical antibiotic

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116
Q

treatment of grade 3 acne

A

grade 2+ oral antibiotics

hormonal therapy

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117
Q

treatment of grade 4 acne

A

retinoids oral indicated in nodulocystic acne not responsive to conventional treatment

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118
Q

drugs causing acne

A 
hormones and steroids 
gonadotropin 
androgens 
antiTB drugs 
anti epileptic
  phenytoin 
 phenobarbitone  
halogens
   bromides 
    iodides 
   halothane
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119
Q

grade 1 acne is

A

primarily comedones

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120
Q

grade 2 acne is

A

comedones + papules

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121
Q

grade 3 acne is

A

comedones +pustules +papules

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122
Q

grade 4 acne

A

nodulocystic acne nodules and cysts leading to scars ,abscess

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123
Q

steroids are contraindicated in roscea t/f

A

true

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124
Q

types of acne are

A
  • acne vulgaris
  • acne conglobata
  • acne fulminans
  • occupational acne
  • drug induces
  • acne excoriee
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125
Q

primary differentiating feature bw acne vulgaris and acne roscea

A

pressence of open and closed comedones in acne vulgaris

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126
Q

hallmark of acne vulgaris is

A

comedones

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127
Q

etiology of acne vulgaris

A
  • obstruction of pilosebaceous unit
  • excessive sebum production
  • propionibacterim
  • insulin like growth factors
  • increased interleukin 1 alfa
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128
Q

most common side effects of retinoids is

A

skin rash

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129
Q

treatment of choice for mild to moderately comedones, papulopustular and nodules

A

topical retinoids +oral antibiotics

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130
Q

treatment of choice for severe nodular acne conglobata

A

oral isotretinoin

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131
Q

a pt taking treatment for acne develops blueblack muddy hyperpigmentation causative drug is

A

minocycline

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132
Q

side effects unique to minocycline are

A

drug induced lupus and blue black pigmentation

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133
Q

max dose of isotretinoin

A

120-150 mg it is given as 0.5 to 1 mg /kg/day

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134
Q

eccrine glands are located in

A

present all over the body
especially
palms,soles,axilla
except vermilion border of lips ,nails,labia minora and inner aspect of prepuce

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135
Q

difference bw opening of sebaceous and eccrine glands

A

eccrine gland open directly under skin

whereas sebaceous glands open into hair follicle

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136
Q

difference between

ans control of eccrine and apocrine glands

A

eccrine gland is under control of sympathetic and cholinergic but apocrine glands are only under control of sympathetic adrenergic

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137
Q

treatment of local hyperhidrosis

A

• topically aluminium chloride hexahydrate
•iontophoresis
passing of current low voltage across skin
•botulinum inj

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138
Q

manifestations of acute generalized hypohidrosis

A

heat stroke it is a emergency

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139
Q

manifestations of chronic generalised hypohidrosis

A

seen in hypohydrotic ectodermal dysplasia with frontal bossing ,saddle nose,everted lips,peg shaped teeth

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140
Q

wht is miliaria crystallina and its manifestations

A

when duct ruptures just below stratum corneum

manifests as tint,clear,crystalline vesicles

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141
Q

wht is miliaria rubra and its manifestations

A

duct ruptures in epidermis

manifests as small ,erythematosus papules often surmounted by vesicles

142
Q

wht is milaria profunda and its manifestations

A

when duct ruptures below dermoepidermal
junction
manifests as large,skin coloured papules

143
Q

apocrine acne is another name of

A

hidradenitis suppurativa

144
Q

hidradenitis supprativa is disease of

A

apocrine gland

145
Q 
true about apocrine gland is all except 
•modified sweat gland 
•modified sebaceous glands 
•present in groin and axilla 
•inf is known as hidradenitis  supprativa
A

modified sebaceous glands

146
Q

name disorders of eccrine sweat glands

A

hyperhydrosis
anhydrosis
miliaria

147
Q

name type disorders of apocrine sweat glands

A 
bromhidrosis 
osmidrosis 
chromhidrosis 
foxfordyce ds 
hidradenitis supprativa
148
Q

bromhidrosis is due to

A

asfoetida
onion
garlic

149
Q

most common cells found in stratum spinosum

A

langerhans cells

they aredendc i

150
Q

types of hair in human body

A

•lanugo hair 》fine,soft hair which are shed in utero rarely retained k/a congenital hypertrichosis lanuginosa
•Terminal hair》long ,coarse,medullated
hair present on scalp,eyebrows, and eye lashes ,beard ,moustaches
•vellus hair 》fine ,short ,nonmedullated hair present on most parts of body

