Growth Rates in Dermatology

Hi everyone. My skin Lecturer just taught me this so I thought let's post this =)

So growth rates !
We need to know 3 of them - Hair , Finger nails and Toe Nails.

Hair is the fastest growing.
So remember just one number for it - 0.37 mm/day.

Now , next fastest is finger nails.
For this divide by 3.
0.12 so 0.1 mm / day is finger nails.

Now divide this by 3 to get the value for Toe nails.
So 0.03 mm/ day is for Toe nails !

That's all for this post !
Stay awesome !
Happy Studying !
~ A.P.Burkholderia

MIL : Tinea (Dermatophytosis)

Hi everyone ! 
This is my 2nd MIL! Hope it's illustrative and informative ! 

(Click on the image to see it in Full View). 

Description : 

This is an Image of Tinea Corporis (Ringworm) infection of the skin. 

Notice - the lesion is annular in shape , has a ring like appearance. 

The lesion seems to be erythematous and  elevated (papular) towards its outside, and shows central area of clearing. 

This is classic of Tinea! 

Tinea is actually a fungal infection caused by Dermatophytes. 

____________________________

Clinical Features -

- Include such a lesion over different body parts which are severely itchy. 

- Occur particularly in summers.

Tinea Corporis = Tinea infection occuring over the body. 

Some common forms are - 

Tinea Cruris = Tinea Infection in the groin area (Jock itch).

Tinea Glutealis = Tinea along the natal cleft and towards the Gluteal regions. 

Tinea Pedis = Athelete's foot, occuring in the feet. 

Tinea Capitis = Scalp and hair. 

- Predisposed to get this in areas of constant sweat and moisture. 

Hence dryness is very important to maintain. 

____________________________ 

Ix : 

Usually a clinical diagnosis. 

Differentiate from Psoriasis : Lesions are not clear centrally ; there are plaques with Scales in Psoriasis and there maybe history of pin point bleeders.

Can confirm using Biopsy / Analysis of skin scraping and obtaining a species specific diagnosis. 

____________________________

Rx : 

A. Topical Anti fungals 

- Resistance is rampant. 

- Most promising ones are Luliconazole and Terbinafine creams.

- Can try Clotrimazole and Ketoconazole Shampoo for the site of lesion.

B. Oral Anti fungals 

- Itraconazole is a wonderful drug , dose being 5mg/kg / day. Roughly 100 mg twice a day is good enough. 

- Griseofulvin was an option but resistance seen now.

C. Anti histaminic for allergy. 

D. Duration of Rx is almost 2-3 months. It's a hard fungus to kill..

E. Steroids not to be used strictly. ( I've seen some horrendous results where the whole body was covered with Tinea when the patient stopped applying the steroids. Best to avoid them as per clinical as well as literature review). 

Hope this was helpful! 

Happy studying ! 

Stay Awesome ! 

~ A.P.Burkholderia 

Koebner Phenomenon

Hi everyone!
Koebner Phenomonon is a much talked about skin phenomenon.
In this post I'll just discuss Koebner's and its variants briefly.

1. What is it ?
- Many skin conditions tend to occur at the sites of previous trauma.
- This propensity of some new disease to be localised to trauma marks from before is called Koebner's. 
- Also called ' Isomorphic Phenomonon'.

2. Why does it occur ?
- So that's kind of unclear ! But it is said that trauma causes some amount of Subacute inflammation.
- This Subacute inflammation is mainly IL1 and 17 mediated.
- Such an inflammatory condition predisposes the site to further Autoimmune damage.

3. Conditions where Koebner Occurs ?

Mnemonic :
Truly , she Pees Very Little.

True Koebner seen in
Psoriasis
Vitiligo
Lichen Planus

4.  What is Pseudo Koebner's  ?
- Now the basis of true Koebner is that on a site for existing trauma, a new autoimmune lesion appears.
- When the trauma site gets secondarily seeded by some organism causing lesions along its line it's called 'Pseudo Koebner's phenomena'.
Examples =
Molluscum contagiosum
Verruca Vulgaris ( Warts).

