General Medical cards Dan Flashcards

1
Q

Which icthyosiform syndromes have PPK?

A
‘Never Kid THe lipid’ 
Nethertons 
KID syndrome 
THiodystrophy with icthyosis - IBIDS/PIBIDS 
Neutral Lipid Storage Disease
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2
Q

List the uncommon causes of multiple facial papules

A

‘MMR ABCDE’ AAAA BB CC
Muir-Torre (sebaceous adenoma, carcinoma, sebaceoma, keratoacanthoma. NB seb carcinoma usually away from face in Muir-Torre)
Milia en plaque (PXE, DLE, LP)
Rosai Dorfman disease
Angiofibromas (TSC, MEN1, Birt-Hogg-Dube)
Acne agminata
AD pilar cysts
Apocrine hidrocystoma (Schöpf–Schulz–Passarge syndrome)
Birt-hogg-Dube (Fibrofolliculomas, acrochordons, Trichodiscomas) or familial trichodiscoma
Brooke-Spiegler (trichoepithelioma, cylindroma, spiradenoma) or AD form of any of these
Cowdens syndrome (trichilemmomas, cobblestone facial papules)
Colloid milium (can look like syringomas, trichoeps or hydrocystomas)
Down syndrome (syringomas, can also be sporadic)
Eruptive vellous hair cyst (Pachyonychia congenita or familial trait)

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3
Q

Causes of erythema nodosum?

A

No cause found in 60%
MY Bi-Lateral SORE SHINS
Mycoplasma Or pneumococcal pneumonia Or psittacosis
Yersinia infection (enterocolitis)
Behcets, Bartonella (cat scratch dx)
Leprosy
Strep infection
OCP (also pregnancy) + other drugs SHOPS in Gold Mine
Rickettsia
EBV and HepB
STDs; HIV, syphilis, chlamydia, gonorrhoea
Histoplasmosis, blastomycsis, coccidioidomycosis
IBD (UC>Crohns)
NHL
Sjogren’s, Sarcoid and TB (granulomatous diseases)

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4
Q

What are the ARA diagnostic criteria for SLE?

A

4 out of these 11 needed to potentially label the patient having SLE;
MD SOAP BRAIN;
Malar rash
Discoid rash
Serositis such as pleuritis or pericarditis
Oral ulcers
Arthritis (usually oligo or polyarticular)
Photosensitivity
Blood dyscrazias: hemolytic anaemia, leukopenia, lymphopenia & thrombocytopenia
Renal involvement with nephrotic picture
ANA (95% of patients)
Immunological abnormalities such as Anti-Sm, Anti-dsDNA, Anti-phospholipid, false positive syphilis serology
Neurological/Psych: mainly seizures and psychosis

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5
Q

List the Annular (figurate) erythemas and their associations

A

Erythema (chronicum) migrans – tick bite/Lyme disease
Erythema gyratum repens –malignancy
Erythema annulare centrifugum – infection, lupus, malignancy
Erythema marginatum (rheumaticum) – acute rheumatic fever

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6
Q

List your Dermatology Sieve

A
SIGN VIP MEN (O)
Squamous
Infective
Granulomatous
Neoplastic
Vascular
Immune
Physical/traumatic
Metabolic
Endocrine
Nutritional 
(O)other – drug side effects
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7
Q

What grouping is Streptococcus Pyogenes?

What are the major post strep complications?

A

Strep pyogenes = Lancefield group A, Beta haemolytic strep
Complications? STREP SICKS
Derm:
Sweets disease
Toxic shock syndrome
Reccurent toxin-mediated perineal erythema
Erythema nodosum, Erythema marginatum
Psoriasis, guttate, PPP(pustular bacterid), Pit lichenoides
Scarlet fever
Infection: Impetigo, cellulitis, erysipelas, ecthyma, perianal strep etc
CSVV (vasculitis) and PAN
Kawasaki disease
Scleredema (type 1)
Non derm:
Glomerulonephritis
Rheumatic fever
PANDAS
Other strep infection – sinusitis, pneumonia, septic arthritis, osteomyelitis, meningitis, vaginitis

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8
Q

What is drug induced SLE?
Who gets it?
What are the features?

A

Acute lupus-like syndrome with fever, arthralgia, myalgia and pleuritis
ANA often positive
Affects people with HLA-DR4 and slow acetylators preferentially.
F:M = 4:1
No nephritis or CNS features
Uncommon in black people, older age of onset than sporadic SLE
Unusual to have cutaneous lupus specific lesions but may have non-specific skin features. Except if due to TNF inhibitor then can have any kind of cutaneous LE
Usually associated with anti-histone Abs except if due to TNF inhibitors – ANA + anti-dsDNA;
or Minocycline – p-ANCA
Especially remember MyHyPIE
Minocycline
Hydralazine - high risk
Procainamide - highest risk
Isoniazid
Etanercept/TNFalpha blockers

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9
Q

what are the Toxic Erythemas?

A
STAK
Scarlet fever
Toxic Shock syndrome
Acute GVHD
Kawasakis disease
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10
Q

What genoderms are associated with cafe au lait macules?

A
Cheer leader with CALMs spins the BATANS
Bloom's syndrome 
Albright (McCune-Albright) syndrome (coast of Maine)
Tuberous sclerosis
Ataxia telangiectasia
NF1
Silver-Russell (Russell-Silver) syndrome 
Also;
Idiopathic
NF1-like syndrome (Legius syndrome)
NF2
Watson syndrome (Allelic to NF1) - CALMs, pulmonary valve stenosis, short stature
Noonans syndrome
LEOPARD syndrome (cafe noir, CALM, lentigines)
Carney complex (cafe noir, lentigines)
Fanconis anaemia
Gorlin’s
Cowdens (sometimes)
MEN1 (sometimes)
Mafuccis
Gaucher
Chediak-Higashi
Hunter syndrome
Multiple mucosal neuroma syndrome
Epidermal naevus syndromes
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11
Q

What is Graham Little syndrome?

A

Subtype of LPP
LP, KP, scarring alopecia, non-scarring hair loss;
4 features not necessarily at same time;
1. Progressive cicatricial alopecia
2. Classical LP lesions of skin or mucosa
3. Non-scarring loss of pubic + axillary hair
4. KP with long spines in plaques on trunk, limbs or face

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12
Q

What is SCORTEN?

How is it scored?

A
Assess SJS/TEN pts for SCORTEN after 24hrs in hospital using highest scores and again on day 3.
1 point each; ABC PUSH; 
Age over 40
Bicarbonate below 20 mmol/L
Cancer
Percent BSA >10% initially and reaches >30%
Urea over 10 mmol/L
Sugar - BGL over 14 mmol/L
Heart rate over 120
Predicted mortality;
0-1 - 3%
2 - 12%
3 - 36%
4 - 60%
5-7 - >90%
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13
Q

List your DD for sporotrichoid spread (nodular lymphangitis)

A
Infections
Most common;
Atypical mycobacteria esp M. marinum (also kansasii, chelonaei, Gordonae)
Deep fungal infection esp sporotrichosis (S schenckii), also other dimorphic fungi e.g Blastomycosis
Rare; NB;
Nocardiosis esp N. brasiliensis
(pyogenic) Bacteria - staph, strep
Very rare in developed world;
Like TO TAG Cats And Cows
Leishmaniasis
Tuberculosis
Opportunistic fungi e.g Fusarium spp, Alternaria spp.
Tularaemia
Anthrax
Glanders (B. mallei) or melioidosis (pseudomallei)
Cats scratch disease
Acanthamoeba spp
Cowpox
NB Orf and Milkers nodules can simulate this pattern if multiple lesions on an extremity
Non-infective causes and mimics;
Lymphoma
Langerhans cell histiocytosis
In transit metastases e.g melanoma
Perineural spread (mimic) e.g leprosy, skin cancers
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14
Q

Which drugs are high risk for SJS/TEN?

