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DERMATOLOGY & ANDROLOGY
clinical notes and photos from the special sense
round
Made by: Abdulla Buhmaid
Contents:
• Psoriasis.
• Lichen planus.
• Fungal skin infections.
• Hair and melanin disorders.
• Viral skin infections.
• Erythema multiforme, nodosum and steven Johnsons syndrome.
• Parasitic skin infections.
• Urticaria.
• Dermatology clinical notes.
• Andrology lectures and clinical notes and pictures. (lots of MCQs came from it)
psoriasis
Primary psoriatic lesion
• Notice the fine silvery scales
Cold dry climates exacerbate psoriasis
Hot humid climates decrease psoriasis
Sun exposure is mostly protective against
psoriasis in the majority of psoriatic patients
but in some it could aggravate it.
Pregnancy
decreases
psoriasis but
psoriasis will be
aggravated
after labor
Hypocalcemia aggravates psoriasis
Removing
scales leads to
HISTOLOGY IMAGE OF PSORIASIS:
• Hyperkeratosis (increased horny
layer thickness)
• Parakeratosis (incomplete
ketinization of the horny layer “you
still see nuclei”)
• Munro-Micro Abscesses
• Absent granular cell layer
• In the dermis there is:
• Dilated tortuous capillaries
• Cellular infiltrate
Psoriatic nail manifestations:
• Onycholysis ( separation of the nail
plate from its bed)
• Thimble pitting (just like the photo,
a thimble is the item seen above).
• Subungual hyperkeratosis.
Management of psoriasis
TOPICAL THERAPY (1st line in mild to moderate plaque psoriasis)
• Topical steroids
• Salicylic acid 3%
• Tar “antimitotic”
• Anthralin
• Topical calcipotriol
PHOTOTHERAPY
• PUVA
• Broad and narrow band UVB
• Sunlight
SYSTEMIC THERAPY (for severe extensive cases “done in hospitals”)
• Methotrexate
• PUVA
• Cyclosporin
• Oral retinoids
• Biologicals
AVOID SYSTEMIC STEROIDS
IN PSORIASIS
!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!
!!!!!!!!!!!!!!!!!!!!!!!!!!!!
Lichen
Planus
Lichen planus is a disease in
which the pathognomonic
clinical picture is severe
itching with flat-topped
violaceous “purple” papules.
There is hypergranulosis; so
you might see white
networks on these papules
called “Wickhams striae”.
Note that lesions in the palms and soles are NOT
itchy, and NOT purple. They are yellow and non itchy.
Wickhams striae due to hypergranulosis in LP
Lichen planus really hates the nails, so the
nail manifestations are particularly brutal:
• Longitudinal ridging.
• Irregular pitting.
• Nail plate splitting.
• Perygium formation.
Pterygium
(in the conjunctivitis chapter of
ophthalmology)
Also pterygium
(but in the nail manifestations of LP in
DERMA)
Not so different right ??
Lichen planus likes flexor
surfaces
Psoriasis likes extensor
surfaces
The etiology of LP is unknown,
but it is hypothesized that it is
due to immune origin.
Lichen planus is associated
closely with
HCV
Histology of lichen planus:
• Hyperkeratosis
• Hypergranulosis
• Sawtooth rete ridges (long and
with pointy end)
• Cellular infiltrate in upper
dermis
• Liquefactive degeneration of the
basal cell layer.
Management of Lichen Planus
1.Topical steroids
2.Intralesional steroids (in cases or oral ulcer or
hypertrophic skin lesion)
3.Oral antihistamines
4.Systemic steroids in extensive lesions
Fungal Skin
Infections
Superficial
fungal infection
dermatophytes
Pit. Versicolor
(yeast like)
Yeast
(Moniliasis)
• Tinea Microsporum
• Tinea Trichophyton
• Tinea Epidermophyton
Malassezia furfur ( FKA pityrosporum
orbiculare)
Candida Albicans
Clinical types of dermatophytes
T. corporis T. Capitis T. Barbae
onychomychosis
T. Pedis
T. Manus
T. Cruris
Notice the ring appearance in
dermatophyte infection. This
is due to the peripheral
extension and central clearing
with progression. Hence the
name ring worm lesion or
Tinea
Tenia capitis
Scaly type
Black dot
type
Inflammatory
type
Favus
• Microsporum
Canis
• Microsporum
audouinii
• Trichophyton
violaceum
• Trichophyton
Tonsaurans
• Animal fungi
• KERION
• PUSTULAR
FOLLICULITIS
• Trichophyton
schoenleinii
OSCE
Description of the lesion:
• A painful inflammatory, inflammatory, boggy, well
circumscribed, bald swelling on the scalp that is studded
with folliculo-pustules and an edematous weeping surface
that could come with thick crusting.
If you pull a hair that overlays the lesion, what do you
expect?
• Sero-pus comes out of the follicle that I pulled the hair
from.
Do you expect hair to regrow after this lesion heals?
• No; it leaves scarring alopecia.
What is your diagnosis?
• KERION (abscess like swelling)
What is the causative organism?
• Animal fungi
KERION (showing extensive scaling)
OSCE
LESION:
• FAVUS
DESCRIBTION:
• Saucer-shaped crusted lesions
(called sulphur cups or scutula)
that form around the infected
hair. They are concave, yellow,
and centered around a single dull
dry hair and have a mousy odor.
CAUSE?
• The chronic scarring form of T.
schoenlinii.
HAIR EXPECTED TO REGROW?
• No.
KERION
BIOGENIC
ABSCESS IN
THE SCALP
ROUGH surface SMOOTH surface
Less painful and no
constitutional symptoms
SEVERE PAIN with
constitutional symptoms
If incised, no pus will drain out (don’t
incise it)
If incised pus will drain out
Some strains of
fungi causing
Tinea capitis give
GREEN
FLORESCENCE
under woods light
(but not all of
them)
MANAGEMENT OF TINEA CAPITIS and
BARBAE
1.SYSTEMIC ANTIFUNGALS (to all cases)
2.TOPICAL ANTIFUNGALS
3.In kerion
• Topical antiseptics to remove the crusts
• Systemic antibiotics for 1 week
DESCRIBE THE LESION AND IDENTIFY THE CAUSE
DESCRIBTION:
• Well defined plaques over the hairless areas of the body. The plaques shows
active spreading with a raised border that is covered by
scales/vesicles/pustules/crusts/papules.
• The causative organism could cause a lesion that spreads peripherally and
clears in the center (picture below), and other causative organism could cause a
lesion that spreads peripherally and DOESN’T clear centrally.
• The lesion below shows concentric rings (the central clearing is developing a
new lesion).
INVESTIGATIONS:
1. Woods light.
2. Scraping the raised border, then using KOH and microscopy.
3. Culture on Sub Araud Agar media.
MANAGEMENT?
• If lesion is localized: topical antifungal.