151
Q

stages of hair cycle are

A
  • anagen》phase of activity and growth
  • catagen 》phase of involution
  • telogen 》phase of resting
152
Q

difference between bulb of anagen and telogen

A

anagen 》angulated bulb

telogen 》club shaped bulb

153
Q

clinical features of alopecia areata

A

hair loss presents as discoid patch of alopecia
no inflammatory or atrophy
•pressence of exclamation marks hair at periphery of region
•regrowth begins from centre of lesion new hair is fine and grey but gradually regain normal colour

154
Q

treatment of alopecia areta with single lesion <6mnths

A

observe spontaneous recovery

155
Q

treatment of single or few lesions >6mnths or rapid progress

A

topical steroids/topical minoxidal/topical psoralen+UVA

156
Q

extensive lesions

alopecia totalis/universalis

A

oral steroids

oral psoralen

157
Q

wht is miniaturisation of hair follicles

A

it is progressive conversion of terminal
hair follicles into vellus hair follicles
ie conversion of medullated to non medullated hair

158
Q

cause of androgenic alopecia

A

miniaturisation is induced by increased end organ sensitivity mediated by 5a reductase which converts testosterone to 5 DHT in scalp

159
Q

how is androgenic alopecia graded in males

A

Hamilton-norwood scale

160
Q

how is androgenic alopecia graded in females

A

ludwig scale

161
Q

clinical features androgenic alopecia in males

A

frontoparietal recession with thinning of vertex

162
Q

clinical features of androgenic alopecia in females

A

widening of central parting

163
Q

wht is telogen effluvium

A

anagen phase of several adjoining hair follicles is aborted and all enter telogen phase at same time all hair are shed simultaneously

164
Q

cause of teloven effluvium

A 
infectious diseases like malaria, dengue 
child birth 
surgery 
emotional 
drugs like retinoids,anticonvulsants
165
Q

trichogram finding of telogen effluvium

A

telogen count>20%

166
Q

causes of cicatricial alopecia

A
  • lichen planopilaris
  • DLE
  • Pseudopelade of brocq ie scarring alopecia with no cause identified presents as patches of cicatricial alopecia with foot prints in snow
167
Q

ophiasis is

A

patients lose hair in band like manner at the periphery of scalp

168
Q

trachyonychia is

A

nail plates are grey brown and hve rough surface due to longitudinal striations as if sandpapered it affects all nails known as twenty nail dystrophy

169
Q

wht is leuconychia

A

white nails seen in pts if hypoalbuminemia

170
Q

half and half nails r seen in

A

chronic renal failure 1/2nails white and 1/2nails red

171
Q

Terry nails are

A

proximal 4/5th of nail is white and distal tip is normal

seen in liver disease

172
Q

beus lines are

A

transverse grooves appear simultaneously on all nails plates
seen in viral illness ,peripheral nerve injury surgery,Kawasaki ds

173
Q

diagnosis of telogen effluvium is confirmed by

A

club like swelling at root end called club hairs and length of hair shorter thn surrounding hair due to premature stoppage

174
Q

anagen effluvium causes

A 
•radiotherapy to head 
•systemic chemotherapy 
esp alkylating agent eg cyclophosphamide 
•mercury ,boric acid,thallium 
•colchicine poisoning 
•vit a poisoning
,severe protein malnutrition
175
Q