A
SATAN drugs - also cause DRESS
Sulphur drugs esp sulphonamides
Allopurinol 
Tetracyclines
Anticonvulsants
NSAIDs esp COX2 and oxicams
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15
Q

what is Rowell’s syndrome?

A

Lupus erythematous + EM-like lesions

with RF+ve + Speckled ANA or Anti-Ro or La

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16
Q

What is metabolic syndrome?

A
Need 3 out of 5 of; 
HOT Bacon Butty
HDL low or treated
Obese - elevated waist circumference >102m/88f cm
Triglycerides high or treated
BP high or treated (>130 sys /85 diast)
BSL>5.5

Causes 2-3x risk DM or CVD, 1.6x mortality risk

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17
Q

What are causes of septal panniculitis?

A

ASPEN migration + vasculitis and infection;
Alpha1 antitrypsin def (lob>septal)
Scleroderma/ morphoea profunda
PAN
Erythema Nodosum + EN migrans (+ eosinophilic panniculitis)
NLD, GA
Superficial or migratory Thrombophlebitis
CSVV and infective causes

  • as well as CSVV, vasculitis is seen in PAN and thrommbophlebitis types
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18
Q

What are the drugs that cause erythema nodosum?

A
SHOPS IN Gold Mine
Sulphur drugs - sulphonamides, sulphonylureas
Halides - Bromides, Iodides
OCP
Penicillin
Salicylates
IsotretinoIN
NSAIDs
Gold
Minocycline
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19
Q

What are the diagnostic criteria for Kawasaki disease?

what is management?

A

CRASH and burn (Kawasaki motorbike)
Conjunctivitis
Rash - polymorphous/macpap/scarletiniform
Adenopathy - cervical
Strawberry tongue + lips red and fissured
Hand swelling/erythema/desquamation
Burn = high fever; over 38 degrees for over 5 days
need the fever and 4 of the other 5 features to make the diagnosis
Mx;
blds; raised WCC, high ESR, high plts
echo
refer - paeds, cardiology
High dose aspirin + IVIg;
80-100mg/kg/day divided over four times per day for two weeks then reduce for next 6-8 wks
IVIG 2g/kg IV over 10-12hrs as single dose; can rpt

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20
Q

What are the categories of acanthosis nigricans?

What are some common causes?

A
Melissa Manahan SAD HO 
Mixed 
Malignant 
Syndromic 
Acral (tripe palms) 
Drug (steroids, hormones)
Hereditary 
Obesity 
causes - PODGE 
PCOS or HAIR-AN
Obesity 
Diabetes 
Gastric cancer adneocarcinoma and other malignancy 
Endocrine – Other endo cause; Cushing’s, Acromegally
also;
congenital generalized lipodystrophy
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21
Q

What is PHACES syndrome?
Who gets it?
How do you procede?

A

Association of a large segmental facial infantile haemangioma with one or more malformations.
90% are female;
PHACES
Posterior fossa defects (Dandy-Walker malformation most common)
Haemangiomas
Arterial anomalies (esp carotid artery)
Cardiac defects (coarctation of aorta most common)
Eye abnormalities
Sternal clefts or pits, supraumbilical raphe (=ventral developmental defects)

Upper face lesions linked with brain,cerebrovascular and eye abnormalities
Lower face lesions linked with ventral developmental defects
Scan head if concerns

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22
Q

What are the features of Sturge-Weber syndrome?

A

STURGE Leper (leptomeningeal vascular malformation)
Sporadic (not inherited)
Tram track calcification (on skull X-ray)
Unilateral portwine stain (sometimes central forehead)
Retardation (learning difficulties)
Glaucoma/angioma of choroid
Epilepsy

Other features;
Hypertrophy of gingivae and other tissues e.g. bone - can occur with any PWS capillary malformation not only in SWS
As can eye enlargement, myopia

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23
Q

What are the features of lumbosacral infantile hameangioma? What is management?

A
(L)LUMBAAR – 
Lumbosacral haemangioma, often ulcerated
Lipoma or other skin lesions
Urogenital anomalies 
Myelopathy (dysraphism)
Bony deformities
Anorectal malformations
Arterial anomalies
Renal anomalies
investigate even if neurologically normal – USS under 4 months of age, MRI if older
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24
Q

What is Mafucci’s syndrome?

A

Presents in infancy
Cutaneous venous malformations + enchondromas
Deformed hands and feet
High risk of malignancy - enchondromas can transform into chondrosarcomas.
Also angiosarcomas, lymphangiosarcomas, fibrosarcomas, osteosarcomas
Also CALMs
F/u long term

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25
Q

What is Blue rubber bleb syndrome?

A

Sporadic or AD
Usually presents in adulthood
Multiple venous malformations of skin, gut, spinal cord and viscera - skin lesions are painful
No glomus cells

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26
Q

What are the side effects of EGFR inhibitors?What other targeted agents have same side effects?

A

Eg. Cetux, pmab, erlotinib, gefitinib
‘EGFR makes(MEK) a fast car’ (rhymes) - if you have a fast car you get ‘MPH PRIDE’
Mucositis
Photosensitivity
Hair changes eg hypertrichosis, hirsuitism, trichomegally of eyelashes + Alopecia (androgenetic or rarely scarring)
Papulopustular eruption
Regulatory changes in hair
Itching
Dryness
Easy breaking nails (brittle) + paronychia + onycholysis + pyogenic granulomas

NB; MEK inhibitors have same side effects eg. Seletanib, trametinib

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27
Q

What is HAIR-AN syndrome?

A
Due to insulin resistance in women
Subtype of PCOS.  Triad of;
Hyperandrogenism HA
Insulin resistance IR
Acanthosis nigricans AN
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28
Q

What is the Arthus reaction?

A

Rare type of local immune complex (type 3) hypersensitivity vasculits due to injection of an antigen, usually esp diphtheria or tetanus toxoid in a sensitized individual.
Local pain, swelling, redness and sometimes purpura or necrosis in 4-10 hrs then settles.

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29
Q

What is Carney complex?

A
AD lentiginosis syndrome
Mutation in PRKAR1A gene
Cutaneous lentigines + atrial myxomas + endocrine tumours and overactivity
2 subsets: NAME and LAMB
Think Name the Lamb PATT
Naevi
Atrial Myxoma
Myxomas of skin
Ephelides
Lentigines
Atrial myxoma
Mucocutaneous myxomas
Blue naevi
Pituitary adenoma
Adrenal Cushings
Thyroid tumours
Testicular tumours
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30
Q

What conditons are knuckle pads asociated with?

A

Idiot Kids Traumatized By Fist Knuckle Pads
Idiopathic in kids
Trauma
Bart-Pumphrey syndrome
Fibromatoses
Keratin 9 Epidermolytic palmoplantar keratoderma - Vorner’s
Papillon-Lefevre syndrome

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31
Q

What is POEMS syndrome?

A
variant of myeloma
Polyneuropathy - sensory and motor
Organomegally - Liver, spleen LNs
Endocrinopathy - mainly DM
M protein - monoclonal gammopathy
Skin changes - hyperpigmentation, hypertrichosis, scleroderma, Terry's nails
treat with chemo and autologous SCT
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32
Q

What is Achenbach’s syndrome?

A

Spontaneous onset of painful haematomas/bruises on fingers in middle aged females
Unknown cause but lesions often triggered by minor trauma
Usually resolves

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33
Q

Which syndromes are associated with multiple lipomas?

A
Lipoma syndromes; 
Dercum's Family Makes Bull Shit
Other syndromes; 1,1,P10, He-man's Garden
Dercum’s disease (adiposis dolorosa) – painful lipomas
Familial multiple lipomatosis
Benign symmetrical lipomatosis
NF1
MEN 1
PTEN syndromes;
Bannayan-Riley-Ruvalcaba 
Proteus
Cowden's
lumbosacral haemangioma
Gardner's syndrome
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34
Q

what are the causes of painful dermal tumours?