• If lesion is extensive: systemic antifungals
PROVISIONAL DIAGNOSIS:
• TINEA CORPORIS
All those pictures show T. corporis, it presents with many
dermatological features and thus it could have many DD:
1. circinate psoriasis
2. Circinate impetigo (inflammatory types are similar)
3. Pityriasis rosea (differ by scraping and looking for fungus)
4. Annular LP
5. Discoid eczema
DESCRIBE and DIAGNOSE
DESCRIPTION: an arch like red plaque in the
groin that extends to the thigh with a well-
defined raised border. In the lower picture the
scrotum is affected BUT usually the genitalia are
spared.
DD: flexural psoriasis, erythrasma, candidiasis,
tinea cruris, dermatitis, flexural psoriasis.
PROVISIONAL DIAGNOSIS: T. Cruris (of course
I would know after investigations only, I can’t
know without them “i’m not a wizard”)
MANAGEMENT?
1. IF LOCALIZED: TOPICAL ANTIFUNGALS
2. IF EXTENSIVE: SYSTEMIC ANTIFUNGALS
M<F
Center is somewhat clear
Wearing tight shoes
for a long time,
hyperhidrosis, hot
weather, and
excessive water use
MACERATION of the
skin in the foot
Tinea pedis infection
(commonest form of
dermatophyte
infection)
Tinea Pedis
Interdigital type
“commonest”
Scaly
hyperkeratotic
type
Vesiculo-bullous
type
More in lateral 3
toe clefts
Sodden (very moist), fissured, has
opaque white scales, with eroded
areas. With bad smell.
The sole has erythema,
fine scaling and
hyperkeratosis. This type
is resistant to treatment
and chronic
Vesicles or bullae that are tense
progress to contain pus and rupture
leaving a collar of scales. Worsens in
hot weather.
dermatophytid reaction is the body's reaction to a dermatophyte
(fungal) infection and is a skin eruption that appears on an area of the
body that is not the area where the infection first began. It is not
dermatophytosis, but it is an allergic reaction. You will see this usually
with vesiculobollus tinea pedis as a sterile vesicular reaction in the
hand in the form of pompholyx.
MANAGEMENT OF TINEA PEDIS
1.AVOID RISK FACTORS
2.FOR INTERDIGITAL TYPE: topical
antifungal
3.FOR HYPERKERATOTIC AND VB TYPES:
systemic antifungals
The commonest
form of Tinea
Manus is the scaly
hyperkeratotic
type
Diffuse powdery scaling and
hyperkeratosis of the palm with
accentuation of flexural creases (50%
unilateral) “TTT SAME AS PEDIS”
DIAGNOSIS:
Onychomycosis
FEATURES:
• Whitish/yellowish discoloration of the free edge of the nail
plate that spreads proximally.
• Subungual hyperkeratosis
• onycholysis
MANAGEMENT:
1. Topical antifungal (Miconazole or Tioconazole)
2. Systemic antifungals
DIFFERENTIAL DIAGNOSIS
PSORIASIS
You will see fine pitting
CANDIDAL ONYCHIA
Paronychia is present; nail dystrophy is proximally and
laterally
Bad prognosis in toe nail
affection especially the
elderly
PityriasisVersicolor
A common macular/patchy eruption of the trunk and proximal limbs. The color
could be erythematous, whitish “hypopigmented”, or brownish “hyperpigmented”.
The surface is covered by fine scales detected by scrabbing the lesion. Remission in
winter and exacerbation in summer. Heals with hypopigmented macules that either
persist or disappear on their own
By woods light: yellow florescence of involved skin
DD: vitiligo (no scaling), pityriasis alba (scaly), erythrasma (coral red on woods
lamp), seborrheic dermatitis (greasy scales).
TREATMENT OF P.VERSICOLOR
TOPICAL OPTIONS:
• Ketoconazole shampoo (5mins daily for 5 days)
• Selenium sulphide or Zinc pyrithione shampoo (10 mins daily for 10
days or overnight once every week) “don’t apply to face or genitals”
• Topical antifungal creams (Clotrimazole or Miconazole; daily for 2-4
weeks)
SYSTEMIC OPTIONS “FOR RESISTANT OR EXTENSIVE CASES”
• Fluconazole 300mg/week for 2 weeks.
• Itraconazole 200mg/day for 1 week.
IN CASES OF POST INFLAMMATORY HYPOPIGMENTATION:
• Takes months to return to normal
CANDIDIASIS
CUTANEOUS NAIL
MUCOUS
MEMBRANE
interdigital intertrigo
Napkin
candidiasis
In groin, axilla and
submammary
Moniliasis after
contact dermatitis or
the diaper
White
macerated
skin at webs
• Nail thickening
• Lateral fold
discoloration
• Irregular
transverse
ridging
• Proximal nail
fold seperation
• Subungual
hyperkeratosis
((paronychia))
oral
vulvovagin
al
balanitis
Oral thrush
Acute atrophic
(denture stomatitis)
Candidal leucoplakia
Oral thrush
NOT SCRABED OFF
EASILY
EASILY SCRABED
OFF
Candidal
leukoplakia
TREATMENT OF CANDIDA INFECTION
1. Treat the causing factor (disease, drug use etc…)
2. Topical treatment:
• Imidazole, nystatin, amphotericin.
• 2-4 weeks for skin and oral candidiasis.
• If nail candidiasis given for 3 months alongside systemic antibiotic.
• If vaginal candidiasis: vaginal cream or tablets must be given “and treat the husband too”
3. Systemic treatment:
1. Oral nystatin (500k units 4 times/day “hold in mouth for some mins then swallow”) “for oral
and vaginal”
2. Fluconazole ( 150mg/day for 3 days if oral candidiasis. And 150mg/week for 2 weeks for vaginal
candidiasis)
3. Itraconazole (200mg/day “for 3 days in vaginal and for 2 weeks in oral”)
ALOPECIA and
melanin disorders
Scarring (cicatricial)
alopecia
congenital Acquired
Trauma, lacerations,
burns
Abscess, kerion, favus,
and lupus vulgaris
Discoid lupus, lichen
planus, scalp cancer
Follicular lichen planus (causes scarring alopecia, not
expected to have their hair grow back)
Discoid lupus scarring the scalp causing permanent scarring alopecia
Note that in SLE the hair becomes brittle and hair
loss is most evident at the hairline. It this case the
hair has a chance of regrowing after the flare of SLE
is controlled. But in discoid lupus lesion, the scarring
that is done causes permanent hair loss that is only
managed by hair restoration treatments after
controlling SLE.
KERION (a large sore caused by a
fungal infection)
Favus (Latin for "honeycomb") or tinea favosa is the severe form
of tinea capitis.
Lupus vulgaris is the TB granuloma of the skin, it is rare to come over
the scalp.