onychogryphosis

A

nail is severly distorted ,thickend ,opaque

brownish nails seen in pressure foot wear in elderly

176
Q

onycholysis is seen in

A
  • psoriasis

* reiter syndrome

177
Q

muehreke’s lines

A

hypoalbuminemia

178
Q

koenen’s periungal fibroma is seenin

A

tuberous

sclerosis

179
Q

fordyce disease mainly involves

A

lips >buccal mucosa

180
Q

sebaceous glands found in eyelids are

A

meibomin glands

181
Q

sebaceous glands found in nipples

A

Montgomery’s gland

182
Q

sebaceous glands found in genitalia are k/a

A

tysoris gland

183
Q

pilosebaceous unit includes

A

sebaceous gland +hair follicles

184
Q

largest gland and greatest density of sebaceous glands are found in

A

face and scalp

185
Q

give classification of sweat glands

A 
#•eccrine sweat gland》hyperhydrosis 
anhydrosis
#•eccrine sweat duct 
》 miliaria 
# apocrine sweat gland 
•bromhidrosis 
•osmidrosis 
•chromhidrosis 
•fox-fordyce disease 
•hidradenitis supprativa
186
Q

causes of cicatericial

alopecia

A 
5L,4F,3S
•lichen planus
•leprosy 
•lupus vulgaris 
•linear scleroderma 
•lupus erythematosus (DLE)
•favus and kerion
•follicular degeneration syndrome(pseudo pelade of broq) 
•frontal fibrosing alopecia of kossard 
•syphilis 
•sarcoidosis 
•secondaries
187
Q

type of alopecia in DLE

A

cicatericial

whereas in SLE there is non cicatericial

188
Q

is ther e alopecia in psoriasis

A

no alopecia inspite of extensive scalp involvement

189
Q

exclamation marks hair is pathognomic of

A

alopecia areata

190
Q

alopecia areta is associated with

A

exclamation sign
atopy
pitting nails

191
Q

male with patchy loss of scalp hair and grey hair in eyebrows and beard diagnosis is

A

alopecia areata

192
Q

pterygium of nail is characteristically seen in

A

lichen planus

193
Q

oil drop and pitting nail dystrophy is seen in

A

psoriasis

194
Q

nail change in alopecia areta is

A
  • fine stippled pitting of nails

* trachyonychia

195
Q

name infections involving nails

A 
paronychia
bacterial 
viral herpes and HIV
fungal 
tinea
196
Q

dermatoses

involving nail

A
  • psoriasis
  • lichen planus
  • eczema
  • dariers disease
197
Q

nail changes in psoriasis

A
  • pitting of nails (thimble nail)
  • oil drop nails
  • onycholysis (detachment of nail plate)
  • discoloration of nail plate
  • subungal hyperkeratosis
198
Q

asymmetric involvement of toe >fingers nail, yellow discoloration , nail thickening and tunneling indicates diagnosis of

A

tinea unguium which can be confirmed by KOH mounting

199
Q

immediate pigmentation is caused by exposure to

A

UVA

200
Q

delayed pigmentation is caused by exposure of

A

both UVA and UVB

201
Q

colour of melanin when it is

in epidermis

A

brown

202
Q

colour of melanin when it is in dermis

A

bluish grey due to tyndall effect

203
Q

causes of hyperpigmentation

A 
#epidermal pigmentation 
1. increased number of melanocytes 
 •lentigenes 
• cafeaulait macules 
•malignant melanoma 
2.increased activity of melanocytes 
•freckles 
•exposure to UV light 
•PUVA treatment 
•endocrine disorders
#dermal pigmentation 
•Mongolian spots 
•naevus of ota
204
Q

lesions of vitiligo

A
  • depigmented macules which hve 3 shades trichome depigmented center, surrounded by hypopigmented rim and normal skin
  • macules hve scalloped outline and form geographical patterns
  • koebners phenomenon is +
  • leucotrichia
205
Q

characteristic of segmental vitiligo

A

•depigmented macules r dermatomal and stops short of midline
most commonly seen along 5th nerve

206
Q

types of vitiligo

A 
segmental 
focal 
acrofacial 
vulgaris is most common 
universalis
207
Q

sites of predilection of vitiligo

A

sites of repeated trauma

208
Q

wht is freckles

A 
ill defined brown macules 
which darken on sun exposure 
occur on photoexposed
areas  
photoprotected area and mucosa is spared
209
Q

wht r lentigenes

A

dark brown to black macules also involves mucosa and photoprotected areas
seen in peutzjegher,,cronkhite Canada