A
Blue ANGEL or BLEND AN EGG
Blue rubber bleb
Angiolipoma
Neuroma
Glomus tumour
Eccrine spiradenoma
Leiomyoma
Blue rubber bleb
Leiomyoma
Eccrine spiradenoma
Neuroma - Morton's, traumatic
Dermatofibroma (sometimes)
Angiolipoma
Neurilemmoma
Endometrioma
Glomus tumour 
Granular cell tumour
also Tufted angioma in 30% of cases
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35
Q

What are the key features of Pellagra?

A
4 D's
Dermatitis
Diarrhoea
Dementia
Death
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36
Q

What are the cutaneous features of antiphospholipid syndrome?

A
U LAD
Ulceration
Livedo reticularis
Atrophie blanche, Acrocyanosis
Degos-like lesions
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37
Q

What is the follicular occlusion tetrad?

A

If you find one, always look for the others;

  1. Hidradenitis suppuritiva
  2. acne conglobata
  3. dissecting cellulitis of scalp
  4. Pilonidal sinus
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38
Q

Diagnostic criteria for DRESS?

A

STAMPER - 7 diagnostic, 6 possible;
Symptoms persist >2 wks after stopping drug
Temp >38 degrees
ALT >100; hepatitis or other visceral inflammation
Maculopapular rash >3wks after starting drug
Palpable LNs
Eosinophilia or high WCC or raised atypical lymphocytes >5%
Re activation of HHV6

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39
Q

What are the top drug causes of AGEP?

A
Mostly antibiotics
Also antifungals, diltiazem, paracetamol + quinolones, HCQ
Do My Pits Pus Today?
Diltiazem
Macrolides
Penicillins, beta lactams
Plaquenil
Terbinafine and azole antifungals
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40
Q

What are the causes of erythroderma?

A
Common derm;
Eczema + variants (seb derm, stasis, contact) 40%
Psoriasis 25%
PRP
CTCL (MF or Sezary) 15%
Pemph foliaceous or other immunbullous
Idiopathic 10%
Rare derm causes;
HOSTING Lovely ladies Double Ds
Hailey-hailey
Ofuji's papuloerythroderma
Sarcoidosis
Toxic Shock Syndrome
Icthyoses
Norwegian scabies
GvHD
Lupus
Lichen planus
Dermatophyte
Dermatomyositis
Non derm causes;
Drugs - 10% - esp CASA 
- Carbamazepine/phenytoin 
- Allopurinol 
- Sulphasalazine 
- Ampicillin/penicillinsSystemic lymphoma/leukaemia
Hypereosinophilic syndrome
HIV seroconversion
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41
Q

What are the complications of skin emergencies?

A

THE INET + Metabolic
Thermoregulation + Thrombosis
Haemodynamic – ARF, CHF/high output cardiac failure, odema
Ectropion + other eye complications
Infection – skin, pneumonia etc
Nutrition, Nails & Nodes (low albumin marker of poor protein status)
Enteropathy (iron, B12, folate, protein and fat malabsorption and deficiency)
Telogen effluvium
Metabolic - electrolyte imbalance

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42
Q

What is APECED syndrome?

A
Autoimmune PolyEndocrinopathy Candidiasis Ectodermal Dystrophy syndrome Type 1 
autoimmune polyendocrine syndrome
Addisons
Hypoparathyroidism
Immune deficiency 
Skin features - CHAV nail;
Candidiasis - chronic mucocutaneous
Hyperpigmentation of Addisons
Alopecia areata
Vitiligo - in most cases
Nail dystrophy
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43
Q

What are the diagnostic criteria for antiphospholipid syndrome?

A

Need at least 1 clinical and 1 lab feature
Clinical;
- One or more episodes of arterial, venous or small vessel thrombosis
- Pregnancy complications
One or more unexplained foetal loss at 10 wks or later (normal foetus)
One or more prem delivery of normal neonate before 34 wks
3 or more unexplained consecutive miscarriages before 10 wks
Laboratory (remember LAB);
- Positive Lupus anticoagulant Ab test on ≥2 occasions ≥12 wks apart
- IgM or IgG Anticardiolipin Abs at mod-high levels on ≥2 occasions ≥12 wks apart
- Positive Beta2-glycoprotein 1 Abs test on ≥2 occasions ≥12 wks apart
NB thrombocytopenia is no longer in the diagnostic criteria

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44
Q

Which plants are common causes of phytophotodermatitis?

A
ARM and Leg - rash seen on extremeties
Apiaceae (Umbelliferae)
-	Parsnip 
-	Celery 
-	carrots
-	Parsley 
-	Cow parsley/hogweed
-	Giant hogweed 
Rutaceae
-	Bergamot lime (Citrus bergamia) also causes berloque dermatitis
-	Citron (Citrus medica) 
-	Pomelo (Citrus maxima) 
-  Ruta spp ('Rue')
Moraceae  
-	Fig 
Leguminosa 
-	Beans  

NB; Phytophoto is a type of phototoxic rcn mainly due to plant furocoumarins, not a photoallergy
compositae [asteraceae] cause ACD but not photoACD or phototoxicity
- Ragweed and parthenium cause airborne bush dermatitis
However it is theorised that a reaction occurs between plant material in this species and human DNA which renders the patient photosensitive accounting for hight rates of compositae allergy in pts with CAD

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45
Q
Define:
Koebner phenomenon
Pseudo koebner
Reverse Koebner
Isotopic response
Pathergy
A

Kebner (isomorphic resposne) = skin condition occuring at site of a scar (healed)
Pseudo Koebner phenomenon = infection such as warts or molluscum at sites of trauma
Reverse Koebner phenomenon = trauma to a site of dermatosis causes resolution
Isotopic response = dermatosis occurring at the site of a previously healed, unrelated dermatosis
Pathergy is more appropriate terms in Behcets, Sweets and PG if the wounds are new

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46
Q

What is Rosai-Dorfman disease?

A

‘Sinus Histiocytosis with massive Lymphadenopathy’
rare type of non-Langerhan’s cell, Non-dendritic cell histiocytosis
affects age 10-30, M>F, all races
>600 reported cases
- Massive, painless cervical lymphadenopathy
- Fever
- Mild anemia and neutrophilia, high ESR
- 40% have extranodal involvement with skin being most common site (bone, CNS, genitourinary, GIT, heart, thyroid)
Skin involved in 10%; can be only extranodal site involved + rare skin-limited form
Multiple red-brown or xanthomatous macules, papules, nodules or plaques of eyelids and malar regions
Often indolent, self-limiting
Many lesions are asymptomatic and heal spontaneously Rare fatal cases
Poor prognosis if; disseminated LN Dx or involvement of liver, kidneys or lungs

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47
Q

What are the types of Porokeratosis?

A

7 types;
Mibelli
Giant
DSP/DSAP (if only on sun-exposed areas)
Linear
Porokeratosis palmaris, plantaris et disseminata (PPPD)
Punctate porokeratosis (may be variant of PPPD)
Porokeratotic Eccrine Ostial and Dermal Duct Naevus (PEODDN)

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48
Q

What is BLAISE?

A

Blaschko Linear Acquired Inflammatory Skin Eruption includes lichen striatus in children and adult blaschkitis

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49
Q

What is Salzberger-Garbe disese?

A

AKA Oid-Oid disease or
Exudative discoid and lichenoid chronic dermatosis
widespread disocid eczema - lesions go through exudative and lichenified (not lichenoid) stages
mainly adult jewish men, cause unknown
penis and scrotum invovlement pathognomonic
Very itchy
can be eosinophilia
can be gynaecomastia
treatment resistant - try pred or AZA
Chronic - months-years

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50
Q

What are the DSM IV diagnostic criteria for trichotillomania?