5. What is Reverse Koebner ?
- When a lesion along a trauma line gets resolved spontaneously it's called Reverse Koebner.
- Seen in Psoriasis and Granuloma Annulare.

6. What is Reverse Remote Koebner ?
- (isn't that about enough with this topic now?! Are they kidding us with this?)
- So it's seen in Vitiligo. When one patch undergoes resolution with surgery etc , patches elsewhere get resolved too. (God knows what this means , but yeah. *yawns* )

7. What is Pathergy test ?
- So this is a somewhat similar reaction.
- In people with Behcet Disease, if they're poked on their forearm with a needle , they tend to develop pustules and ulcers over it.! It's almost diagnostic of Behcet's.

So, that's all in this post !
Hope this was helpful.
Happy Studying!
Stay awesome!

~ A.P.Burkholderia.

MIL : Pemphigus Vulgaris

Hi everyone ! This is my first MIL post ! 

Step 2 CK: Confusing vesicular skin manifestations

Skin manifestations that sometimes confuse us:

1) Dermatitis herpetiformis: It is a skin manifestation of celiac disease (adult and pediatric) - clusters of vesicles, pustules on extensor surfaces of elbow, knees etc.
Treatment:  Gluten free diet and anti-inflammatory drugs (Dapsone, Sulfapyridine)

2) Eczema herpeticum: Infection of eczematous skin by HSV (fluid filled , honey crusted vesicles on red, indurated skin of eczema).
Treatment: Acyclovir, Valaciclovir.

IkaN addition: I know honey crust makes us think of impetigo right away but put the presentation and distribution whenever inferring the diagnosis. I've got a number of questions wrong on the USMLE practice tests because of the honey crust bias.

This mini note was submitted by Disha Sharma :)

Desmosomes and its disorders

Hello friends,
This post is about the importance of desmosomes in various dermatological conditions.

Basics:
Desmosomes are present in stratum spinosum of epidermis.  They are calcium channel dependent adhesion molecules (cadherins)  and hence form intercellular connections.

Desmosomes are seen all through the epidermis, but are obvious as spines in spinous layer.

They have many constituents. Important transmembranous  parts are:
•Desmoglein (DSG)
•Desmocollin (DSC).

Now we will focus on Desmoglein (DSG) .
•DSG-3 is present mainly in basal layer of epidermis and strongly seen in mucosae.
•DSG-1 is present in superficial epidermis and is not seen in mucosae.

Clinical importance:
* If DSG-3 is damaged --->
   early, severe mucosal involvement.
   Lower level of damage to epidermis.
* If DSG-1 is damaged --->
    No mucosal involvement.
    Superficial epidermal damage.

° If IgG antibody is formed against DSG-3, then the resulting disease is known as Pemphigus vulgaris.
° If IgG antibody is formed against DSG-1, then the resulting disease is known as Pemphigus foliaceous.

A mnemonic to remember DSG-3 for basal layer and mucosal involvement :

Thanks for reading
Madhuri.

MIL: Lichen Planus

Read more about Medicowesome Image Library (MIL) here.

Image: Plaques of Lichen Planus

Submitted by: Dr. Manasi Shirolikar

MIL: Impetigo

Read more about Medicowesome Image Library (MIL) here.

Image: Impetigo contagiosa

Submitted by: Sagar

MIL: Psoriasis

Read more about Medicowesome Image Library (MIL) here.

Image: Plaques of psoriasis

Submitted by: Dr. Manasi Shirolikar

Drug of choice : Dermatology

Hello everyone!
Here's a collection of Drugs of choice (DOC) for some Dermatology conditions. These are some of the most commonly asked questions in Post Graduation entrance exams.

1. DOC for severe erythrodermic psoriasis?
Cyclosporin

2. DOC for erythrodermic psoriasis?Methotrexate

3. DOC  for pustular psoriasis?
Acitretin

4. 2nd choice for pustular psoriasis?Methotrexate

5. DOC  for arthritis mutilans?
Etanercept

6. DOC for impetigo herpetiformis?
Systemic steroids

7. DOC for psoriatic arthritis?
Methotrexate

8. DOC for psoriatic erythroderma in pregnancy?
Systemic steroid

-Md Mobarak Hussain (Maahii)

Diagnostic criteria of neurofibromatosis type 1 mnemonic

The criteria are met in an individual if two or more of the features listed are present.