210
Q

difference bw vitiligo and OCA

A

VT》

•begins later in life
•depigmented area may regress or progress
•eye changes r not seen
•partial or near complete response to treatment

 #OCA
•present at birth 
•eye changes are present
211
Q

difference bw piebaldism and OCA

A 
piebaldism 
•present at birth 
•localised areas of depigmented macules with islands of hyperpigmentation 
•white forelock +
•depigmented eye brow and lashes
OCA 
•at birth 
•generalized depigmentation 
•all hair hve pigment dilution 
•photophobia, translucent irides,red reflex
212
Q

piebaldism is frequently associated with

A

waardenburg syndrome characterized by dystopia canthorum ie lateral displacement of inner canthi,but normal interpuppilary distance broad nasal root,sensorineural hearing loss and piebaldism

213
Q

eye changes must be present to make diagnosis of albinism t/f

A

true

214
Q

morphology of seborrheic keratosis lesions

A

usually multiple lesions start as macules and change into papules with distinctive stuck on morphology greasy surface
currant bun appearence

215
Q

currant bun appearence is found in

A

seborrheic keratosis

216
Q

cause of melanocytic naevi

A

clustered proliferation of melanocytes

217
Q

wht r Mongolian spots

A

bluish ill defined macules present on lumbosacral region

regress by 4 yrs

218
Q

other name of pityriasis versicolor

A

tinea versicolor

219
Q

causative agent of tinea versicolor

A

pityriasis versicolor is caused by malassezia furfur

220
Q

pathogenesis of pityriasis versicolor

A

PV represent shift of host and resident yeast flora yeast becomes pathogenic in hot and humid climates it realeses azelaic acid thus causing hypopigmentation

221
Q

morphology of pityriasis versicolor lesion s

A

hypopigmentation sometimes erythematosus or hyperpigmented
so called versicolor
scaly perifollicular macules
surmounted by branny scales which can be accentuated by scratching with glassslide

222
Q

perifollicular character is invariably retained in

A

pityriasis versicolor

223
Q

KOH mount shows _____ in case of pityriasis versicolor

A

spaghetti and meat ball appearence

224
Q

difference between pityriasis and vitiligo

A

there is no scales in vitiligo but scaling is present in pityriasis
• in vitiligo repigmentation
starts perifollicular after treatment
but in case of pityriasis lesion itself are perifollicular

225
Q

causative agent of pityriasis rosea

A

unknown HHV-7 Is frequently associated

226
Q

1 st lesion in case of pityriasis rosea is

A

herald patch

227
Q

wht is herald patch

A

characteristic annular lesion with wrinkled salmon pink centre and collarete of scales at periphery
scales are attached just within leading edge and free towards centre

228
Q

fir tree appearence is characteristically seen in

A

pityriasis rosea long axis of patches runs downward

and outward from spine along the lines of ribs

229
Q

main diffrential of pityriasis rosea is

A

secondary syphilis

230
Q

course of pityriasis rosea is

A 
•self limiting 
its clinical features are 
•Her 
•young 
•mother 
•smokes 》secondary syphilis like lesion 
•fir tree 
•  cigarette paper collarette of scales
231
Q

characteristic lesions of pityriasis rubra pilaris

A

•scaly
pink to orange
follicular papules
grouped papules coalese to form large plaques these papules spread in cephalocaudal direction there are islands normal unaffected skin (nappy claires )
keratodermic sandals
follicular accentuation
it can progress to genralised erythrodermal

232
Q

nutmeg grater feel occurs in

A

it is present in pityriasis rubra pilaris

follicular lesion on dorsal aspect of digits

233
Q

keratodermic sandals are found in

A

pityriasis rubra pilaris

yellow brown discoloration of palms and soles

234
Q

piebaldism is

A

autosomal dominant conditions characterized by congenital stable areas of vitiligo like amelanotic patches of skin which remains unchanged for life with white forelock and islands of normal or hypermelanotic skin