A
  1. Recurrent pulling of ones own hair causing hair loss
  2. Increasing sense of tension when resisting and immediately before hair pulling
  3. Pleasure, relief or gratification after pulling out hair4. Not part of another mental disorder
  4. Causes problems or distress with social life or work or other areas of functioning
    Can support diagnosis by creating a ‘hair growth window’ – weekly shave a small area of involved scalp and see normal confluent growth at end of week
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51
Q

What are the associations of geographic tongue

A
Psoriasis
Eczema
Scrotal/fissured tongue
Downs
Diabetes
Reiter's syndrome
hormonal disturbance
Anaemia
Lithium
EGFR inhibitors
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52
Q

What are the associations of scrotal tongue?

A
Melkersson-Rosenthal syndrome
Down syndrome
Less often;
Cowdens syndrome
Acromegally (with macroglossia)
Pachyonychia congenita
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53
Q

What are the causes of atrophic glossitis?

A

Malabsorption - Crohn’s, coeliac, any other cause
Vitamin deficiency – B12, folate, iron, riboflavin (B2)
Geographic tongue (benign migratory glossitis)
Median rhomboid glossitis
Allergic contact stomatitis e.g. foods, cosmetics etc
Strawberry tongue – characteristic of Kawasaki Dx and Scarlet fever
Sometimes seen in toxic shock syndrome or familial dysautonomia
Trauma
Necrolytic migratory erythema (glucagonoma) - painful beefy glossitis + angular cheilitis in 1/3
Pemphigus vulgaris (rarely)

54
Q

What are the causes of macroglossia?

A
Congenital;
Downs syndrome
Neurofibromatosis
Lingual thyroid
Storage diseases
Rare syndromes
Acquired;
Diabetes
Hypothyroidism
Acromegally
Amyloidosis
TB/ other mycobacterial infectionT
umour
55
Q

What are the causes of desquamative gingivitis?

A
Gum involvement in several disease not a specific diagnosis
LP
Lichenoid (contact) mucositis
Pemphigus vulgaris
MM pemphigoid, Linear IgA, EBA
LE
GVHD
EM
FDE
chronic ulcerative stomatitis
56
Q

What are the causes of complex recurrent apthosis?

what are the DDs?

A
Behchets
IBD
cyclic neutropenia
vit def
coeliac or other malabsorption
EBV
HIV
PFAPA syndrome
DDs
EM/SJS
fixed drug eruption
allergic/irritant contact stomatitis
recurrent HSV
57
Q

What is PFAPA syndrome?

A
Periodic Fever
Aphthous stomatitis
Pharyngitis
Adenitis
occurs in young children
58
Q

what are the causes of Angular Cheilitis (Perleche)?

A
ill fitting dentures or braces
oral candida
thumb sucking in kids
prominent skin fold in older people
Nutritional def - iron, zinc, riboflavin
diabetes
HIV or immunodeficiency states needs exclusion
Secondary syphilis causes split papules
59
Q

At what sites do you develop verucous carcinomas?

A

Oral
laryngeal
Anogenital (Buschke Lowenstein)
Plantar surface of foot

60
Q

What is orofacial granulomatosis?

A

2 meanings;
Was originally coined to describe idiopathic granulomatous cheilitis either alone or as part of Melkersson-Rosenthal syndrome - in this use it specifically excludes other causes of granulomatous change of the lips such as Crohn’s disease
It is also used more loosely as a cover-all term for all kinds of granulomatous change of the lips and oral areas

61
Q

What are the causes of oral apthae?

A

BRILLIANCE
B - Bullous – PV, Paraneo pemph, BP, MMP, LinIgA, EB, DH
R - Recurrent apthous stomatitis, Reiters
I - Infections and immune deficiency – Hand-foot-mouth, Herpangina (coxsackie A16), HSV, HIV, leishmaniasis
L - Lupus, LP
L - Low nutrition
I - Iatrogenic/drugs/trauma – GVHD, dental work, heat, cold, chemicals, XRT, artefact,
A - Amyloidosis, Angina bullosa haemorrhagica
N - Neutrophilic - Behcets, sweets, vasculits (wegeners, PAN, GCA) and Neoplasia –myelodysplasia, leukaemia, cyclic neutropenia, SCC, melamonoma, sarcoma, lymphoma
C - Crohns, UC(rare), coeliac
E - EM, SJS/TEN

Also PFAPA syndrome, systemic dimorphic fungal infection, eosinophilic ulcer, necrotizing sialometaplasia

62
Q

Outline Rx for oral ulcers

A

Good oral hygiene and chlorhex mouthwash
Control w potent TCS gel TDS or inhaler reduces pain and healing time
Topical tacrolimus
TCS
ILCS
May need oral pred.
Topical analgesia/local anaesthetic may help pain
Complex disease may need colchicine/dapsone/thalidomide

63
Q

What are the types of Lichen planus?

A
Types of LICHEN PLANUS
Little/atrophic
Increased (hypertrophic), Inverse
Classic
Hair – LPP, GL, FFA
Exanthematous
Nails
Pemphigoide/bullous/pigmentosus
Linear
Annular
Nitidus
Ulcerative, erosive, vulvovaginal-gingival
Sun (actinicus), Substances – drug, photodrug, FDE
64
Q

What are the diagnostic criteria for Behcet’s disease?

A
International criteria for Behcet’s disease ICBD 
–need 4 or more points; GOO2 CVSP
Genital ulcers = 2
Oral ulcers = 2
Occular manifestations = 2
CNS manifestations = 1
Vascular manifestations = 1
Skin manifestations = 1
Positive pathergy test if performed = 1
65
Q

what causes of infestation need to be considered in a pt with infestation or possible delsuions of parasitosis?

A
BOTS
Bird mites
Onchocerciasis
Thrips
Scabies
66
Q

Which conditions are associated with HLA B27?

A
PPAIR
Psoriatic arthritis with spondylitis Or 
Pustular psoriasis
Ankylosing spondylitis (strongest)
IBD
Reiter's disease
67
Q

What is the treatment ladder for Behcets disease?

A
General measures
Topicals;
Tacrolimus/pimecrolimus (1st line)
Potent TCS
minocycline swish and spit
ILCS for resistant apthosis
Systemic Rx of Behcets – Rx ladder
1st line – topicals + a systemic below;
Colchicine 0.6mg TDS
Oral zinc sulphate 100mg TDS
Sucralfate 1g QDS before meals
2nd line
Dapsone 100-200mg OD (as effective but more AEs/monitoring)
Thalidomide 100-300mg daily
MTX
Prednisolone taper for severe flare ups
3rd line for recalcitrant orogenital ulceration
IFNα
TNFα blocker - Infliximab 5mg/kg, Etanercept
Isotretinoin
AZA, CsA, cyclophosphamide, MMF
Many others listed in reports
68
Q

What is Fox-Fordyce disease?

A
Apocrine miliaria
blocked apocrine sweat ducts
affects young women esp
axillae, pubic region, inframammary, nipples
itchy small red-pink papules
reduced sweating
persistant
Rx with topical retinoids, steroids or antibiotics
69
Q

What is Carcinoma en cuirasse?

A

Dermal infiltration causing sclerosis (scleredermoid in appearance)
DDx: post radiation morphoea VS recurrence of breast cancer

70
Q

What is Carcinoma erysipeloides?

A

Inflammatory metastatic carcinoma
Resembles erysipelas but without the pyrexia or toxaemia
Tumour cells lie within dilated lymphatic vessels in skinoften in breast region

71
Q

What is Mondor’s disease?