Non scarring
alopecia
CONGENITAL AQUIRED
Circumscribed diffuse
Alopecia
areata
Androgenetic
alopecia
Traumatic
(constant rubbing and
pulling)
Secondary
syphilis and
mild T.capitis
Telogen
effluvium
Anemia and
malnutrition
Chronic liver
disease, Mg,
and SLE
DM,
hypo/hyperth
yroid
Hypopituitarism
and
hypoparathyroid
Cytotoxic drugs,
colchicine,
antithyroid and
anticoagulants
Alopecia areata Androgenetic alopecia
Exclamation “!” mark hair at the
periphery of a bald area is a
characteristic feature of alopecia
areata
Ophiasis is when alopecia areata lesions extend to form a band along
the scalp margin
Moth eaten alopecia. Pathognomonic for secondary
syphilis
Telogen effluvium is the
increased loss of hair after
severe stress, expect hair to
regrow within 6-12 months.
VITILIGO
Albinism (congenital abnormality in melanin formation
that affects the skin, hair, and eyes).
The following types of vitiligo show bad
response to treatment:
1. Segmental vitiligo
2. Vitiligo over bony prominences
3. Vitiligo on the palms and soles
4. Acrofacial vitiligo
5. Vitiligo affecting mucous membranes
Viral skin lesions
Lesion: multiple
vesicles on an
erythematous base
Diagnosis: herpes
simplex
Treatment: topical
acyclovir with oral
acyclovir 200x5x10
Lesion: started as papules that
changed into vesicles that ruptured
and formed crusts. This lesion
shows centripetal distribution.
Causative organism: Varicella
zoster virus (primary infection).
Name of disease: chicken pox.
Management: symptomatic TTT
only. But immunocompromised
patients need Acyclovir 800x5x7
Lesion: grouped vesicles on an
erythematous base with a
characteristic unilateral
DERMATOMAL distribution.
Causative organism: reactivated
latent Varicella Zoster virus
Name of disease: herpes zoster
Management: oral acyclovir
800x5x7 and analgesics
Lesion: dome shaped
papule, sessile, firm, and
with ROUGH SURFACE.
Causative organism: HPV
Management: must destroy
(by chemical, cryo, or
electrocautery) “this is not
the only type of warts”
Lesion: multiple umbilicated
papules.
Name of disease: Molluscum
contangiosum
Causative agent: Pox virus
Management: Currettage
Erythema multiforme
Erythema multiforme “TARGET LESIONS”
The lesion fades within two weeks with residual pigmentation that stays for months. The
commonest precipitating factor is herpes simplex virus (HSV).
Steven-Johnson syndrome and toxic epidermal necrolysis
Toxic epidermal necrolysis (<30% detachment)
Epidermal necrolysis is almost always drug induced
Erythema
nodosum (which is
the inflammation
of subcutaneous
fat “allergic
reaction”
The lesion takes 2 to 6 weeks to resolve leaving a bruised
appearance. Those are nodules not macules
Give NSAIDS for pain and treat the causing factor.
+Remember this lesion is connected to IBD and is
infamous for recurrence
DRUG REACTIONS
Severe
reactions
Exenthema
tous R.
photose
nsitivity
blistering SLE like Acneform hyperpigm
entation
alopecia Fixed
eruption
anaphylactic
shock
-penicillin and
plasma
products
Exfoliative
erythroderma
-BDZ
-allopurinol
-sulfa and
gold
Epidermal
necrolysis
Morbiliform
Urticarial
-penicillin
-opiate
-aspirin
-radiocontrast
Purpuric
E.M.
Lichenoid
-captopril
-chloroquine
P. Rosea like
-metronidazol
-captopril
-gold
-psoralen
-thiazide
-tetracycline
-phenothiazide
-penicillin
-
penicillamine
- captopril
-
procaineami
de
-hydralazine
-ACTH
-Steroids
-Iodide
-INH
-OCP
-Gold
-
Antimalaria
-
CHEMO
-NSAIDS
-Sulphonamide
-Phenopthaline
Parasitic skin lesions
ORGANISM:
- Mite (Sarcopetes scabii var hominis).
How long is its incubation period?
- 2 weeks to 2 months
What skin disease does it cause
and what is its characteristic
lesion?
- Scabies, and the characteristic lesion is Burrows.
What is the characteristic
symptom of this disease?
- Severe itching that is worse at night.
Is itching here localized or
generalized?
- It is generalized, because its due to the allergic
reaction of the body to the mite.
Anterior aspects of wrists and ulnar
border of hands and forearm and
elbow
Around the nipples
Finger webs
Medial aspects of the
thigh
Natal cleft and
lower buttox
The axilla
Dorsal foot and
around the ankle Male genitals
Abdomen and
periumbilical
H&N of infants only
Characteristic
sites for scabies
IDENTIFY THE LESIONS
INDICATED BY THE
ARROWS AND DESCRIBE
THEIR SIGNIFICANCE:
- lesion: Burrows
- Significance: they are the
characteristic lesions for
scabies
You can catch scabies from infested animals
like a dog “ANIMAL SCABIES”. So don’t touch
any dog on the street and if you do touch one
make sure you wash your hands with soap and
water and change your clothes or take a
shower as soon as possible
Animal scabies is characterized by:
1- short IP
2- not transmitted man to man
3- burrows are absent
4- self limiting
5- finger webs and genitals are free
•Yes, only if the patient is
immunodeficient. Or is on
steroid therapy.
Can one have scabies and not
have itching?
IDENTIFICATION
Norwegian (crusted) scabies
PATHOPHYSIOLOGY
It’s a severe form of scabies with a huge number of mites and eggs and
thickened horny layer. It is due to the abnormal immune response of the
host. It is seen in the mentally retarded, immunosuppressed, AIDS, sensory
neuropathy, and elderly debilitated patients.
C/P:
- Crusted eruptions on the hands and feet
- Subungual hyperkeratosis
- Red scaly plaques on the head, neck and
trunk
- With or without severe itching
IDENTIFICATION
NODULAR SCABIES
DESCRIPITION
Nodular lesions that are itchy, NON-INFESTED,
reddish brown in color, that may persist for weeks
after treating scabies
Mostly seen at:
- Axilla
- Male genitals
- Groins
- umbilicus
Management?
Intralesional
steroids or surgical
excision
Norwegian scabies
Management?
1. Cut the nails short and apply a topical
scabicide under the nails.
2. Several applications of keratolytic creams
3. Several applications of topical scabicides
4. Two doses of oral ivermectin separated by
an interval of a week (could be repeated
more as needed)
Microphotograph of mineral oil scabies preparation
showing mite (below heavy black arrows), eggs (orange
arrows), and scybala “fecal pallets”(yellow arrows).In
preparing an ex vivo scabies preparation, mineral oil
preserves scabies’ scybala, whereas potassium hydroxide
does not.
The red circle shows the
triangular structure (delta
sign or triangle sign), which
indicates the head parts of
scabies. The body of scabies is
relatively translucent. There is
a classic “S” shaped burrow
above the triangular structure.
TREATMENT OF SCABIES
GENERAL MEASURES
• Boiling all clothes and bed sheets, etc… (disinfection)
• Treating the other people in the house and spouses.
TOPICAL SCABICIDES (applied to entire skin except head and neck unless infant or old)
• Permethrin 5%(2 successive nights) “safe”.