235
Q

congenital

unilateral single stable well defined hypopigmented patch is mostly

A

nevus achromicus

236
Q

vitiligo is mostly associated with

A
  • diabetes mellitus
  • alopecia areata
  • addison’s ds
  • thyroid disease
237
Q

pityriasis rosea like drug eruptions are seen in

A 
GAMB
G gold 
A ace inhibitor 
M metronidazole 
B beta blockers
238
Q

lichenoid like drug eruptions are seen in

A 
A Anti Gold Thai 
Queen 
A》ace inhibitor 
anti》antimalarial 
Gold 
Thiazide
quinidine
239
Q 
an adult presents with oval scaly hypopigmented macules over chest and back the diagnosis is 
•leprosy 
•lupus vulgaris 
•pityriasis versicolor 
•lichen planus
A

pityriasis versicolor

240
Q

24 yr old man had multiple, small, hypopigmented macules on upper chest and back for last 3 mnths .the macules were circular,arranged around the follicles many had coalesced to form large sheets .the macules had fine scales he had similar lesions 1 yr ago which subsided on treatment
the most appropriate investigation to confirm diagnosis is

A

KOH preparation of scales

241
Q 
all are given for treatment of pityriasis versicolor except 
•selenium sulphate 
•clotrimazole 
•ketoconazole 
•griseofulvin
A

griseofulvin it is used systematically for dermatophytes but is ineffective topically and has no role in treatment of versicolor or candidiasis

242
Q

wht is pityriasis alba

A

present characteristically with recurrent scaly hypopigmented macules on cheeks and face of young children it requires no active treatment

243
Q

treatment of ptyriasis rubra pilaris is

A
  • oral retinoids
  • methotrexate
  • photochemotherapy
244
Q

wavelength of woods lamp is

A

320-400nm UVA light with nickel oxide and silicon filter to diagnose pityriasis versicolor, tinea capitis ,vitiligo, porphyria, pseudomaonas pyocyanea
erythrasma

245
Q

color of wood s lamp in case of tinea capitis

A

yellow green fluorescence

246
Q

color of woods lamp on case of pityriasis versicolor

A

golden yellow or apple green

247
Q

color of woods lamp in case of erythasma and acne

A

coral red /pink

248
Q

pseudomonas pyocyanea

A

yellow green

249
Q

colour of woods lamp in case of vitiligo

A

total white

250
Q

colour of woods lamp in tuberous sclerosis ash leaf macules

A

blue white

251
Q

SCC of skin gives ____ colour of flourescence on wood lamp

A

red flourescence

252
Q

non scaly hypopigmented macules are seen in

A 
1.indeterminate leprosy 
more common in children 
more common in pts belonging to high leprosy prevalence 
anaesthetic 
epidermal atrophy 
2. tuberous sclerosis 
ash leaf macules 
shahgreen patch 
adenoma sebaceum 
seizure ,mental retardation 
3.vitiligo 
sharply defined 
non pigmented patches 
anywhere
253
Q

recurrent scaly non anaesthetic hypopigmented macules

A 
▪pityriasis  alba 
(predominately face involvmemt)
self limiting benign condition mostly affecting head and neck region around face in children 
macule with powdery white scales 
▪pityriasis versicolor 
scales are dust like fine or furfaceous
254
Q

pityriasis rubra pilaris starts feom

A

face as scaly macules

255
Q

characteristic histological hallmark of atopic dermatitis is

A

spongiosis of epidermis

lesions show hyperkeratosis and acanthosis

256
Q

diagnostic criteria of atopic dermatitis is

A 
hanifin and rajka criteria 
major criteria is 
pruritis 
involvement of face snd convexities in infant <2yrs and flexures in older children and adults 
tendency to chronicity 
personal or family history
257
Q

finding of infantile phase of atopic dermatitis

A

begins after 3 mnths
starts from face
napkin area is spared
excoristion and lichenification
after 6 mnths when itching tendency develops
when child begins to crawl extensor surface of knee is involved

258
Q

presentation of atopic dermatitis in s child

A

develops after 2-3yrs
involving flexural aspect
side of neck show reticulate pigmenta

259
Q

hertoghe sign is

A

thining of lateral half of eyebrows seen in atopic dermatitis

260
Q

head light sign is seen in

A

chelitis and inflammation of skin on and around lips

261
Q

antenna sign is seen in f

A

follicular opening are filled with horny plugs seen in atopic dermatitis

262
Q

diagnostic lesion of nummular eczema

A

well demarcated coin shaped erythematosus plaque arising from confluence of thin walled papules and papulovesicles
later central clearing and peripheral extension leads to annular ring shaped lesion
secondary lesions in a mirror shaped configuration on opposite side of bodu and reactivation of apparently dominant lesions is very characteristic

