Theory Preparation-2

  • Arthropods

House-dust mite:

Follicle mites/ Demodicidae

American trypanosomiasis  Larva Curens  Anklyostomiasis, Strongyloidiasis  Trypanosomiasis,

 

These are very imp too and comes frequently in theory exam

HIV AND THE SKIN:

Pigmentary disorders

Coagulopathies

Inflammatory dermatosis

Seborrhoeic dermatitis

Erythroderma

Atopic eczema

Psoriasis

Eosinophilic folliculitis

Pruritic papular eruption

 

Granuloma annulare

Porphyria cutanea tarda

Bacterial infections

Viral infections

Fungal infections

Protozoal infections

Scabies

Miscellaneous

Neoplasms

KAPOSI SARCOMA

MELANOMA AND NON MELANOMA SKIN CANCERS

LYMPHOMA

HAIR AND NAILS

ORO-PHARYNX

HIV IN CHILDREN

IRIS/IRD/IRAD

Indicator conditions in case definition of AIDS

Investigations

Dds of primary HIV infection

#pearls topic is HIV.

 

1-Most common pathogen to cause onychomycosis…..T.ruburm

Treatment of fungal infection… Same as in Non HIV. Oral terbinafine is safe.

 

2-Stain used for cutaneous histoplasmosis is Gomori methenamine silver stain

Stain used for systemic histoplasmosis is wright stain.

 

3-Cryptococcal infection …stain used is mucicaramine or tznack smear

Poor progsis if CNS involvement .

 

4-Leishmaniasis is difficult to treat compared to the one in normal person.it is associated with rheumatoid nodulosis.

 

5-Crusted scabies may b localized to sole or genitalia. On histo , eccrine ductal and follicular mucinosis can be seen.

 

6-kaposi sarcoma,a spindle cell tumor,risk increase if topical tacrolimus used in HIV.In children or non HIV person transmission is by saliva.

 

7-ratio of SCC:BCC 1:7

 

 

8- long term voriconazole therapy ,associated with multiple BCC.

 

9-melanoma ,a non AIDS defining cancer, has poor prognosis if CD4 count is low

 

10-most common BCC is superficial spreading type,treated with topical imiquimod

 

11- hodgkin disease with mixed cellularity and lymphocyte depleted ,more common in HIV.

 

12-most common lymphoma is NHL.

 

13 T.ruburm ,most common cause of onychomycosis

 

14- grey nail seen at CD4 count< 200 ×10⁶/L.

 

15-Oral hyperpigmentation is sign of low CD4 count (<200) .

 

16-If pt has hairy cell leukemia, 75% chance to develop AIDS with in 2 to 3 years.

 

17-concrum oris(noma), seen in malnourished HIV infected children.

 

18- hydroxyurea , cause melanonychia.

 

19- indinavir and zidovudine cause hair and nail pigmentation

 

20- foscarnet … side effect :Penile ulceration and eosinophilic folliculitis

LICHEN PLANUS AND LICHENOID DISORDERS:

Clinical features

Annular atrophic LP 👇

CLINICAL VARIANTS👇🏻

1️⃣ LP principally  involving mucous membranes

Oral LP

Oral LP with reticulate pattern and Wickham’s striae

Erosive LP

Vulval LP

Vulvo vaginal gingival syndrome

Penile LP

2️⃣ Lichen plano pilaris

Lichen planopilaris

Frontal fibrosing alopecia

Graham Little Picardi syndrome

3️⃣ Hypertrophic LP

4️⃣ LP of palms and soles

5️⃣ Actinic LP

6️⃣ Lichen planus pigmentosus

7️⃣ Annular lichen planus

8️⃣ Guttate LP

9️⃣ DLE/LP overlap

🔟 Bullous LP and LP pemphigoides

Bullous LP

LP pemphigoides

NAIL CHANGES IN LICHEN PLANUS 👇🏻

  1.  longitudinal ridging
  2. Nail plate thinning
  3. Distal splitting of the nail plate
  4. onycholysis
  5. Subungual hyperkeratosis
  6. Pterygium formation
  7. complete nail loss, appearing as irregular grooves and pitting on the nail surface

Trachyonychia

Trachyonychia is rough nail(s) with excessive longitudinal ridging due to proximal nail matrix damage.

 is characterised by brittle nails that show diffuse longitudinal ridging and can be accompanied by pitting, loss of lustre, or a roughened nail plate.

Trachyonychia, also known as ‘rough nails’ or ‘sandpaper nails’, can involve any number of nails. Twenty-nail dystrophy refers to trachyonychia that affects all 20 nails.