• Sulfur “10% adult 5% child” (every night for 4 nights) “safe but has bad smell and stains so rarely
used”
• Gamma Benzine Hexachloride 1% (one application for 12 hours) “not safe for children >10y,
pregnant women, & epileptics”
• Benzyl benzoate 25% (for 2 nights)
• Crotamiton 10% (for 2 nights) “preferred for infants and young children, and postscabitic pruritus”
• Malathion 0.5% (for 12 hours then washed)
SYSTEMIC TREATMENT
• Ivermectin (antiscabetic) 6mg/15Kg
• Antihistamines and antibiotics.
PEDICULOSIS HUMINIS VAR.CORPITIS (HAIR LICE)
This is a “nit”, which is
the egg of head louses
that are adherent to
the hair. We usually
don’t see the adult lice,
but we can clearly see
the nits in the hair in
cases of pediculosis
capitis
Management of pediculosis capitis
1- CUT THE HAIR SHORT.
2- GIVE CO-TRIMOXAZOLE if there is impetigo
3- GIVE PEDICULOSIDES AFTER CONTROLLONG BACTERIAL INFECTIONS:
• Malathion 0.5% lotion (12 hours then wash)
• Ivermectin lotion (12 hours then washed)
• GBH 1% shampoo (5 mins then washed)
• Repeat after 1 week and all family members should do the exact same.
4- ORAL IVERMECTIN (6mg/15Kg repeated in 10days)
5- REMOVE NITS
• Make a white vinegar solution diluted in water (1:1)
• Leave it for 1-2 hours until the cement dissolves
• Wash and comb the hair with a fine-toothed comb
This is pediculosis pubis also known as
Pubic lice. It is sexually transmitted and
could be seen at the groin hair, axilla,
eyelashes, beard, any body hair tuft.
Management:
1- topical pediculocide (choose 1 agent and
repeat the TTT in one week, must apply it to
all the body even if not affected)
2- in cases of topical TTT failure, or perianal
or eyelash involvement, give oral ivermectin
on day 1 and 8
3- don’t forget the spouse
URTICARIA
Urticaria (many wheals
are seen) and
angioedema of the face.
MANAGEMENT: (after removing the cause!!!)
1.Adrenaline
2.Antihistamines
3.Systemic steroids if severe
4.Local soothing lotion (calamine
lotion)
5.Calcium gluconate
DERMOGRAPHIC
URTICARIA
Aquagenic urticaria is a rare condition in which a
person's skin develops red,itchy hives after exposure to
water. (aka water allergy)
CHOLINERGIC
URTICARIA
stimulus might be
considered to be heat;
the actual
precipitating cause is
sweating. “so, anything
that increases your
core temperature leads
to this”
Solar urticaria
(sun allergy)
Papular urticaria (hypersensitivity reaction to an
insect bite)
Clinical sessions of
dermatology
Identify the disease and describe the
lesions and their distribution and the
causative agent:
Disease: Hand, foot and mouth disease
Description: multiple oval vesicles (or
crusts if the rupture) that are seen on the
oral region, palmar aspect of the hand,
and plantar surface of the foot. WITH NO
LESIONS ON THE TRUNK (to differ it
from chicken pox).
Causative agent: coxsackievirus
Psoriasis of the scalp
Seborrheic dermatitis of
the scalp
Area of affection: primarily the frontal
hair line “crown”
Scales: DRY and WHITE.
Auspitz sign: +ve.
Area of affection: the temporal and
occipital regions.
Scales: GREASY and YELLOWISH
Psoriasis in the palm Eczema in the palm
• Fiery red erythema
• Well defined border
• Oozes blood when scratched
• Auspitz sign +ve
• Less marked erythema
• Hazy border
• The 1ry lesion is vesicles so it oozes watery
fluid when scratched
Condyloma Accuminata (HPV)
Condyloma Lata (secondary syphilis)
Pathophysiology of Acne vulgaris
comedones
COMEDONES
Pityriasis Alba
Peri-ungual wart
Woods lamp
CORAL RED appearance under woods
light in Erythrasma
Vitiligo under woods light
Clinical andrology notes
The male urethra ( 4 parts):
1. Prostatic urethra “3 cm”
2. Membranous urethra “1.2cm and no glands open to it”
3. Bulbar urethra “widest part, receives openings for cowper
glands”
4. Penile urethra “Littres gland open here”
Epithelium of the male urethra:
Prostatic and membranous urethra: transitional epithelium
Bulbar and penile urethra and ducts: pseudostratified columnar
Fossa navicularis: stratified squamous
Histology of the
testes is important
to understand the
books scripts.
Priapism is the prolonged painful erection
more than 4 hours. It is mostly seen in
blood dyscriasis!!!!!!!!!!! And it is a medical
emergency!!!!!!!
Seminal vescicles prostate Cowpers glands
• Forms main bulk of
seminal fluid.
• Adds sodium
bicarbonate.
• Adds fructose.
• Adds semen coagulator.
• Adds zinc (Zn).
• Adds semen liquifactor.
• PSA.
• adds mucus (lubricant)
• Adds antioxidants
• Adds nutrients
chancre chancroid
• Caused by syphilis (Treponema
pallidum)
• It is painless
• Caused by Hemophilus Ducreyi
• It is painful!
((mnemonic to remember: if you have
chancroid, you DO CRY. “because it
sounds like ducreyi ”)
Causative organisms
• Chancre: syphilis/treponema pallidum
• Chancroid: Hemophilus Ducreyi
• Granuloma inguinale/Donovanosis: Klebsiella
Granulomatis ( have safety pin appearance)
• LGV: chlamydia (L1,2,3)
• Moniliasis: candida albicans
• Trichomoniasis: Trichomonas vaginalis “protozoa,
remember the strawberry appearance of the cevix”
Drugs of choice
• Syphilis: Benzathine penicillin G.
• Genital Gonorrhea: Ceftriaxone or spectinomycin.
• Disseminated gonorrhea: Ceftriaxone of Cefotaxime.
• Chlamydia: Azithromycin or Doxycycline.
• Chancroid: ceftriaxone or azithromycin.
• Granuloma inguinale: Doxycycline.
• LGV: Doxycycline for 3 weeks.
• Moniliasis: antifungals (nystatin or miconazole)
• Commonest cause of male infertility: Varicocele “got this info from the
lecture”
• Most painful genital ulcer: chancroid
• Commonest STD: HPV
• Commonest cause of urethral discharge: Gonorrhea
• Commonest cause of genital ulcers: HSV
• Commonest cause of female abnormal discharge: moniliasis
Commonest causes:
Stages of HIV infection:
1. Subclinical stage
• Very infectious
• CD4+ T cells are more than 500 cells/mm3
2. Persistent generalized lymphadenopathy
• Unexplained, lasting more than 3 months.
• Should be in at least 2 extrainguial sites.
• Painless.