263
Q

most serious complications of atopic dermatitis is

A

widespread herpes simplex virus1 infection resulting in kaposi varicelliform eruption

264
Q

clinical featured eczema herpeticum

A

history of herpes labialis in a parent in previous wks
after incubation period of 5-12 days ,multiple itchy vesiculopustular lesions erupt in disseminated pattern
vesicular lesion are umblicated tend to crop become hrgic and leave large areas of denudation which is prone to superadded bacterial infections
these lesions tend to occur on areas of atopic dermatitis

265
Q

most common area of irritant contact dermatitis

A

hands it is due to chronic contact of patient with wet work ,soaps or detergents

266
Q

most common agent causing allergic contact dermatitis

A

nickel

267
Q

gold standard test for diagnosis of allergic dermatitis is

A

patch test

268
Q

patch test is read after

A

48 hrs

269
Q

early fernadez reaction is read after

A

2 days

270
Q

in TB induration is read after

A

3 days

271
Q

skin doubling time in psoriasis is

A

4 days

272
Q

kveim test is read after

A

2 weeks

273
Q

late mistuda reaction is read after

A

3 weeks

274
Q

normal skin doubling time is

A

4 weeks

275
Q

wht is urticaria

A

edema involving superficial layer of dermis

276
Q

wht is angioedema

A

localised edema of deeper layers of dermis

involving subcutaneous tissue

277
Q

most common site for urticaria

A

extremities and face

278
Q

most common site for angioedema is

A

periorbital and lips

279
Q

wht causes cholinergic urticaria

A

pruritic wheals of large size surrounded by erythema attacks are precipitated by fever,hot bath,excercise
as any activity which increases core body temp stimulates release of cholinergic nerve ending

280
Q

most common manifestations of mastocytosis is

A

urticaria pigmentosa

281
Q

clinical features of urticaria pigmentosa

A

pale yellow tan to red dish brown macules to raised papules develop in symmetrical distributions
highest conc on trunk and thighs
lesions are not sharp they are pigmented

282
Q

wht is dariers sign

A

urticaria, erythema and itching around the lesion ie a brown patch after mild trauma including scratching or rubbing of lesion is seen in urticaria pigmentosa

283
Q

diagnosis of atopic dermatitis is by

A

clinical examination

284
Q

diagnosis of contact dermatitis is made by

A

patch test

285
Q

a diagnosis of donovnosis made by

A

microscopic finding of donovan bodies or safety pin appearence

286
Q

diagnosis of syphilis is by

A

dark fields

VDRL

287
Q

diagnosis of chancroid

A

gram staining school of fish or rail road appearence

288
Q

tinea diagnosis is by

A

KOH smear

289
Q

diagnosis of lupus vulgaris is by

A

biopsy

290
Q

an infantpresentewith erythematosushrash on cheeks and extensor aspect of limbs mother has a history of bronchial ashtma likely diagnosis is

A

atopic dermatitis

291
Q

atopic dermatitis is most severe in which season

A

rainy seasons

292
Q

drugs causing exanthematous eruption are

ec

A

beta lactama
sulfonamides
NRTI
phenylbutazone

293
Q

after wht time of drug ingestion fixed drug eruption appear

A

30 min to 8-16 hrs

294
Q

most common site involved in fixed drugs eruption are

A

genital and perianal skin lesions evolve from macules to . bullae and lead to ulceration
heal with hyperpigmentation
lesion appear at the same site everytime the drug is taken

295
Q

lichen nitidis characteristically involves which sites

A

shaft of penis

trunk ,flexures of upper extremities dorsae of hands

296
Q

difference between lichen nitidus and lichen planus

A

lichen nitidus is aysmptomatic wheras lichen planus is itchy
no wickham’s stria in lichen nitidus