Causes of trachyonychia

It can be idiopathic or associated with:

Alopecia areata/alopecia universalis

Lichen planus

Psoriasis

Ichthyosis vulgaris

Atopic dermatitis

Vitiligo.

🌹 LICHEN NITIDUS 🌹

NEKAM DISEASE

Associations of LP

Disease course and prognosis

Investigations

Management

GRAFT VERSUS HOST DISEASE:

Definition

Risk factors

Pathophysiology

Pathology

Markers

🔰 ACUTE GVHD

Clinical features👇🏻

Disease course and prognosis👇🏻

Investigations

Management

🔰 CHRONIC GVHD

Management

Acute is within 90 days and chronic after 90 days

 

Acute tens like pic,<100days

Chronic lichenoid >100days

 

Acute

Maculopapular morbiliform rash

Palmo planter erythema

Ten like

 

Chronic

Sclerodermoid

Lichenoid

Morheaform

 🔰 Acute GVHD

 🔰 Chronic GVHD

🔰 *IMPORTANT*🔰

 

For this chap too, listen to voice notes for quick revision, memorize the tables from rooks and practice mcqs only.

 

🔰 Eczema can be covered  well from mcqs.

Juz solve the mcqs for the  safe side.

U all have managed so many pts in the opd and know well how to manage them. Dun waste ua time reading  this chap from rooks.

URTICARIA:

Subtypes of Urticaria👇🏻

Age and gender incidence 👇🏻

Associated diseases👇🏻

Pathophysiology 👇🏻

Acute spontaneous urticaria

1️⃣ Allergic / Immune mediated histamine release 👇🏻

2️⃣ Non allergic/Non immune mediated histamine release👇🏻

*Chronic spontaneous urticaria*

 

 Idiopathic

Food additives

Natural salicylates

Amines

Spices

Green tea

Alcohol

  1. Pylori infection

Parasitic infestation with Ancylostoma and Strongyloides

Histopathology👇🏻

🔰 INDUCIBLE URTICARIAS 👇🏻

1️⃣ Dermographism

2️⃣ Delayed pressure urticaria

3️⃣ Vibratory angioedema

4️⃣ Temperature dependent urticaria

5️⃣ Cholinergic urticaria

6️⃣Other types of inducible urticaria

Differential diagnosis👇🏻

Course and prognosis👇🏻

Investigations 👇🏻

Management👇🏻

🔰 *Important*

 

For this chap “Urticaria”  only listen to above voice notes and u ll never need to go through rooks for this chap.

Revise by solving mcqs from different books

Happy learning😊

AUTOINFLAMMATORY DISEASES OF SKIN:

1️⃣ Familial Mediterranean fever

🔰Imp points to remember👇🏻

2️⃣ Cryopyrin associated periodic syndrome / Familial cold autoinflammatory syndrome / Muckle Wells syndrome

🔰Mneumonic for CAPS and Muckle Wells👆🏻

3️⃣ Tumour necrosis factor associated periodic syndrome (TRAPS)

🔰 Mneumonic👇🏻

4️⃣ Blau syndrome/ Familial juvenile sarcoidosis

5️⃣ Autoinflammatory syndromes with pustulosis

6️⃣ Schnitzler syndrome

Dds👇🏻

 

  1. Adult onset Still disease
  2. Hypocomplementaemic urticarial vasculitis
  3. Cryoglobulinaemia
  4. SLE

7️⃣ Adult onset Still disease

🔰Summary👇🏻

DERMATOLOGICAL MANIFESTATIONS OF RHEUMATOID DISEASE:

1️⃣ Rheumatoid arthritis

🔰Rheumatoid nodules

🔰Linear subcutaneous bands and interstitial granulomatous dermatitis

🔰 Rheumatoid neutrophilic dermatosis👇🏻

🔰 Vascular lesions in RA👇🏻

🔰Important tip to remember👇🏻

🔰 Leg ulcers👇🏻

Felty syndrome

2️⃣ Sjogren syndrome 👇🏻

Clinical features

Dds, complications and disease course/prognosis

Investigations

Management

Associations

🔰 For this chap, no need to read rooks.

Above voice notes are enough, listen and practice by solving mcqs

 

Happy learning😊

GENETIC DISORDERS OF PIGMENTATION:

🔰 Quick fix for this chap👆🏻

🔰 Important note

 

Above shared tables are really v helpful for a quick revision before exams.

Practice mcqs again n again fron etas and other books.