3. Aids related complex (ARC)
• At least 2 C/P combined with at least 2 lab findings (next slide)
4. AIDS
• Proven HIV infection
• CD4+ T cells less than 200/mm3
• Opportunistic infections or rare malignancies
Clinical picture Laboratory findings
• Night sweats
• Weight loss more than 10%
• Unexplained fever
• Extreme fatigue
• Unexplained diarrhea
• CD4+ T cells between 499-200
cells/mm3
• Helper/suppressor ratio less than 1
• Cytopenia's
• Cutaneous anergy
• Increased Ig levels
Gonorrhea discharge (pus-like)
Commonest cause of female genital
discharge is CANDIDIASIS
Clue cells are seen in bacterial vaginosis
Bacterial vaginosis discharge is
whitish and
Has a fishy odor

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DERMA-ANDRO NOTES.pdf

  • 1. DERMATOLOGY & ANDROLOGY clinical notes and photos from the special sense round Made by: Abdulla Buhmaid
  • 2. Contents: • Psoriasis. • Lichen planus. • Fungal skin infections. • Hair and melanin disorders. • Viral skin infections. • Erythema multiforme, nodosum and steven Johnsons syndrome. • Parasitic skin infections. • Urticaria. • Dermatology clinical notes. • Andrology lectures and clinical notes and pictures. (lots of MCQs came from it)
  • 4. Primary psoriatic lesion • Notice the fine silvery scales
  • 5.
  • 6. Cold dry climates exacerbate psoriasis Hot humid climates decrease psoriasis Sun exposure is mostly protective against psoriasis in the majority of psoriatic patients but in some it could aggravate it. Pregnancy decreases psoriasis but psoriasis will be aggravated after labor Hypocalcemia aggravates psoriasis
  • 8.
  • 9. HISTOLOGY IMAGE OF PSORIASIS: • Hyperkeratosis (increased horny layer thickness) • Parakeratosis (incomplete ketinization of the horny layer “you still see nuclei”) • Munro-Micro Abscesses • Absent granular cell layer • In the dermis there is: • Dilated tortuous capillaries • Cellular infiltrate
  • 10. Psoriatic nail manifestations: • Onycholysis ( separation of the nail plate from its bed) • Thimble pitting (just like the photo, a thimble is the item seen above). • Subungual hyperkeratosis.
  • 11. Management of psoriasis TOPICAL THERAPY (1st line in mild to moderate plaque psoriasis) • Topical steroids • Salicylic acid 3% • Tar “antimitotic” • Anthralin • Topical calcipotriol PHOTOTHERAPY • PUVA • Broad and narrow band UVB • Sunlight SYSTEMIC THERAPY (for severe extensive cases “done in hospitals”) • Methotrexate • PUVA • Cyclosporin • Oral retinoids • Biologicals AVOID SYSTEMIC STEROIDS IN PSORIASIS !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!! !!!!!!!!!!!!!!!!!!!!!!!!!!!!
  • 13. Lichen planus is a disease in which the pathognomonic clinical picture is severe itching with flat-topped violaceous “purple” papules. There is hypergranulosis; so you might see white networks on these papules called “Wickhams striae”. Note that lesions in the palms and soles are NOT itchy, and NOT purple. They are yellow and non itchy.
  • 14. Wickhams striae due to hypergranulosis in LP
  • 15. Lichen planus really hates the nails, so the nail manifestations are particularly brutal: • Longitudinal ridging. • Irregular pitting. • Nail plate splitting. • Perygium formation.
  • 16. Pterygium (in the conjunctivitis chapter of ophthalmology) Also pterygium (but in the nail manifestations of LP in DERMA) Not so different right ??
  • 17. Lichen planus likes flexor surfaces Psoriasis likes extensor surfaces
  • 18. The etiology of LP is unknown, but it is hypothesized that it is due to immune origin. Lichen planus is associated closely with HCV
  • 19. Histology of lichen planus: • Hyperkeratosis • Hypergranulosis • Sawtooth rete ridges (long and with pointy end) • Cellular infiltrate in upper dermis • Liquefactive degeneration of the basal cell layer.
  • 20. Management of Lichen Planus 1.Topical steroids 2.Intralesional steroids (in cases or oral ulcer or hypertrophic skin lesion) 3.Oral antihistamines 4.Systemic steroids in extensive lesions
  • 22. Superficial fungal infection dermatophytes Pit. Versicolor (yeast like) Yeast (Moniliasis) • Tinea Microsporum • Tinea Trichophyton • Tinea Epidermophyton Malassezia furfur ( FKA pityrosporum orbiculare) Candida Albicans
  • 23. Clinical types of dermatophytes T. corporis T. Capitis T. Barbae onychomychosis T. Pedis T. Manus T. Cruris
  • 24. Notice the ring appearance in dermatophyte infection. This is due to the peripheral extension and central clearing with progression. Hence the name ring worm lesion or Tinea
  • 25. Tenia capitis Scaly type Black dot type Inflammatory type Favus • Microsporum Canis • Microsporum audouinii • Trichophyton violaceum • Trichophyton Tonsaurans • Animal fungi • KERION • PUSTULAR FOLLICULITIS • Trichophyton schoenleinii
  • 26. OSCE Description of the lesion: • A painful inflammatory, inflammatory, boggy, well circumscribed, bald swelling on the scalp that is studded with folliculo-pustules and an edematous weeping surface that could come with thick crusting. If you pull a hair that overlays the lesion, what do you expect? • Sero-pus comes out of the follicle that I pulled the hair from. Do you expect hair to regrow after this lesion heals? • No; it leaves scarring alopecia. What is your diagnosis? • KERION (abscess like swelling) What is the causative organism? • Animal fungi
  • 28. OSCE LESION: • FAVUS DESCRIBTION: • Saucer-shaped crusted lesions (called sulphur cups or scutula) that form around the infected hair. They are concave, yellow, and centered around a single dull dry hair and have a mousy odor. CAUSE? • The chronic scarring form of T. schoenlinii. HAIR EXPECTED TO REGROW? • No.