A
Superficial obliterative phlebitis affecting the thoraco-epigrastric, lateral thoracic, or superior epigastric vein
Ages 30-60F >> M
Red linear 2-3mm thick cord running from lateral margin of breast, crossing costal margin, and extending to abdominal wall
Subsides in few weeks and no known complications
Risk factors:
Large pendulous breasts
Strenuous physical activity
Direct trauma
Breast surgery
Sentinel node biopsy
Infection near affected vessel
Breast cancer (occasional cause)
72
Q
What substances are used to make the following tattoo pigments?
White
Red
Brown
Yellow
Green
Blue
Purple
Black
A

White - titanium or zinc oxide
Red - cinnabar(mercury sulphide) or cadmium red, sienna(Ferric hydrate) sandalwood, brazilwood
Red/brown - iron (ferric) oxide
Yellow - cadmium sulfide
Green - chromium salts, Phthalocyanine dyes
Blue - Cobalt
Purple - manganese, aluminium
Black - carbon(India ink), iron oxide, logwood

73
Q

What are the types of Keratosis Pilaris atrophicans?

A

Keratosis pilaris atrophicans faciei (bearded face) Erythromelanosis follicularis faciei et colli (face and neck) Ulerythema ophryogenes (eyebrows)
Keratosis follicularis spinulosa decalvans (scalp) Atrophoderma vermiculata (cheeks)

74
Q

What are the congenital causes of poikiloderma?

A

Werners
Blooms
Rothmund-Thompson
Dyskeratosis Congenita
Kindler syndrome
XP
Trichothiodystrophy (photosensitive type-PIBIDS)
Hartnup disease
Mendes da Costa syndrome (erythrokeratoderma variabilis)
Hereditary acrokeratotic poikiloderma of Weary (one family described only)
Hereditary sclerosing poikiloderma of Weary
Degos –Touraine syndrome
Neutral lipid storage disease

75
Q

What is Degos –Touraine syndrome?

A

Incontinentia pigmenti with poikiloderma and GI symptoms

76
Q

What are the acquired causes of poikiloderma?

A
Poikiloderma of Civatte
Dermatomyositis
Cutaneous lupus
LP
Systemic sclerosis
MF
Poikiloderma with neutropenia (syndrome)
Pre-lymphomatous poikiloderma (chronic superficial scaly dermatosis that has developed atrophy and reticulate pigmentation)
Chronic cold or heat exposure
XRT
Acrodermatitis chronica atrophicans (lyme)
77
Q

What are the features of PXE?

What is the gene and inheritence?

A

AR
ABCC6 gene on Chr 16 (A Big Cucoo Clock 6 ‘o clock)
Calcium accumulates in elastic fibres of skin + tissues
skin changes often present in childhood
CHICS (skin looks like chicken skin)
Comets, Angioid streaks + peau d’orange of eyes
Haemorrhage (upper GI bleed)
Ischaemic heart disease
Claudication (PVD) >age 30
Squeaky valves; MR/AR/ aortic dissection
NB also;
May get reticulate pigmentation on abdo
acneiform lesions
Usually arises before 30. Occasionally old age.
Persists indefinitely
Changes similar to skin occur on all mucosal surfaces
Exaggerated horizontal or oblique mental crease pathognomonic finding
Eye changes due to calcification of Bruch’s membrane of retina
Risk of;
Bleeding - GI, intracranial
Miscarriage

78
Q

What is Ascher’s syndrome?

A

blepharochalaxis + progressive enlargement of the upper lip due to hypertrophy and inflammation of the labial salivary glands
May be excessive salivation

79
Q

What are the features of Marfan’s syndrome?

A
AD mutation in fibrillin-1 gene (FBN1)
30% new mutations
MARFANS
Mitral valve prolapsed, Myopia
Aortic Regurge, Aneurysm, Dissection
Retinal detachment
Fibrillin gene, Chr Fifteen + PH(marPHan)- Pectus excavatum, High arched palate
Arachnodactyly
Negative Nitroprusside test (differentiates from homocystinuria), neural deafness (6%)
Subluxated lens (Upward/up + lateral dislocation of Lens)
Skin features - HESP
Hyperexensible skin
Elastosis perforans serpiginosa
Striae atrophicae
Papraceous scars
80
Q

What are the associations of elastosis perforans serpiginosa?

A
A DERM POP
Acrogeria
Down’s syndrome
EDS
Rothmund-Thomson
Marfans
PXE
Osteogenesis imperfecta
Penicillamine: produces abnormal elastin. (Disrupts desmosin cross links within elastin)
81
Q

What is SCARF syndrome?

A
skeletal abnormalities
cutis laxa, craniostenosis
ambiguous genitalia
retardation
facial abnormalities
82
Q

What are the DDs of Cutis Verticus Gyrata?

A
Leonine facies - many causes
Extensive congential cerebriform melanocytic naevus on scalp
Pachydermoperiostosis
Acanthosis nigricans
Dissecting cellulitis of scalp
83
Q

What is MAGIC syndrome?

A

Mouth and Genital Ulcers with Inflamed Cartilage

Combination Behcet’s + relapsing polychondritis

84
Q

What are the risk factors for Keloid scarring?

A

Age (peak between puberty and 30)
Race (B>W), Afro Caribeans
Sites = ear lobes/ shin / neck/ shoulders/ upper trunk/ LL and sites that stretch
Mechanism of injury; burns, scalds
Infected wound
Foreign material = sutures/ endogenous hair
Scarring acne on back
FHx
Recent Roacutane + laser
Polyfibromatosis syndrome = Dupuytren’s
Other associations; acromegaly, post thyroidectomy, Dubowitz, Rubinstein-Taybi, EDS, pachydermoperiostosis
Linear keloids in athletes taking anabolic steroids
Keloid scarring can be triggered by pregnancy
Spontaneous keloids - presternal region of chest, probably micotrauma. Can be seen in in syndromes; rubinstein-taybi, noonan and Dubowitz, Goeminne

85
Q

Diagnostic criteria of PXE?

A

Dx: 1 major from 2 systems
Probable: 2 major from same cat or 1 major + 1 minor from another category
Major:
1) Skin: yellow papules/plaques neck or body,Or
bx with histo changes from affected skin
2) Eye: angioid streaks Or peau d’orange
3) Genetics: mutation of both alleles of ABCC6, Or
1st degree relative

Minor:

1) eye: 1 streak shorter than 1 disk Diameter, comets in retina, 1 or more wing signs
2) Genetics: 1 allele mutation

86
Q

Which conditions have apple jelly diascopy?

A
granulomatous infiltrates;
Sarcoidosis 
Lupus vulgaris 
Acne agminata
Lupoid leishmaniasis
87
Q

what are features of Felty’s Syndrome?

A
RA + 3 Ls
Large spleen (Splenomegaly)
Leg ulcers
Leukopenia
Clinical: Rheumatoid arthritis with leg ulcers, splenomegaly with leukopenia and granulocytopenia
88
Q

what are features of Letterer-Siwe Disease?

A
Let's See HOPE for these poor kids
Letterer Siwe
Hepatosplenomegally
Osteolytic bone lesions
Pulmonary lesions
Enlarged LN
89
Q

What are the associations of granuloma annulare?

A
None definite
Possibly;
Localized GA associated w/ autoimmune thyroiditis esp in women
type 1 diabetes (not type 2)
uveitis
Plummers syndrome (toxic nodular goitre)
malignancy
90
Q

How many NLD pts have diabetes?

How many diabetic pts have NLD?

A

2 thirds of necrobiosis pts have diabetes esp type 1 and insulin-dependent
Many more have abnormal GTT
0.3% of diabetic pts get NLD
2.8% of pts with MODY

91
Q

T/F

Diabetics with NLD have inc risk of retinopathy and nephropathy

A

True

92
Q

What percentage of pts with xanthelasmata have raised serum lipids?

A

approx 50%

93
Q

Which skin conditions or systemic conditions with skin manifetsations may be triggered by EBV infection?

A

Eruptive pseudoangiomatosis

94
Q

What are the diagnostic criteria for HS?