297
Q

histological findings in lichen planus

A 
thickened granular layer 
basal cell degeneration 
max josephs spaces 
colloid bodies ie necrotic basal cells become incorporated into inflammed pappilary dermis and form eosinophilic cytoid/civatte bodies 
saw tooth dermoepidermal junction
298
Q

histological changes in psoriasis

A
  • hyperkeratosis
  • acanthosis
  • munro microabscess if neutrophils collect in stratum corneum
  • torturous capillaries
  • spongiform pustule of kogoj if neutophils collect in spinous layer
  • increased epidermal cell turn over 4 days normal 4 wks
299
Q

wht are papulosquamous

disorders

A

elevated lesions ,papules or plaques with scales

300
Q

primary papulosquamous disorders are

A 
psoriasis 
parapsoriasis 
all pityriasis except pityriasis versicolor as it has macules 
lichen planus 
bowens disease 
seborrheic dermatitis
301
Q

systemis causes of papulosquamous disease

A

secondary
syphilis
sarcoidosis
SLE

302
Q

grattage test

A

scratching with glass slide accentuate scale formation

303
Q

auspitz sign

A

removal of scales lead to appearence

of punctuate /pin point bleeding

304
Q

oral form of psoriasis is

A

geographical tongue benign migratory glossitis or glossitis areata migrans

305
Q

lesions of psoriasis are surrounded by a ring called

A

wornoff ring there are lesions which are mildly or not pruritic

306
Q

difference between psoriatic arthritis and rheumatic arthritis

A

psoriatic arthritis 》
•MHC class 1 disease fibroblastic response ,sacroilitis,enthesitis ,dactylitis ,and juxtaarticular new bone formation is present whereas such findings are not present in rheumatoid arthritis
RA
MHC class 2

307
Q

psoriatic arthritis characteristically involves which joint

A

DIP

308
Q

commonest complication of psoriasis is

A

erythrodermic psoriasis seen due to use of irritant substances and withdrawal of systemic steroids

309
Q

rupioid psoriasis is seen which syndrome

A

reiter syndrome
HLA B27 preceding chlamydia and shigella dysentr6
circinate balanitis and keratoderma blennorhagicum

310
Q

von zumbusch disease is

A

generalized pustular psoriasis
suddenly developing skin first becimes erythrodermic and then sheets of sterile pustules develops over trunk and limbs tht confluent to form lake of pus

311
Q

pustular psoriasis of pregnancy is k/a

A

impetigo herpetiformis

312
Q

Toc for psoriasis type chronic plaque psoriasis on face ,neck flexures ,and genitalia

A

topical corticosteroids

even low concentrations tar and dithranol is tolerated

313
Q

TOC for psoriatic erythroderma and psoriasis with AIDS

A

systemic retinoid +PUVA is drug of choice

even in case of gross edema no diuretic is given as with treatment of psoriasis diuresis will occur

314
Q

DOC for psoriatic arthritis is

A

methotrexate

315
Q

safest drug for treatment of pustular psoriasis is

A

prednisone

316
Q

pustular psoriasis of pregnancy is called

A

impetigo herpetiformis

317
Q

which UV rays is used in treatment for photochemotherapy

A

UV A

puva

318
Q

uv rays causing sun burns,skin cancers is

A

UVB

319
Q

circulating lymphocytes are most senstive to

A

UV-C filtered by ozone layer

320
Q

interface dermatitis is seen in

A

lichen planus

321
Q

causes of erythroderma are

A

pityriasis rubra pilaris, psoriasis
lichen planus
eczema, drugs

322
Q

treatment of exfoliative dermatitis

A

steroids

323
Q

other name of exfoliation dermatitis

A

erythroderma

324
Q

microabscess are found in

A

psoriasis

mycosis fungoides

325
Q

pautrie microabscess are found in

A

mycosis fungoides

326
Q

munro microabscess are made up of

A

seen in stratum corneum

only contains neutrophils

327
Q

PUVA is used in

A 
psoriasis 
mycosis fungoides 
sezary syndrome
vitiligo 
atopic dermatitis 
generalized licen planus 
urticaria pigmentosa 
generalized granuloma annulare 
cutaneous graft vs host
328
Q

wht is pseudo koebners phenomenon

A

autoinoculation seen in infectious diseases like plane warts ,molluscum contagiosum
eczematous lesions