  • 29. KERION BIOGENIC ABSCESS IN THE SCALP ROUGH surface SMOOTH surface Less painful and no constitutional symptoms SEVERE PAIN with constitutional symptoms If incised, no pus will drain out (don’t incise it) If incised pus will drain out
  • 30. Some strains of fungi causing Tinea capitis give GREEN FLORESCENCE under woods light (but not all of them)
  • 31. MANAGEMENT OF TINEA CAPITIS and BARBAE 1.SYSTEMIC ANTIFUNGALS (to all cases) 2.TOPICAL ANTIFUNGALS 3.In kerion • Topical antiseptics to remove the crusts • Systemic antibiotics for 1 week
  • 32. DESCRIBE THE LESION AND IDENTIFY THE CAUSE DESCRIBTION: • Well defined plaques over the hairless areas of the body. The plaques shows active spreading with a raised border that is covered by scales/vesicles/pustules/crusts/papules. • The causative organism could cause a lesion that spreads peripherally and clears in the center (picture below), and other causative organism could cause a lesion that spreads peripherally and DOESN’T clear centrally. • The lesion below shows concentric rings (the central clearing is developing a new lesion). INVESTIGATIONS: 1. Woods light. 2. Scraping the raised border, then using KOH and microscopy. 3. Culture on Sub Araud Agar media. MANAGEMENT? • If lesion is localized: topical antifungal. • If lesion is extensive: systemic antifungals PROVISIONAL DIAGNOSIS: • TINEA CORPORIS
  • 33. All those pictures show T. corporis, it presents with many dermatological features and thus it could have many DD: 1. circinate psoriasis 2. Circinate impetigo (inflammatory types are similar) 3. Pityriasis rosea (differ by scraping and looking for fungus) 4. Annular LP 5. Discoid eczema
  • 34. DESCRIBE and DIAGNOSE DESCRIPTION: an arch like red plaque in the groin that extends to the thigh with a well- defined raised border. In the lower picture the scrotum is affected BUT usually the genitalia are spared. DD: flexural psoriasis, erythrasma, candidiasis, tinea cruris, dermatitis, flexural psoriasis. PROVISIONAL DIAGNOSIS: T. Cruris (of course I would know after investigations only, I can’t know without them “i’m not a wizard”) MANAGEMENT? 1. IF LOCALIZED: TOPICAL ANTIFUNGALS 2. IF EXTENSIVE: SYSTEMIC ANTIFUNGALS M<F Center is somewhat clear
  • 35. Wearing tight shoes for a long time, hyperhidrosis, hot weather, and excessive water use MACERATION of the skin in the foot Tinea pedis infection (commonest form of dermatophyte infection)
  • 36. Tinea Pedis Interdigital type “commonest” Scaly hyperkeratotic type Vesiculo-bullous type More in lateral 3 toe clefts Sodden (very moist), fissured, has opaque white scales, with eroded areas. With bad smell. The sole has erythema, fine scaling and hyperkeratosis. This type is resistant to treatment and chronic Vesicles or bullae that are tense progress to contain pus and rupture leaving a collar of scales. Worsens in hot weather.
  • 37. dermatophytid reaction is the body's reaction to a dermatophyte (fungal) infection and is a skin eruption that appears on an area of the body that is not the area where the infection first began. It is not dermatophytosis, but it is an allergic reaction. You will see this usually with vesiculobollus tinea pedis as a sterile vesicular reaction in the hand in the form of pompholyx.
  • 38. MANAGEMENT OF TINEA PEDIS 1.AVOID RISK FACTORS 2.FOR INTERDIGITAL TYPE: topical antifungal 3.FOR HYPERKERATOTIC AND VB TYPES: systemic antifungals
  • 39. The commonest form of Tinea Manus is the scaly hyperkeratotic type Diffuse powdery scaling and hyperkeratosis of the palm with accentuation of flexural creases (50% unilateral) “TTT SAME AS PEDIS”
  • 40. DIAGNOSIS: Onychomycosis FEATURES: • Whitish/yellowish discoloration of the free edge of the nail plate that spreads proximally. • Subungual hyperkeratosis • onycholysis MANAGEMENT: 1. Topical antifungal (Miconazole or Tioconazole) 2. Systemic antifungals DIFFERENTIAL DIAGNOSIS PSORIASIS You will see fine pitting CANDIDAL ONYCHIA Paronychia is present; nail dystrophy is proximally and laterally Bad prognosis in toe nail affection especially the elderly
  • 41. PityriasisVersicolor A common macular/patchy eruption of the trunk and proximal limbs. The color could be erythematous, whitish “hypopigmented”, or brownish “hyperpigmented”. The surface is covered by fine scales detected by scrabbing the lesion. Remission in winter and exacerbation in summer. Heals with hypopigmented macules that either persist or disappear on their own By woods light: yellow florescence of involved skin DD: vitiligo (no scaling), pityriasis alba (scaly), erythrasma (coral red on woods lamp), seborrheic dermatitis (greasy scales).
  • 42. TREATMENT OF P.VERSICOLOR TOPICAL OPTIONS: • Ketoconazole shampoo (5mins daily for 5 days) • Selenium sulphide or Zinc pyrithione shampoo (10 mins daily for 10 days or overnight once every week) “don’t apply to face or genitals” • Topical antifungal creams (Clotrimazole or Miconazole; daily for 2-4 weeks) SYSTEMIC OPTIONS “FOR RESISTANT OR EXTENSIVE CASES” • Fluconazole 300mg/week for 2 weeks. • Itraconazole 200mg/day for 1 week. IN CASES OF POST INFLAMMATORY HYPOPIGMENTATION: • Takes months to return to normal
  • 43. CANDIDIASIS CUTANEOUS NAIL MUCOUS MEMBRANE interdigital intertrigo Napkin candidiasis In groin, axilla and submammary Moniliasis after contact dermatitis or the diaper White macerated skin at webs • Nail thickening • Lateral fold discoloration • Irregular transverse ridging • Proximal nail fold seperation • Subungual hyperkeratosis ((paronychia)) oral vulvovagin al balanitis Oral thrush Acute atrophic (denture stomatitis) Candidal leucoplakia
  • 44. Oral thrush NOT SCRABED OFF EASILY EASILY SCRABED OFF Candidal leukoplakia
  • 45. TREATMENT OF CANDIDA INFECTION 1. Treat the causing factor (disease, drug use etc…) 2. Topical treatment: • Imidazole, nystatin, amphotericin. • 2-4 weeks for skin and oral candidiasis. • If nail candidiasis given for 3 months alongside systemic antibiotic. • If vaginal candidiasis: vaginal cream or tablets must be given “and treat the husband too” 3. Systemic treatment: 1. Oral nystatin (500k units 4 times/day “hold in mouth for some mins then swallow”) “for oral and vaginal” 2. Fluconazole ( 150mg/day for 3 days if oral candidiasis. And 150mg/week for 2 weeks for vaginal candidiasis) 3. Itraconazole (200mg/day “for 3 days in vaginal and for 2 weeks in oral”)
  • 47. Scarring (cicatricial) alopecia congenital Acquired Trauma, lacerations, burns Abscess, kerion, favus, and lupus vulgaris Discoid lupus, lichen planus, scalp cancer
  • 48. Follicular lichen planus (causes scarring alopecia, not expected to have their hair grow back)
  • 49. Discoid lupus scarring the scalp causing permanent scarring alopecia
  • 50. Note that in SLE the hair becomes brittle and hair loss is most evident at the hairline. It this case the hair has a chance of regrowing after the flare of SLE is controlled. But in discoid lupus lesion, the scarring that is done causes permanent hair loss that is only managed by hair restoration treatments after controlling SLE.
  • 51. KERION (a large sore caused by a fungal infection)
  • 52. Favus (Latin for "honeycomb") or tinea favosa is the severe form of tinea capitis.
  • 53. Lupus vulgaris is the TB granuloma of the skin, it is rare to come over the scalp.