The mnemonic is "FANCOOL"

F: Family history
A: Axillary freckles (known as CROWE'S SIGN)
N: Neurofibromas (2 or more)
C: Café-au-lait macules (6 or more)
O: Optic gliomas
O: Osseous  (sphenoid dysplasia)
L: Lisch nodules in the eyes.

Thanks for reading.

Madhuri

 

Image based MCQ on pediatric infections

Hey Awesomites

Yesterday we posted an MCQ on a pediatric infection with characteristic appearance of rash on face, involving both cheeks.

Cutaneous manifestations of Streptococcus

Hello awesomites!
Here's a collection of Cutaneous infections/diseases caused by Streptococcus pyogenes

Direct infections of skin or subcutaneous tissue-

1. Cellulitis
2. Impetigo
3.Ecthyma,Erysipelas
4. Vulvovaginitis
5. Perianal infection
6. Streptococcal ulcers
7. Blistering distal dactylitis
8. Necrotizing fasciitis

Secondary infection-

Eczema, infestations, ulcers, etc.

Tissue damage from circulating toxins-

1. Scarlet fever
2. Toxic‐shock‐like syndrome
3. Recurrent toxin‐mediated perineal erythema

Skin lesions due to allergic hypersensitivity to Streptococcal antigens

1. Erythema nodosum
2. Vasculitis

Skin disease provoked or influenced by Streptococcal infection (mechanism uncertain)-

1. Psoriasis, especially guttate forms.
2. Kawasaki disease.

That's all!

MD Mobarak Hussain (Maahii)

Steven-Johnson syndrome (SJS) / Toxic epidermal necrolysis (TEN) -Part 2

Hello :)

Have you heard of SCORTEN SCORE?

It is a score used to assess the severity of illness in TEN.

Go to the link below:-

https://image.slidesharecdn.com/delayedtypedrughypersensitivityinterhospitalconference-100803104905-phpapp01/95/delayed-type-drug-hypersensitivity-35-728.jpg?cb=1280833217

-We can assess the nutritional status by the body weight.

-Body is in the condition of hyper metabolism which will lead to excessive proteolysis.

-For the above thing, check albumin levels.

-Due to excessive fluid loss body will undergo dehydration and hypotension.

-Temperature should be noted. As each degree increase in temperature over normal, increases metabolism by 5-8%.

-Ocular examination is important part.

-Check for LFT and RFT.

-Late ophthalmic complications are mainly due to functional alteration of the conjunctival epithelium with dryness and abnormal lacrimal film. This leads to chronic inflammation, fibrosis, entropion, trichiasis, and symblepharon. Long-term irritation and deficiency of stem cells in the limbus may result in metaplasia of corneal epithelium with painful ulcerations, scarring, and altered vision.

- Esophageal, intestinal, urethral, and anal strictures may also develop in rare cases. 

Nutrition: -

 Consist 2 parts

1) parentral

2) Entral

Parentral nutrition consist of dextrose.

Entral is important for this patient.

-Protein powder.

-Dal.

-Fruits e.g. Banana

-We use various feeding devices like nasogastric tube or ryles tube.

Treatment:-

-Stop all the drugs

-airway breathing circulation fluids

-Symptomatic treatment

MEDICATIONS

Antibiotic to treat and prevent infections.

Used to treat and prevent severe skin inflammation.

Ranitidine reduces the acidity.

BETADINE MOUTH GARGLE: Oral antiseptic for relief of painful infections and inflammatory conditions of mouth and pharynx

Anti-inflammatory, Anti-pruritic, and Vaso-constructive properties. To cure mouth ulcers.

-Burns guideline (but lesser fluids)

That's all for today .