A

modified Dessau definition - 3 features must be present;
Typical lesions present – deep-seated painful nodules/ blind boils
Lesions must be in one or more of the typical sites for HS
Clear history of chronicity or recurrence

95
Q

What are causes of a lobular/mixed panniculitis?

A

SKEPTICAL
Sarcoidosis - subcutaneous
Kids - Sclerema neonatorum, Fat necrosis of the newborn (needle-shaped clefts within lipocytes); sclerema is a screamer - bad prognosis; fat nec has good prog
Erythema induratum (Bazin or Whitfield)(w/ vasculitis)
Pancreatitis (necrosis is early feature)
Traumatic - blunt trauma, injectable substances (oil, DA etc), cold panniculitis, sclerosing lipogranuloma
Idiopathic Nodular panniculitis
Infectious
Calcifying panniculitides - pancreatic, crystal (gout, oxalosis), alpha1 antitrypsin deficiency, calciphylaxis
AI - Dermatomyositis, Lupus profundus, RA, Hashimotos, Crohns (w/ vasculitis)
Lipodermatosclerosis
Lipodystrophies (Cold panniculitis, Nodular cystic fat necrosis)
Lepra reactions; Lucio’s phenomenon or Erythema nodosum leprosum (NOT type 1 rcn) (w/ vasculitis)

96
Q

what is a female hormone panel for cutaneous hyperandrogenism?

A

Totally Bitch SLAPPED
do at 8am on day 3-5 of menstrual cycle (not on OCP for last 2 months);
Total and free testosterone
BetaHCG
SHBG
LH and FSH
Androstenedione
Prolactin (NB baseline test should ideally be after 11am)
17α-hydroxyProgesterone (8am on day 1-3)
oEstradiol
DHEAS
+
Worth doing the TFTs and 8am cortisol routinely
8AM cortisol – high in Cushings or late CAH
- 8am 17α-hydroxyprogesterone high in late CAH (usually due to mutation in 21-hydroxylase)
- Dexamethasone suppression test confirms Cushings (alternative is 24hr urinary cortisol repeated x 2)

97
Q

What are the diagnostic criteria for PCOS?

A
PCOS – Rotterdam diagnostic criteria 
(need 2 of 3 of HOP - Peacocks hop!);
Hyperandrogenism - evidenced by;
- Raised testosterone or;
- Hirsuitism or male pattern hair loss (AGA)
Oligo/anovulation
Polycystic ovaries on USS 
(12 or more 2-9mm follicles in each ovary and/or ovarian vol >10mls)
Also may have;
Raised LH (LH:FSH ratio may be raised (>3:1) but not always – FSH is normal or low)

And need to exclude DDs; NCAH, androgen secreting ovarian/adrenal tumour, Cushings, Hypothyroidism (oligomenorrhoea), hyperprolactinaemia, Pregnancy and premature ovarian failure are also causes of amenorrhoea

98
Q

In what conditions can you see revertant mosaicism?

A

This is like natural gene therapy where areas of thr skin revert to wildtype causing islands of sparing;
Icthyosis en confetti
Some types of EB esp Dystrophic EB types

99
Q

What are the features of Reiter’s/ Reactive arthritis?

what are the causes?

A

SARA RUCA
Sexually Acquired Reactive Arthritis
Rash - mucocutaneous features
Urethritis (non-gonococcal)
Conjunctivits (or; epislceritis, iridocyclitis, Keratitis)
Arthritis
mucocutaneous features;
oral ulcers
scaly red patches/plaques resembling psoriasis
keratoderma blennorrhagicum
balanitis circinata (scaly/eroded rash on glans)
papules and pustules on fingers and toes
paronychia
Mostly due to Chlamydia trachomatis can be salmonella or campylobacter, HIV, HSV or CMV

100
Q

what are the cross reactants with PPD allergy?

A

PABA and its derivatives;

  • IPPD
  • PABA containing sunscreens
  • ester local anessthetics (benzocaine on ABS)
  • Parabens (preservative in lignocaine)
  • Sulphonamides
  • Sulphonylureas
  • Thiazides
101
Q

What are the types of angiokeratomas?

A
My Ford Car Solely Plays CDs
Angiokeratoma of Mibelli
Angiokeratoma of Fordyce (scrotal angiokeratoma)
Angiokeratoma Circumscriptum
Solitary Papular angiokeratoma
angiokeratoma Corporis Diffusum
102
Q

what HLA types are associated with actinic prurigo?

A

DRB1*0407 is very supportive of diagnosis

DRB1*0401 is supportive

103
Q

What are the causes of childhood facial scarring?

A

Spontaneous atrophic scarring of the cheeks - Atrophia maculosa varioliformis cutis (AMVC)
KP atrophicans variants;
- Vermiculate Atrophoderma (AD, sporadic, Rombo; cheeks, preauricular)
- KP atrophicans faciei (AD; eyebrows, forehead)
- Keratosis follicularis spinulosa decalvans (infancy, cheeks, alopecia)
Follicular atrophoderma (Bazex, others)
Lipid proteinosis
Erythropoeitic protoporphyria
Hyper IgE syndrome (Job syndrome)
Hydroa vacciniforme
DA
Varicella scars, acne scars, actinic prurigo scars, DLE scars etc

104
Q

What are features of Swimmer’s itch?

what is treatment?

A

Allergic response to microscopic larvae of non-human schistosomes (flukes) (humans not primary host)
Starts 12-24 hrs after exposure
Usually fresh water, can be salt water
Esp summer in temperate climates (UK, USA, southern Aus)
Mainly affects exposed areas not covered by swimsuit
Starts with prickling sensation after leaving water; lasts for 1-2 hrs
Subsides in under 12h if not sensitized
If sensitized turns into itchy papules and plaques over 24hrs and lasts 1-2 weeks
Histo – spongiosis w/ collections of neuts and eos in epi. Can see cercariae (tadpole shaped larva) in outer epi if taken within 48 hrs
Vigorous towelling after swimming may prevent cercariae penetrating skin
Rx - shower, topical menthol or calamine for itch
NB - the same clinical syndrome can be the presenattion of acute human schistosomal infection in endemic countries (Schistosomiasis AKA Bilharziasis) - look out for acute systemic disease 2-8wks later

105
Q

What are features of Sea bathers eruption?

what is treatment?

A

= nematocyst dermatitis, ‘sea lice’
Irritant contact rcn to the nematocysts (sting organ) of the larval stage of cnidaria (jelly fish and sea anemones and coral)
Itchy, erythematous papules and weals occur predominantly under swimwear, and lesions are usually concentrated in tight-fitting areas
The organisms become trapped under bathing costume and discharge of nematocysts is triggered
subsides in mins to hrs
Rx - shower, topical menthol or calamine for itch

106
Q

What is Sneddon syndrome?

A

Rare syndrome of widespread livedo racemosa and multiple cerebral ischaemic episodes
Leads to progressive neurological impairment
May be vasculitis, vasculpoathy or coagulaopathy – unclear
Histo is characteristic - A subendothelial pad of smooth muscle cells (‘intimal proliferation’) with subtotal or total occlusion of the lumen in at least one arteriole or small artery
With correct clinical and histo signs must exclude antiphospholid syndrome to make the diagnosis

107
Q

What is livedoid vasculopathy?

A

Uncommon condition can present with livedo reticularis
Multiple recurrent painful ulcers on the lower legs – heal slowly leaving atrophie blanche scars
Fibrin in vessel walls and perivascular stroma and hyaline thrombi in lumen

108
Q

T/F

Raynaud’s with either positive ANA, anticentromere or anti-Scl70 Abs indicates a CTD until proven otherwise

A

T

109
Q

Causes of acquired nasal destruction/saddle nose?