  • 54. Non scarring alopecia CONGENITAL AQUIRED Circumscribed diffuse Alopecia areata Androgenetic alopecia Traumatic (constant rubbing and pulling) Secondary syphilis and mild T.capitis Telogen effluvium Anemia and malnutrition Chronic liver disease, Mg, and SLE DM, hypo/hyperth yroid Hypopituitarism and hypoparathyroid Cytotoxic drugs, colchicine, antithyroid and anticoagulants
  • 56. Exclamation “!” mark hair at the periphery of a bald area is a characteristic feature of alopecia areata
  • 57. Ophiasis is when alopecia areata lesions extend to form a band along the scalp margin
  • 58. Moth eaten alopecia. Pathognomonic for secondary syphilis
  • 59. Telogen effluvium is the increased loss of hair after severe stress, expect hair to regrow within 6-12 months.
  • 60.
  • 62. Albinism (congenital abnormality in melanin formation that affects the skin, hair, and eyes).
  • 63.
  • 64.
  • 65. The following types of vitiligo show bad response to treatment: 1. Segmental vitiligo 2. Vitiligo over bony prominences 3. Vitiligo on the palms and soles 4. Acrofacial vitiligo 5. Vitiligo affecting mucous membranes
  • 66.
  • 68. Lesion: multiple vesicles on an erythematous base Diagnosis: herpes simplex Treatment: topical acyclovir with oral acyclovir 200x5x10
  • 69. Lesion: started as papules that changed into vesicles that ruptured and formed crusts. This lesion shows centripetal distribution. Causative organism: Varicella zoster virus (primary infection). Name of disease: chicken pox. Management: symptomatic TTT only. But immunocompromised patients need Acyclovir 800x5x7
  • 70. Lesion: grouped vesicles on an erythematous base with a characteristic unilateral DERMATOMAL distribution. Causative organism: reactivated latent Varicella Zoster virus Name of disease: herpes zoster Management: oral acyclovir 800x5x7 and analgesics
  • 71. Lesion: dome shaped papule, sessile, firm, and with ROUGH SURFACE. Causative organism: HPV Management: must destroy (by chemical, cryo, or electrocautery) “this is not the only type of warts”
  • 72. Lesion: multiple umbilicated papules. Name of disease: Molluscum contangiosum Causative agent: Pox virus Management: Currettage
  • 74. Erythema multiforme “TARGET LESIONS” The lesion fades within two weeks with residual pigmentation that stays for months. The commonest precipitating factor is herpes simplex virus (HSV).
  • 75. Steven-Johnson syndrome and toxic epidermal necrolysis
  • 76. Toxic epidermal necrolysis (<30% detachment) Epidermal necrolysis is almost always drug induced
  • 77.
  • 78.
  • 79. Erythema nodosum (which is the inflammation of subcutaneous fat “allergic reaction” The lesion takes 2 to 6 weeks to resolve leaving a bruised appearance. Those are nodules not macules Give NSAIDS for pain and treat the causing factor. +Remember this lesion is connected to IBD and is infamous for recurrence
  • 80. DRUG REACTIONS Severe reactions Exenthema tous R. photose nsitivity blistering SLE like Acneform hyperpigm entation alopecia Fixed eruption anaphylactic shock -penicillin and plasma products Exfoliative erythroderma -BDZ -allopurinol -sulfa and gold Epidermal necrolysis Morbiliform Urticarial -penicillin -opiate -aspirin -radiocontrast Purpuric E.M. Lichenoid -captopril -chloroquine P. Rosea like -metronidazol -captopril -gold -psoralen -thiazide -tetracycline -phenothiazide -penicillin - penicillamine - captopril - procaineami de -hydralazine -ACTH -Steroids -Iodide -INH -OCP -Gold - Antimalaria - CHEMO -NSAIDS -Sulphonamide -Phenopthaline
  • 82. ORGANISM: - Mite (Sarcopetes scabii var hominis). How long is its incubation period? - 2 weeks to 2 months What skin disease does it cause and what is its characteristic lesion? - Scabies, and the characteristic lesion is Burrows. What is the characteristic symptom of this disease? - Severe itching that is worse at night. Is itching here localized or generalized? - It is generalized, because its due to the allergic reaction of the body to the mite.
  • 83. Anterior aspects of wrists and ulnar border of hands and forearm and elbow Around the nipples Finger webs Medial aspects of the thigh Natal cleft and lower buttox The axilla Dorsal foot and around the ankle Male genitals Abdomen and periumbilical H&N of infants only Characteristic sites for scabies
  • 84. IDENTIFY THE LESIONS INDICATED BY THE ARROWS AND DESCRIBE THEIR SIGNIFICANCE: - lesion: Burrows - Significance: they are the characteristic lesions for scabies
  • 85. You can catch scabies from infested animals like a dog “ANIMAL SCABIES”. So don’t touch any dog on the street and if you do touch one make sure you wash your hands with soap and water and change your clothes or take a shower as soon as possible Animal scabies is characterized by: 1- short IP 2- not transmitted man to man 3- burrows are absent 4- self limiting 5- finger webs and genitals are free
  • 86. •Yes, only if the patient is immunodeficient. Or is on steroid therapy. Can one have scabies and not have itching?
  • 87. IDENTIFICATION Norwegian (crusted) scabies PATHOPHYSIOLOGY It’s a severe form of scabies with a huge number of mites and eggs and thickened horny layer. It is due to the abnormal immune response of the host. It is seen in the mentally retarded, immunosuppressed, AIDS, sensory neuropathy, and elderly debilitated patients.
  • 88. C/P: - Crusted eruptions on the hands and feet - Subungual hyperkeratosis - Red scaly plaques on the head, neck and trunk - With or without severe itching
  • 89. IDENTIFICATION NODULAR SCABIES DESCRIPITION Nodular lesions that are itchy, NON-INFESTED, reddish brown in color, that may persist for weeks after treating scabies Mostly seen at: - Axilla - Male genitals - Groins - umbilicus Management? Intralesional steroids or surgical excision
  • 90. Norwegian scabies Management? 1. Cut the nails short and apply a topical scabicide under the nails. 2. Several applications of keratolytic creams 3. Several applications of topical scabicides 4. Two doses of oral ivermectin separated by an interval of a week (could be repeated more as needed)
  • 91. Microphotograph of mineral oil scabies preparation showing mite (below heavy black arrows), eggs (orange arrows), and scybala “fecal pallets”(yellow arrows).In preparing an ex vivo scabies preparation, mineral oil preserves scabies’ scybala, whereas potassium hydroxide does not.
  • 92.
  • 93. The red circle shows the triangular structure (delta sign or triangle sign), which indicates the head parts of scabies. The body of scabies is relatively translucent. There is a classic “S” shaped burrow above the triangular structure.
  • 94. TREATMENT OF SCABIES GENERAL MEASURES • Boiling all clothes and bed sheets, etc… (disinfection) • Treating the other people in the house and spouses. TOPICAL SCABICIDES (applied to entire skin except head and neck unless infant or old) • Permethrin 5%(2 successive nights) “safe”. • Sulfur “10% adult 5% child” (every night for 4 nights) “safe but has bad smell and stains so rarely used” • Gamma Benzine Hexachloride 1% (one application for 12 hours) “not safe for children >10y, pregnant women, & epileptics” • Benzyl benzoate 25% (for 2 nights) • Crotamiton 10% (for 2 nights) “preferred for infants and young children, and postscabitic pruritus” • Malathion 0.5% (for 12 hours then washed) SYSTEMIC TREATMENT • Ivermectin (antiscabetic) 6mg/15Kg • Antihistamines and antibiotics.