-Upasana Y. :)

x

Steven-Johnson syndrome (SJS) / Toxic epidermal necrolysis (TEN) -Part 1

Hello! :)

TOXIC EPIDERMAL NECROLYSIS

-A severe form of adverse cutaneous drug reaction

-Idiosyncratic reaction

-Immunologically Mediated

- Fever and mucocutaneous lesions

-Epidermal sloughing

CLASSIFICATION

1. SJS= <10% BSA detachment

2. OVERLAPPING SJS/TEN= 10-30% detachment

3. TEN = >30% detachment

EPIDEMIOLOGY

-Both are rare but occur as a medical emergency.

-Incidence of SJS 1-7 Cases per million.

-SJS > TEN by 3: 1

-TEN tend to be older

-Worldwide distribution

-HIV positive cases have increased incidence.

ETIOLOGIES

-Drugs being the most common cause

-Infection (viral e.g. HSV, bacterial, fungi)

-Vaccination

-systemic disease (lupus)

-Physical agents (UV light, radiation)

-Idiopathic 25%

Drugs that result in this are:-

-Antibiotics = sulfonamides > penicillin > cephalosporin

-Anti-gout: allopurinol

-Anti-epileptics; carbamazepine, Dilantin

-Anti-psychotics

-Analgesic including NSAIDS

RISK FACTORS:

GENETIC SUSCEPTIBILITY:-

-HLA-B*1502 associated with greater risk with carbamazepine use in southeastern Asians.

-HLA-B*5801 confers risk with allopurinol associated reactions.

-HLA-B*44 Caucasians

HIV:-

-Slow acetylators so results in prolonged exposure to medications.

-Immune dysregulation

-Other infections

-40 Fold increased risk of SJS/TEN with cotrimoxazole (Remember! It is used as a prophylactic drug in HIV patients.)

CLINICAL PRESENTATION:-

-Drug exposure 1-3 weeks prior to onset of symptoms

-PRODROME=fever, flu-like, 1-3 days

-symmetrical lesion distribution

-starts on face and trunk before spreading

-skin blistering with sloughing for 2-3 days progressively then stabilizes

-Erythroderma

-Facial edema

-Skin pain- burning

-Palpable purpura

-Skin necrosis (Nikolsky sign)

-Blisters or epidermal detachment

-SJS tragetoid, TEN target lesions atypical

-Mucous membrane erosions or crusting

-tongue swelling

-conjuctival irritation

-Dysuria

-GI bleed

-Pulmonary bleed

LABORATORY FINDINGS

-Anemia

-Lymphopenia

-Neutropenia (poor prognosis)

-Elevated transaminases

-Cultures, If infected

-Skin biopsy-Rule out other conditions

-BUN/CR ratio

-Serum electrolytes

PATHOGENESIS

-not well understood

-Suspected immunologic

1. GRANULYSIN: Cytolytic protein from cytotoxic T-cell and NK - cells

(Highly expressed in SJS /TEN patients)

2. DEATH RECEPTOR CD95 (fas): Elevated fas ligand leading to apoptosis

3. Perforin, TNF-alpha and granzymes-B in higher concentration, associated with NON-APOPTOTIC death.

HISTOLOGY

-Early perivascular inflammation of T-lymphocytes, primarily CD8

-Monocytes infiltration

-Lymphocytes surrounding basal keratinocytes

-Subepidermal vesiculation

-Full thickness necrosis

-Increased adhesion molecules: VCAM, ICAM

EVALUATION AND DIAGNOSIS

-Clinical diagnosis on the basis on exclusion

-prior drug history or illness+fever+skin lesions with sloughing

DIFFERENTIAL DIAGNOSIS

-toxic shock syndrome (staphylococcus and streptococcus)

-Scalded skin syndrome (staphylococcus)

-Phototoxic eruptions (Sun exposure areas and known medications)

-Paraneoplastic pemphigus (Lymphoma)

-Erythematous drug eruptions (Lack mucosal involvement)

-Drug hypersensitivity syndrome /DRESS/DIHS (eosinophilia)

-Acute generalized exanthematous pustulosis (AGEP) (lack of pain and noted pustules)