For 1st time readers listen to detailed voice notes of this chap👇🏻

🔰 HYPOPIGMENTATION DISORDERS

1️⃣ Piebaldism 👇🏻

Waardenburg syndrome👇🏻

🔰 *Mneumonic* 👇🏻

 

Type IV is Shah sahb ( Shah wardenburg synd ) who is a bit mental (neurological symptoms ) deaf and play with Spring (hirshprungs) he buys SOX (SOX10) from Edenrobes (EDNR8)

3️⃣ Oculocutaneous albinism 👇🏻

4️⃣ Hermansky -Pudlak syndrome 👇🏻

Platelets with absent dense bodies on the right side vs normal on the left

5️⃣ Chediak Higashi syndrome👇🏻

 🔰 Imp for identification in toacs

6️⃣ Griscelli Prunieras syndrome

7️⃣ Hypomelanosis of Ito👇🏻

ACQUIRED DISORDERS OF NAILS AND NAIL UNITHypomelanosis of Ito:

Clubbing

Koilonychia

Pincer nail

🔑 🗝 🔐 Pincer nails deformity

 

*hereditary disease*

 

▪️autosomal dominant Mendelian

▪️Clouston

 

 *acquired pincer nails*

 

▪️gastrointestinal malignancies,

▪️renal failure,

▪️Kawasaki disease,

▪️amyotrophic lateral sclerosis, and

▪️systemic lupus erythematosus

Nail shedding

Onycholysis

Pterygium

Longitudinal grooves👇🏻

Transverse grooves and beau’s lines

Trachyonychia

Onychoschizia/ lamellar dystrophy

Nail plate pigmentation

Subungual disturbances

Nail bed changes

Leuconychia

Colour changes due to drugs and chemicals

YELLOW NAIL SYNDROME

Red lanulae

Longitudinal erythronychia

Splinter hemorrhage

🔰 *Causes of Splinter hemorrhage*

 

Liver disease

Endocarditis

Connective tissue disease

Meningococcal disease

Psittacosis

Disseminated histoplasmosis.

 

 *Skin disease*

 

 psoriatic nail disease

lichen planus 

 

 *Systemic diseases*

 

 microemboli or injury to vessel walls associated with vasculitis

Primary antiphospholipid syndrome

 

Systemic lupus erythematosus

 

Raynaud disease

 

Behcet disease

 

Cutaneous vasculitis

 

Scurvy.

 

chronic kidney disease on haemodialysis or post-renal transplant

 

 *Drugs*

 

Tyrosine kinase inhibitors (seen in 60–70% of patients taking sunitinib and sorafenib)

 

Nitrofurantoin

 

Ganciclovir

 

Terbinafine

 

Tetracyclines.

📝 Hutchinson eye sign …in herpes zoster ..

 

Hutchinson nail sign.. melanoma.. ( others are pseudo Hutchinson and micro Hutchinson)

 

Hutchinson triad in congenital syphilis ..

 

Hutchinson summer prurigo which is actinic prurigo.

 

Hutchinson malignant freckle which is lentigo maligna

What is the significance of this… Black streak…

 *Melanonychia*

 

Here there can be the following *possibilities*

 

 *1.functionsl melanonychia* ( melanocyte activation,common in dark individuals, can be due to trauma ,)

 

 *2.melanocytic nevi*

 

 *3.inflammatory skin conditions* like lp and other pigmentary disorders which can be correlated clinically)

 The pigmentation varies from brown dark brown to black

Pseudo Hutchinson can be seen too.

 

 Most commonly involves thumb but other nails can be involved as well

 

 

 *_Mostly a naevi  in matrix !*_

mostly these are *matrix naevi*  leading to band, so focal matrix ablation might lead a nail plate dystophy lateron which might look uglier than this

 

Would the nail appearance be normal after this procedure and complete healing?

 

 *Yes only the transverse lenght* *will be shortened* , rest it will be perfact

 

Grabbing this opportunity to revise *ABCDEFGHI*  , to R/O *subungual melanoma* in such cases

 

*A: Age (* 50–70 years old); African, Japanese, Chinese, and Native American heritage

 

 *B: Brown-black* pigmented band ≥3mm with blurred borders

 

 *C: Change or lack of change* despite treatment in the nail band or nail morphology

 

 *D: Digit most* commonly involved (thumb, big toe, or index finger)

 

 *E: Extension* of pigment into the skin surrounding the nail (Hutchinson sign)

 

 *F: Family or personal history* of melanoma or dysplastic nevus (atypical mole)

 

 *G – Geometry* of lesion like triangular band

 

 *H – Hyponychial involvement*

 

 *I – irregular pigment pattern* (like different color bands) , irregular spaces , irregular thickness

🔰 Racquet nails

🟥 *causes?* 🔑

*Genetic disorders*

▪️Larsen syndrome, 

▪️Brooke–Spiegler syndrome, 

▪️Rubinstein–Taybi syndrome, 

▪️Hajdu–Cheney syndrome, 

▪️cartilage–hair hypoplasia, 

▪️pycnodysostosis, 

▪️acrodysostosis,

▪️brachydactyly type D.