  • 96. This is a “nit”, which is the egg of head louses that are adherent to the hair. We usually don’t see the adult lice, but we can clearly see the nits in the hair in cases of pediculosis capitis
  • 97. Management of pediculosis capitis 1- CUT THE HAIR SHORT. 2- GIVE CO-TRIMOXAZOLE if there is impetigo 3- GIVE PEDICULOSIDES AFTER CONTROLLONG BACTERIAL INFECTIONS: • Malathion 0.5% lotion (12 hours then wash) • Ivermectin lotion (12 hours then washed) • GBH 1% shampoo (5 mins then washed) • Repeat after 1 week and all family members should do the exact same. 4- ORAL IVERMECTIN (6mg/15Kg repeated in 10days) 5- REMOVE NITS • Make a white vinegar solution diluted in water (1:1) • Leave it for 1-2 hours until the cement dissolves • Wash and comb the hair with a fine-toothed comb
  • 98. This is pediculosis pubis also known as Pubic lice. It is sexually transmitted and could be seen at the groin hair, axilla, eyelashes, beard, any body hair tuft. Management: 1- topical pediculocide (choose 1 agent and repeat the TTT in one week, must apply it to all the body even if not affected) 2- in cases of topical TTT failure, or perianal or eyelash involvement, give oral ivermectin on day 1 and 8 3- don’t forget the spouse
  • 100. Urticaria (many wheals are seen) and angioedema of the face. MANAGEMENT: (after removing the cause!!!) 1.Adrenaline 2.Antihistamines 3.Systemic steroids if severe 4.Local soothing lotion (calamine lotion) 5.Calcium gluconate
  • 102. Aquagenic urticaria is a rare condition in which a person's skin develops red,itchy hives after exposure to water. (aka water allergy)
  • 103.
  • 104. CHOLINERGIC URTICARIA stimulus might be considered to be heat; the actual precipitating cause is sweating. “so, anything that increases your core temperature leads to this”
  • 106. Papular urticaria (hypersensitivity reaction to an insect bite)
  • 108.
  • 109. Identify the disease and describe the lesions and their distribution and the causative agent: Disease: Hand, foot and mouth disease Description: multiple oval vesicles (or crusts if the rupture) that are seen on the oral region, palmar aspect of the hand, and plantar surface of the foot. WITH NO LESIONS ON THE TRUNK (to differ it from chicken pox). Causative agent: coxsackievirus
  • 110. Psoriasis of the scalp Seborrheic dermatitis of the scalp Area of affection: primarily the frontal hair line “crown” Scales: DRY and WHITE. Auspitz sign: +ve. Area of affection: the temporal and occipital regions. Scales: GREASY and YELLOWISH
  • 111. Psoriasis in the palm Eczema in the palm • Fiery red erythema • Well defined border • Oozes blood when scratched • Auspitz sign +ve • Less marked erythema • Hazy border • The 1ry lesion is vesicles so it oozes watery fluid when scratched
  • 114.
  • 120. CORAL RED appearance under woods light in Erythrasma
  • 122.
  • 124.
  • 125. The male urethra ( 4 parts): 1. Prostatic urethra “3 cm” 2. Membranous urethra “1.2cm and no glands open to it” 3. Bulbar urethra “widest part, receives openings for cowper glands” 4. Penile urethra “Littres gland open here” Epithelium of the male urethra: Prostatic and membranous urethra: transitional epithelium Bulbar and penile urethra and ducts: pseudostratified columnar Fossa navicularis: stratified squamous
  • 126.
  • 127.
  • 128. Histology of the testes is important to understand the books scripts.
  • 129. Priapism is the prolonged painful erection more than 4 hours. It is mostly seen in blood dyscriasis!!!!!!!!!!! And it is a medical emergency!!!!!!!
  • 130.
  • 131.
  • 132.
  • 133. Seminal vescicles prostate Cowpers glands • Forms main bulk of seminal fluid. • Adds sodium bicarbonate. • Adds fructose. • Adds semen coagulator. • Adds zinc (Zn). • Adds semen liquifactor. • PSA. • adds mucus (lubricant) • Adds antioxidants • Adds nutrients
  • 134.
  • 135.
  • 136. chancre chancroid • Caused by syphilis (Treponema pallidum) • It is painless • Caused by Hemophilus Ducreyi • It is painful! ((mnemonic to remember: if you have chancroid, you DO CRY. “because it sounds like ducreyi ”)
  • 137. Causative organisms • Chancre: syphilis/treponema pallidum • Chancroid: Hemophilus Ducreyi • Granuloma inguinale/Donovanosis: Klebsiella Granulomatis ( have safety pin appearance) • LGV: chlamydia (L1,2,3) • Moniliasis: candida albicans • Trichomoniasis: Trichomonas vaginalis “protozoa, remember the strawberry appearance of the cevix”
  • 138. Drugs of choice • Syphilis: Benzathine penicillin G. • Genital Gonorrhea: Ceftriaxone or spectinomycin. • Disseminated gonorrhea: Ceftriaxone of Cefotaxime. • Chlamydia: Azithromycin or Doxycycline. • Chancroid: ceftriaxone or azithromycin. • Granuloma inguinale: Doxycycline. • LGV: Doxycycline for 3 weeks. • Moniliasis: antifungals (nystatin or miconazole)
  • 139. • Commonest cause of male infertility: Varicocele “got this info from the lecture” • Most painful genital ulcer: chancroid • Commonest STD: HPV • Commonest cause of urethral discharge: Gonorrhea • Commonest cause of genital ulcers: HSV • Commonest cause of female abnormal discharge: moniliasis Commonest causes:
  • 140. Stages of HIV infection: 1. Subclinical stage • Very infectious • CD4+ T cells are more than 500 cells/mm3 2. Persistent generalized lymphadenopathy • Unexplained, lasting more than 3 months. • Should be in at least 2 extrainguial sites. • Painless. 3. Aids related complex (ARC) • At least 2 C/P combined with at least 2 lab findings (next slide) 4. AIDS • Proven HIV infection • CD4+ T cells less than 200/mm3 • Opportunistic infections or rare malignancies
  • 141. Clinical picture Laboratory findings • Night sweats • Weight loss more than 10% • Unexplained fever • Extreme fatigue • Unexplained diarrhea • CD4+ T cells between 499-200 cells/mm3 • Helper/suppressor ratio less than 1 • Cytopenia's • Cutaneous anergy • Increased Ig levels
  • 143. Commonest cause of female genital discharge is CANDIDIASIS
  • 144. Clue cells are seen in bacterial vaginosis
  • 145. Bacterial vaginosis discharge is whitish and Has a fishy odor