A
Endemic/venereal syphilis esp congenital
Leprosy
Rhinoscleroma
Mucocutaneous leishmoniasis (Tapir nose)
Paracoccidiodomycosis
Tuberculosis
Glanders
Zygomycosis due to Mucorales species (mucormycoses)
Other infection e.g. pseudamonas
Wegner’s granulomatosis
Relapsing polychondritis
NK/T-cell lymphoma, nasal type  
cocaine use
110
Q

which are the slow growing mycobacteria?

A
MASKUT BS
Take 2-3 wks to culture in lab
Mycobacterium......
Marinum
Avium
Scrofulaceum
Kansasii
Ulcerans
Tuberculosis
Bovis
Szulgai
111
Q

List the rapid growing mycobacteria

A
Rap(id) A Smeg For CHristmas
Take 3-5 days to grow
Mycobacterium......
Abscessus
Smegmatis
Fortuitum
Cholenaei
112
Q

What investigations should be done for suspected calciphylaxis?
what are the treatments?

A

Investigations;
• Biopsy
Histo
- Calcification of tunica media of small subcut vessels + necrosis of overlying tissue
- Can be calcification of septae in subcutis and of adipocytes
- May see thrombosed vessels
- Can be dermal inflammation only if before ulceration phase
- Can be bullae
Sometimes repeated biopsy is required to find the calcified small vessels
• Xray may show calcification of small vessels in skin
• Check ELFTs, serum calcium, phosphate, PTH and protein C and S

Treatments;
Low calcium and phosphate dialysate
Non-calcium phosphate binders
Parathyroidectomy
Drugs to alter calcium metabolism
• sodium thiosulphate (increases solubility of calcium depsois + antioxidant action – more useful in pts w/out hyperparathyroidism)
• bisphosphonates e.g. pamidornate
• cinacalcet (calcimimetic which lowers PTH and calcium-phosphorus product – esp useful if pt has hyperparathyroidism)
Daily dressings and strict antispesis – infection is  major cause of mortality
Debride if ulcerated
Antibiotics if secondary infection
Hyperbaric oxygen
Tissue plasminogen activatior
113
Q

Causes of Purpura?

A

Non-inflammatory “SHORE PICC ME”
Systemic alteration in coagulation – APLS, protein C/S defcy, warfarin necrosis, B12/folate/vit C defcy (scurvy), vit K defic, anti-thrombin III def, Factor V Leiden mut, DIC
Hyperviscosity - Hypergammaglobulinaemic purpura of Waldesntrom, paraproteinaemia
Organisms – vessel invasive fungi, ecthyma gangrenosum, disseminated strongyloides
RBC occlusion – sickle cell disease, severe haemolytic anaemia, severe malaria, polycythaemia
Emboli – cholesterol, oxalate crystal, endocarditis, myxoma, decompression sickness
Platelet d/o – heparin necrosis, decr/incr plt, myeloproliferative d/o, TTP, ITP paroxysmal noctural haemoglobinuria, VWd, aspirin/drug effect, Dengue
Intravascular lymphoma (B cell)
Conditions – livedoid vasculopathy, Degos, Sneddon’s, Calciphylaxis
Cold-related – cryoglobulins, cryofibrinogens, cold agglutinins
Mechanical – CT d/o, incr intravasc pressure, decr support (Amyloidosis, Ehlers Danlos, solar, senile, steroids)
External – trauma/artefact, Gardner Diamond
Inflammatory;
Vasculitis
- Small vessel – palpable purpura e.g. CSVV, HSP
- Medium vessel – inflammatory retiform purpura e.g. mixed cryoglobulinaemia, rheumatic, PAN, MPA, WG, CSS
Occlusion – livedoid vasculopathy, perniosis, septic/infective vasculitis, Thromboangitis Obliterans (Buergers disease), levamisole cut cocaine

114
Q

Treatment ladder for Darier disease?

A

General measures
Educate esp on signs of secondary infection
Lightweight clothes - cotton
Sunscreen – UV flares skin and increases skin Ca risk and reactivates HSV
Prevent aggravation due to heat, sweating and sun exposure
Daily skin antimicrobial cleansers to reduce colonization and malodor
Keratolytic emollients to reduce scaling and irritation - urea, sal acid
Psychoscial support, support groups, psych for depression, carers if very mentally handicapped
Genetic counseling
Avoid lithium

Topical
topical retinoids (adapalene, tazarotene, tretinoin) – starting with alternating days increasing to daily as tolerated as can be irritating. Esp good for localized/linear disease
Addition of TCS can alleviate irritation
Also addition of antibiotic with TCS can be used as superinfection common (BetC)
Tacrolimus
Efudix – has caused temporary remission in reported cases

Systemic
oral retinoids mainstay of Rx in widespread disease (isotretinoin 0.5-1mg/kg/day or acitretin 10-25mg/day initially) – use continuously or intermittently
Cyclosporine
Prednisone for vesiculobullous variant

Physical – esp for resistant flexural disease
Laser ablation (CO2, erbium:YAG), PDL has also been used
BoTox to reduce sweating if hyperhidrosis
PDT
Electron beam XRT
Dermabrasion deep to pap dermis
Electrosurgery
Surgical debridement
Surgical excision and flap with tissue expanders or split-thickness skin grafting
Nail removal and partial distal matrix excision for nail disease

115
Q

Treatment ladder for Hailey-Hailey disease?

A

General measures
Education on disease, gen measures and recognizing infection
Lightweight clothing to avoid friction and sweating, weight loss
Antimicrobial cleansers +/- antibiotics to treat secondary bacterial, fungal, viral infections
Analgesia
Patch test if concerns as high risk for ACD esp to medicaments
Genetic counseling
Support groups

Topical
TCS combined with topical antimicrobials and cleansers – NB need to be aware of SFX of TCS in flexures eg) alternating days. Lowest effective strength TCS
antimicrobials; clindatech or clioquinol
Intralesional steroids can be used
Tacrolimus/pimecro good option to spare steroid use
calcitriol
efudix - has been tried

Systemics
No clear evidence for retinoids
dapsone/CsA only anecdotal reports but can try if topical failed
pred – short course may help
biologics – few reports but increasing
Low dose naltrexone 
Antivirals if secondary HSV

Procedural
Dermabrasion
Laser – erbium YAG better or CO2
PDT – painful and limited success reported
Electron beam XRT
Botox to reduce sweating, breast reduction to reduce submammary maceration
Surgery – Excision and 2nd intention or SSG – last resort

116
Q

Treatment ladder for Grovers disease?

A

General measures
Avoid soap, simple emollients, colloidal oatmeal baths
Wet compresses with zinc oxide or calamine
Remain cool to reduce sweating
Prantal powder - diphemanil methylsulfate (20mg/g) (antiperspirant; opposes action of parasympathetic nerves that control sweating)

Topical
Moderate to potent TCS in a cream or lotion
1% menthol in Aq cream
Calcipotriol bd

Systemic
acitretin / isotretinoin
pred
high dose vitamin A – 50,000 units TDS for 2 weeks

Physical
PUVA / UVA1 (PUVA can also trigger Grovers)

117
Q

What are the features of endothrix infections?

what are the main organisms?

A

Non-fluorescent arthroconidia within hair shaft
Anthropophilic species
Nearly always Trychphyton
esp Tonsurans and Violaceum also Soudanense (esp in Africa)
remember ‘TVSets are IN houses’
Clinically can be; scale only/ black dots /alopecia

118
Q

What are the features of ectothrix infections?

what are the main organisms?

A

Hyphae and arthroconidia grow outside hair shaft – cause destruction of cuticle
Mostly Microsporon esp Canis
Mostly zoophilic (T. ferrugineum and M. audouinii are exceptions)
May fluoresce under Wood’s lamp
Clinically can be scaly and patchy alopecia up to kerion

119
Q

What are common/important causes of tinea capitis in Aus?