 *Acquired racquet nail*

associated with 

▪️acroosteolysis and 

▪️psoriatic arthropathy.

▪️diagnostic of bone resorption in hyperparathyroidism.

Anonychia

🔰 Important tip for this chap👇🏻

Leprosy

Joplings

Clinical features

  1. Indeterminate leprosy
  1. Tuberculoid leprosy👇🏻
  1. Borderline leprosy👇🏻

Lepromatous leprosy👇🏻

Nerve involvement in leprosy👇🏻

Systemic involvement👇🏻

Bone changes👇🏻

Testes changes👇🏻

Renal involvement👇🏻

Muscle and lymph node 👇🏻

Other systemic involvement in leprosy👇🏻

Cause of death in leprosy👇🏻

Uncommon presentations of MB leprosy👇🏻

🔰 Chap 2 Relapse, reactivation, reaction and reinfection 👇🏻👇🏻

Chap 2.3 LEPROSY IN CHILDREN

Chap 2.4 PURE NEURITIC LEPROSY👇🏻

Chap 2.5 SPECIAL SCENARIOS 👇🏻👇🏻

Chap 3.2 HISTOPATHOLOGY OF LEPROSY👇🏻👇🏻

Indeterminate leprosy👇🏻

Primary Tuberculoid leprosy👇🏻

Secondary Tuberculoid leprosy👇🏻

Borderline tuberculoid👇🏻

Borderline lepromatous leprosy👇🏻

Lepromatous leprosy👇🏻

 

Histo of Tuberculoid leprosy👆🏻

 

Histopathology of lepromatous leprosy👆🏻

🔰 REACTIONS IN LEPROSY

Chap 5 Reactions in leprosy👇🏻

Type 1 reaction👇🏻

Type 2 reaction👇🏻

Lucio phenomenon

Acute exacerbation 👇🏻

Diagnosis

Immunology👇🏻

Immunology👇🏻

Treatment👇🏻

🔰 Important note

 

This detailed explanation of leprosy is only for those who wanna go through joplings

 

Juz listen to these once.

 

For exam, only go through the voice notes of leprosy given in long case grp, go through the tables of jopling only and listen to dr  Asher’s video on leprosy.

 

Tht wud be more than enough

INFLAMMATORY DERMATOSES:

PSORIASIS

Pathogenesis of Psoriasis👇🏻

🔰 Pustular psoriasis

General discussion👇🏻

More detail👇🏻

PALMOPLANTAR PUSTULOSIS👇🏻

Acrodermatitis continua of Hallopeau👇🏻

🔰 PSORIATIC ARTHRITIS👇🏻

General discussion👇🏻

 🔰 Imp for identification in toacs

Other specified forms of psoriasis

Classification of severity

https://youtu.be/a8FCOK_21Y8?si=niqKuu1nwERSkzWA

Modified napsi score 👇🏻

onycholysis or oil-drop dyschromia 

0 No onycholysis or oil drop dyschromia present

1–10%

2 11–30%

3 > 30%

 

Pitting

0 0

1 1–10

2 11–49

3 > 50

 

 

Score Percent of nail with crumbling present

0 No crumbling

1 1–25%

2 26–50%

3 > 50%

 

Following findings can be graded as

 

0 absent

1 present

 

Leukonychia:

Splinter hemorrhages:

Red spots in the lunula:

Differential diagnosis of psoriasis

Complications and comorbidities👇🏻

Disease course and prognosis👇🏻

Investigations👇🏻

Management👇🏻

General discussion

More detail👇🏻

PHOTOTHERAPY

UVB PHOTOTHERAPY👇🏻

UVB combination therapies

Targeted phototherapy

 Excimer laser

GRENZ RAY THERAPY

PUVA PHOTOCHEMOTHERAPY👇🏻

Summary of PUVA

Topical preparations for psoriasis👇🏻

 

 Psoriatic ointment

Clobetasol 25%

Salicylic acid 3%

Liquor pices carbonis 5%

WSP 67%

 