-Toxic skin reaction (chemical irritant)

-Toxic erythema (Intoxication)

-Kawasaki's (diagnostic criteria)

EMM (ERYTHEMA MULTIFORME):

-targeted papules and plaques

-Acrally distributed

-Fever mild

-Significant skin detachment uncommon

-Histology: inflammation EMM>SJS

TREATMENT:-

-Immediate removal of possible triggers (especially drugs with longer half-life)

-SUPPORTIVE CARE

 - Wound care: burn unit with improved outcomes

 *avoid silver sulfadizine (Sulfonamide associated with SJS)

 -Fluid and electrolyte management (RL or NS)

 -Pain control (Local anesthetic cream)

 -Temperature regulation: caloric expenditure 

 -Monitor for infection: pseudomonas

 -Nutrition (High protein diet, Banana) (I will discuss it in next post)

 -Ocular care (Important)

 You can also refer this link 

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3018455/

That's all for today.

I will discuss the case we have seen in the emergency ward on the same. And also the treatment aspect. 

-Upasana Y. :)

x

Staphylococcal Scalded Skin Syndrome vs Bullous Impetigo

How do you differentiate Staphylococcal Scalded Skin Syndrome (SSSS) from Bullous Impetigo (BI)?

The exfoliative toxins are restricted to the area of infection in BI. In SSSS, infection is diffuse.

In BI, bacteria can be cultured from the blister contents. Cultures from blisters are negative in SSSS.

Blood cultures are usually negative in SSSS (positive in BI).

In SSSS, Nikolsky sign is positive. It is negative in BI.

In BI, patients are usually not ill appearing.

That's all!
-IkaN

Parkinson's disease associated with melanoma: Research update

Hey Awesomites

Patients with movement disorder such as the Parkinson's are at four-fold higher risk for malignant melanoma, and vice versa. This is likely due to mutual genetic, environmental and pathogenic ( immune system ) abnormalities and factors that they both share, as suggested by a research study at Mayo clinic.
( Source )

- Jaskunwar Singh

MCQ Pointers - Pityriasis Versicolor.

Hello!

If you see some of the below "pointer" words in MCQs the ans would most likely be pointing towards Pityriasis Versicolor.

-Acquired lesions.
-Hypopigmented small macules coalescing to form Patches classically on the chest (m/c),back,face.
-Perifollicular (around hair follicles) distribution.
-Fine scaling on lesions which becomes prominent on scratching - Scratch sign+.
-Pale yellow fluorescence of the lesions on Wood's lamp examination.

Finally the classic - Indicating the causative organism : Malasessia.
Spaghetti and meat balls appearance or Banana and Grapes appearance on KOH mount.

Lemme know more of pointers you know about.
Let's Learn Together!
-Medha.

Melanoma marker mnemonic

The immunohistological marker for melanoma is HMB 45.

You can remember it by remembering the gorilla named 'Harambe' (HaraMBe) of Cincinnati zoo who was in the news as he unfortunately had to be put down because a child entered his enclosure.

You can correlate melanoma's black pigment with that of Harambe's black fur.

That's​ all!

- Sushrut Dongargaonkar

Paraneoplastic Dermatoses - Bazex Syndrome.

Hello everybody,

So to continue our series on cutaneous manifestations of internal malignancies
Let's quickly learn about Bazex Syndrome.

Bazex syndrome — acrokeratosis
paraneoplastica is a paraneoplastic phenomenon associated with squamous cell carcinoma of the upper digestive tract.

Presents more commonly in Males and over the age of 40.

Presentation: Erythematous to violaceous psoriasiform plaques predominantly located in acral areas (especially the fingers, toes, nose, and helices).

Nail dystrophy, palmoplantar keratoderma, and alopecia are common.

In most patients, manifestations of Bazex syndrome precede the diagnosis of malignancy or the malignancy is diagnosed concurrently.

The lesions of Bazex syndrome are usually resistant to targeted therapies, but treatment of the neoplasm usually leads to resolution of the cutaneous findings, although not always.

Let's learn together!
-Medha!