A

Cash Allows Very Many TV Sets
M. Canis (cats, dogs) - griseo for this only
M. Audouinii (anthropothilic)
M. Verrucosum (from cattle, very slow growing, kerion)
T. Mentangrophytes (quite common, guinea pigs, kerion)
T. Tonsurans
T. Violaceum
(T. Soudanense rare in Aus unless refugee etc)
(T. Schoenleinii rare, favus - rare in Aus unless refugee)
*CAVM are ectothrix, TVS are endothrix as ‘TV Sets are IN houses’

120
Q

What are the species of dermatophyte which fluoresce?

A
FACDs
T ferrugineum (yellow)
M audouinii (green-yellow)
M canis (green)
M distortum (yellow)
T schoenleinii (blue-white/pale-dull green)
T triple M T
121
Q

Why must you look at the eyes in a child with JXG of the skin?

A

0.5% of kids w/ skin JXG have eye JXG
40% of kids w/ eye JXG have skin JXG at diagnosis – ALWAYS MULTIPLE
NB: eye JXG can cause hyphema (bleeding) and glaucoma leading to blindness therefore if child has 2 or more JXGs must look at eyes and refer to ophthalmology

122
Q

What do you get by going barefoot?

A
Mossy foot (Podoconiosis - nonfiliarial elephantiasis)
Foot inuries in neuropathies
TB
Madura foot (mycetoma)
Human hook worm 
Dog/cat hook worm (larva migrans)
Strongyloides (larva currens)
Bushfeet
123
Q

which non-melanocytic lesions can have pigment network?

A

SADS
seb K
accessory nipple
dermatofibroma
solar lentigo
(according to ACD module)
Other features of melanocytic lesions found in non-melanocytic lesions are;
Globules - SebK, pigmented BCC, dermatofibroma, talon noir
Streaks - SebK, pigmented BCC
Homogenous blue - Kaposi sarcoma, pigmented BCC, XRT tattoo

124
Q

What are common causes of plant ACD in Australia?

what are the allergenic chemicals?

A
  • Grevillea esp Robyn Gordon type (allergen is pentadecylresorcinol)
    Grevillea (in Proteaceae family) can cross react with members of the Anacardiaceae family esp mango tree, cashew tree and brazillian pepper tree (all 3 contain resorcinol) and less often rhus (in Aus) and other toxicodendrons (both also anacardiaceae) eg Poison Ivy, poison oak and poison sumac (in USA; main allergens are catechols)
  • Mango tree sap also common allergen
    NB; all the above plant allergens cross react as they contain urushiols - mixtures of catechols and resorcinols
  • Tea tree is common ACD but usually contact is via use as a medicament rather than with the plant; the same is true for feverfew (a compositae) and balsam of Peru (Myroxylon pereirae)
  • Compositae (allergen sesqueterpine lactone) allergy is common but usually causes an airborne contact or presents as allergy to cross reactants e.g. Balsam of Peru, colophony
  • Alliaceae - includes onion, chives and garlic - garlic allergy most common esp in chefs or home cooks (main allergen is diallyl sulfide)
125
Q
what are treatments for;
M. marinum
M. ulcerans (Buruli ulcer) 
Nocardiosis
Sporotrichosis
chromoblastomycosis
phaeohyphomycosis
A

For all of these infections excision may be considered for smaller isolated lesions in amenable sites. Also always involve ID
M. marinum; clarithro 500mg bd 12 wks+/-rifampicin Or Mino 100mg od Or Bactrim
M. Ulcerans; Rifampicin 300bd + clarithromycin 8wks-12wks if severe Or excision +ABs and/Or heat Rx reported AND high dose pred if paradoxical rcn
Nocardiosis; Bactrim mainly, 6wks to months or combination IVs if resistant
Sporotrichosis; Terbinafine 250mg/d Or Itraconazole 200mg/d Or SSKI all taken until lesions resolved-many months (3-6 or more)
chromoblastomycosis;
- Small lesions; can excise + oral antifungals
- Itraconazole 200mg/day for at least 6 months – cure in 80%+
- Terbinafine 250mg/day for at least 6 months
- Others; 5-Flucytosine + oral thiabendazole or IV amphotericin B or an oral triazole
- Heat
- Cryotherapy
+ Antibiotics if secondary bacterial infection
phaeohyphomycosis; excise if possible Or Itraconazole 200mg bd for 12 months

126
Q

What are the main features of Scurvy?

A

5 H’s
Haemorrhage - perifollicular + purpura + Gums + GI + intrarticular, intramuscular, cerebral
Haematologic abnormality - anaemia, low folate
Hypochondriasis - anxiety, depression
Hyperkeratosis of follicles - KP + phrynoderma + corkscrew hairs
Hypertrophy of gums + loose teeth + bleeding gums
At risk;
alcoholics, the elderly or disabled with reduced access to fresh foods, food faddists or those on dietry restrictions
Increased requirements occur with drugs such as aspirin, indomethacin, tetracycline, OCP and corticosteroids
Smokers (lowers vit C)
Dialysis – Vit C is lost in dialysis (haem and peritoneal)

127
Q

What are the HLA associations of coeliac disease?

A

HLA-DQ2 or HLA-DQ8

+ve in almost 100% of pts and v unlikely to ever get coeliac if negative

128
Q

What can you eat and not eat if gluten intolerant?

How can you confirm adherence to gluten-free diet in coeliac?

A

Gluten: Barley, Rye, Oats, Wheat (‘BROW’)
Hidden-gluten products: beer, meat products containing breadcrumbs, some icecreams, malt vinegar, vegemite,
Gluten-free: meat, dairy, fruit, vegetables, corn, rice, polenta
Gluten-free flours: corn, rice, coconut, lentil, polenta, potato
Measure serum TTG level - goes down to normal if stay off gluten

129
Q

What foods contain a lot of zinc?

How do you assess and manage suspected Zinc deficiency/ acrodermatitis enteropathica in an infant?

A

High Zn - meat, fish, shellfish, eggs and legumes
High Zinc in human breast milk is also highly bioavailable (Zn in formula less bioavailable)
Investigations;
measure serum elemental zinc, LFTs and albumin. + FBC may show anaemia
Rubber blood tube stoppers can cause false high zinc result
Can measure urinary zinc – excretion will be low
Measure mums breast milk elemental zinc if currently breast fed baby
Biopsy is non specific but may r/o DDs
Swab for secondary infection - highly likely
Rx
Usually Zinc sulphate or gluconate PO 1-3mg/kg/day or zinc chloride for parenteral Rx. Treat mum if breastmilk deficient otherwise Rx case. Lifelong treatment required for AE + high zinc diet. Improve quickly. Caution high zinc can impair copper absorption and cause anaemia. Zinc toxicity can occur so don’t OD
Genetic testing and counselling/screen parents
Serum Zinc, Cu, Fe, ALP levels every 3-6 months to ensure within normal range
Treat any secondary impetiginisation with oral antibiotics, condys crystal soaks, topical emollient

130
Q

What are the derm associations of coeliac disease?

A
DH
Psoriasis
IgA pemphigus
Alopecia
Mouth ulcers
Thrombocytopenic purpura
Systemic associations with possible skin manifestations;
SLE
RA
Sjogrens
Sarcoidosis
Diabetes
AI thyroid disease
Addisons
Anaemia
Autoimmune hepatitis, PBC, PSC
MS and neuropathies
131
Q

How do you do a low nickel diet?

A

Difficult as Nickel in may things
Allow tap to run before using water
Avoid nickel-plated cookware and cutlery and avoid cooking acidic foods in stainless steel cookware
Avoid all canned foods
Avoid high nickel content foods such as;
cocoa, chocolate, soya beans, oatmeal, nuts, almonds and fresh and dried legumes
Take other nickel-containing foods in moderation - including most fruits and veges
Milk products and cereals are fine
Meats are generally lower in Nickel than fruit and veg