 Lassar paste

Zinc oxide 24%

Starch 24%

Salicylic acid 2%

WSP 50%

*Treatment of patients with TB along with psoriasis*

ATT give 1 month of ATT followed by both ATT and  immunosuppressive therapy or biologics with close monitoring

 

Preferred treatment is

Phototherapy

Acitretin

Apremilast

Secukinumab

 

 *Treatment options in patients of hiv with psoriasis..*

 

Antiretroviral therapy

Topical therapies with following

Retinoid

Phototherapy

Apremilast

Secukinumab

 

Less favourable options MTX, Cyclosperin, TNF inh and ustekinumab

 

 

 *Treatment options in hep b/c patients with psoriasis*

 

Systemic therapy

Acitretin

Ciclosporin

Apremilast

Biologics esp etenercept

Ustekinumab, secukinumab, ixekizumab and brodalumab

 

 *Do not prescribe MTX*

 

 

 *Treatment of Psoriasis and malignancy*

TNF inh

Ustekinumab

Apremilast

Acitretin

*Treatment options in children*

Topical calcineurin inh for face and intertriginous areas

Vit D analogues +/- mid potency steroids

Mtx

Ciclosporin

Etanrecept greater then 5 yr children

Ustekinumab  greater then 12 yr old child

 

 *Treatment options in pregnancy*

NB UVB Phototherapy

Ciclosporin (Category C drug)

TNF inh (discontinue at 30 weeks of gestation).live vaccine to infant is postponed till 7th month of age

Topical agents

Systemic steroid only in pustular psoriasis

🔰 *IMPORTANT*👇🏻

Psoriasis is indeed the most important chap. U can never pass the exam without mastering this very disease. 
For theory listen to above voice notes once to have the concept. If needed u may go through rooks after these. 
Once done, practice by solving mcqs and revise psoriasis from long case grp which is focussed more on the management part of psoriasis which is most frequently asked in exams. Save time and energy. 
Happy learning 😊

CUTANEOUS PHOTOSENSITIVITY DISEASES:

1️⃣ Polymorphic light eruption👇🏻

Predisposing factors👇🏻

Clinical presentation👇🏻

Differential diagnosis👇🏻

Disease course and prognosis👇🏻

Complications👇🏻

Investigations👇🏻

Management👇🏻

General investigations done in acquired photodermatoses:

🔰 IMPORTANT TIP

 

The above voice notes have detailed discussion on idiopathic photodermatoses. Listen to them to get the concept and then practice from mcqs.

ETAS has given the best mcqs so far for this chap.

ACNE:

Associated diseases👇🏻

1️⃣ Polycystic ovarian syndrome

2️⃣ Late onset congenital adrenal hyperplasia / Non classical congenital adrenal hyperplasia

3️⃣ Cushing disease / Cushing syndrome

4️⃣ Acromegaly

5️⃣ SAPHO syndrome (Synovitis, acne, pustulosis, hyperostosis, Osteitis)

6️⃣ HAIR- AN syndrome (Hyperandrogenism, insulin resistance, acanthosis nigricans)

7️⃣ SAHA syndrome (Seborrhoea, acne, hirsutism, androgenetic alopecia)

8️⃣ PAPA syndrome (Pyogenic sterile arthritis, pyoderma gangrenosum, acne)

 

9️⃣ Apert syndrom

🔟 Premature adrenarche

🔰 Syndromes associated with protective effects against acne

🔰 Drug induced acne

CHINa MTV is the mneumonic

🔰 Predisposing factors for acne

🔰 Pathophysiology

🔰 Clinical features

🔰 Variants of Acne

1️⃣ Acne associated with Psychological problems👇🏻

🔯 Acne excoriee

🔯 Other psychological disorders

2️⃣ Granulomatous acne

3️⃣ Acne mechanica

🔰 Differential diagnosis

🔰 Clinical severity

🔰 S/s tht may indicate an underlying endocrinopathy suggesting the need for investigation👇🏻

🔰Complications

🔰Management

1️⃣ Comedonal acne

2️⃣ Mild to moderate Papulopustular acne

Systemic antibiotics

How to avoid bacterial resistance

How to suspect poor response to antibiotics

🔰 Hormonal therapy in papulopustular acne

1️⃣ Oral contraceptives

2️⃣ Androgen receptor blockers

3️⃣ Spironolactone

🔰 Severe acne

🔯 Oral Isotretinoin

Pharmacokinetics, adverse effects, contraindications and drug interaction has been covered in the drugs group

🔰 Other treatment modalities for acne