329
Q

clinical features of lichen planus are

A

Wickham’s
I infilteration of lymphocytes ie interface dermatitis
C ivatte bodies
K oebner phenomenon
Ha hepatitis C,hyperpigmentation
M mucosal involvement
S spontaneous healing,scarring alopecia, SCC ,steroids are mainstay of therapy

330
Q

lichen scrofulosorum and lichnen nitidus are not variants of lichen planus t/f

A

true

331
Q

hepatitis c is associated with

A

lichen planus
sjogren syndrome
porphyria cutanea tarda

332
Q

only definatiive

indication of systemic steroids in psoriasis is

A

impetigo herpetiformis ie genralised pustular psoriasis in pregnancy

333
Q

pathogenesis of pemphigus

A

igG antibodies agnst polypeptide complexes present in intercellular substance of epidermis leads to kkeratinocyte realesing serine proteasee which dissolve intercellular substance
keratinocyte then seprate from adjoining cells

334
Q

Patients present with the following signs:

  1. Hyperkeratotic papules present over the seborrheic area of the body.scalp,forehead,nasolabial folds,retroauricular groove
  2. V-shaped nicking present at the tip of the nails.
  3. Red and white longitudinal nail lines.
  4. oral mucosa has cobble stone appearence
    wht is likely diagnosis
A

dariers ds

335
Q

Microscopically the lesions show a “dilapidated brick wall” appearance in the epidermis
is seen in

A

Hailey–Hailey disease, or familial benign chronic pemphigus[1]:559 or familial benign pemphigu

336
Q

tzank smear finding of herpes simplex and herpes zoster

A

eosinophilic cowdry type A intranuclear inclusion bodies

337
Q

nikolsky sign is seen in

A 
pemphigus  all types not pemphigoid 
steven Johnson 
TEN 
SSSS
epidermolysis bullosa simplex and dystrophic
herpes 
leukemia 
mycosis fungoides
338
Q

level of split in EB simplex

A

basal or suprabasal

defect is in keratin 5 and 14

339
Q

level of split in EB Junctional

A

Lamina lucida of basement membrane zone and defect in laminin gene

340
Q

level of split in dystrophic EB

A

below lamina densa of BMZ defect is in collagen 7

341
Q

mitten like deformity with digits encased in epidermal coccon is seen in

A

epidermolysis bullosa

342
Q

gold standard for confirm level of bulla is in

A

electron microscopy

343
Q

how is epidermolysis bullosa acquisita differentiated from porphyria cutanea tarda and bullus pemphigoid

A

PCT hve deposited of immune complexes also around blood vessels in addition to dermoepidermal junction
BP AND EBA
direct and indirect immunoflorescence on salt split skin
if deposit on roof side of dermoepidermal junction then it is bullous pemphigoid and on floor side of dermoepidermal junction it is EBA

344
Q

mucous involvement is in
pemphigus follacious
pemphigus vulgaris
bullous pemphigoid i

A

in PF 》mucosa is always spared
in PV》
nearly all pts hve mucosal lesions
in BP》mucosal involvement is infrequent but if present it is limited to buccal mucosa mostly

345
Q

fishnet pattern is seen in

A

pemphigus vulgaris

346
Q

linear florescent pattern in blood vessels is found in

A

porphyria cutanea tarda
bullous pemphigoid
epidermolysi s bullosa acquisita

347
Q

contact leucoderma

A

external chemicals destroying melanocytes

causing vitiligo patches

348
Q

wht is urticaria pigmentosa

A

it is a tumor of mast cells where mast cells irritate the basal melanocytes and lead to inc brown pigmentation of the skin
⬇️
when these patches are scratched this leads to break down of those mast cells thus lesions become red and erythematosus
⬇️
dariers sign

349
Q

target /bulls eye lesion are seen in

A

erythema multiforme

350
Q

tinea incognito is seen with

A

steroids

351
Q

wht is norweign scabies

A

scabies seen in HIV +ve patients
⬇️
immune response to scabies is very poor due to which there are no itching, no scratching no removal of mite no of mite
no of mites reach till 20000
⬇️
characteristically there is hyperkeratosis and crusting

352
Q

wht is nodular scabies

A

more inflammation to scabies resulting in nodules formation

Skin (4 decks)

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