dermatology Flashcards
1
Q
why do we use dermatological diagnostic skills
A
prevent or reduce internal organ damage by early diagnosis
detect internal malignancy
2
Q
what is an example of a multi organ systemic disease targeting skin
A
sarcoidosis
3
Q
what is an example of an internal disorder causing flushing in the skin
A
carcinoid syndrome
4
Q
What underlying skin condition does pyoderma gangrenosum suggest?
A
inflammatory bowel disease
5
Q
List the 9 different subheadings used when making a differential diagnoses
A
Autoimmune
Idiopathic
Metabolic
Infection
Neoplastic
Genetic
Traumatic
Inflammatory
Drug-induced
6
Q
List the investigations that are frequently undertaken in dermatology
A
blood tests
microbiology
imaging
skin biopsy
specific
7
Q
what do you test/look for in blood tests (eg FBC)
A
FBC
renal profile
LFTs
inflammatory markers
autoimmune markers
8
Q
what do you test/look for in microbiology tests
A
viral/bacterial serology
swabs for bacteria
C&S, viral PCR
tissue culture/PCR
9
Q
what do you look for in imaging
A
internal organ involvement
vascular supply
10
Q
what do you do with skin biopsies
A
look under microscope
11
Q
what do you do with specific tests
A
urinalysis
nerve conduction studies
endocrine investigations
12
Q
what is a punch histology
A
the cells are examined for any inflammatory patterns or cellular abnormalities that can suggest neoplasia or invasive cancer
It can also be sent for immunofluorescence in which autoAbx can be detected.
13
Q
what are the 2 main groups of lupus erythematosus
A
Systemic lupus erythematosus
Cutaneous (discoid) lupus erythematosus
(these can overlap)
14
Q
What are the musculocutaneous findings that are a part of the diagnostic criteria of systemic lupus erythematosus (SLE)?
A
Oral ulcers
Cutaneous lupus - acute OR chronic
Alopecia
15
Q
What 2 signs are seen in cutaneous acute lupus?
A
Chilblains - small, itchy red patches that can appear after you have been in the cold
Photodistributed (sun-exposed red areas) erythematous rash
16
Q
What other organs affected in SLE are part of the diagnostic criteria and what do they manifest as?
A
Joints - synovitis
Kidney - renal disorder
Lungs and heart - serositis (pleurisy or pericarditis)
Brain - neurological disorder
17
Q
What haematological findings are a part of the diagnostic criteria of SLE?
A
Haemolytic anaemia
Thrombocytopenia
Leukopenia
18
Q
What immunological findings are a part of the diagnostic criteria of SLE?
A
ANA - antinuclear antibodies so immune system has launched misdirected attack on your own tissue
Anti-dsDNA - likely lupus
Anti-Sm - consistent with diagnosis of lupus erythematosus
Antiphospholipid - higher risk of blood clot
Low complement
Direct Coomb’s test - presence of antibodies against RBC antigens
19
Q
List the skin signs that may be present in SLE.
A
Photodistributed rash
Cutaneous vasculitis - inflammation of blood vessel walls and skin lesions
Chilblains
Alopecia - patchy baldness
Livedo reticularis -spasms of blood vessels or abnormal circulation near skin makes the skin, usually on the legs, look mottled and purplish, in sort of a netlike pattern with distinct borders
Subacute cutaneous lupus (SCLE)
20
Q
List the skin sign that is present in cutaneous (discoid) lupus erythematosus (CLE)
A
Discoid lupus erythematosus
SCLE
21
Q
what does Palpable purpura (small vessel cutaneous vasculitis) look like
A
purple splodges on skin area
22
Q
what skin finding can be present in both SLE and CLE
A
Subacute cutaneous lupus (SCLE) - can be a chronic skin finding → can be present in both SLE or CLE (overlap).
23
Q
which is more common - SLE or CLE
A
CLE (95% of cases)
24
Q
what organ is affected in CLE
A
only the skin
25
What is the distinctive feature of CLE?
scarring in the ear/cheek /scalp region
26
what is the underlying condition which affects newborns with lupus
neonatal lupus
27
what AB is positive in neonatal lupus
Ro antibodies
28
what test should be immediately done for neonatal lupus
ECG because 50% of neonates with this condition have a risk of heart block and need a pacemaker
29
What is dermatomyositis?
Autoimmune connective tissue disease, in which there’s a photo-distributed pink-violet rash favouring scalp, periocular regions and extensor surfaces.
There is also proximal extensor inflammatory myopathy (disorder of the muscles)
30
what are some other signs of dermatomyositis
ragged cuticles
shawl sign - redness of the trunk
heliotrope rash - erythema of the eyelids
photo distributed redness
31
what are the clinical features for dermatomyositis with antibody profile Anti Jo-1
fever
myositis
gottron's papules
32
what are the clinical features for dermatomyositis with antibody profile Anti SRP
necrotising myopathy
33
what are the clinical features for dermatomyositis with antibody profile Anti Mi-2
Milde muscle disease
34
what are the clinical features for dermatomyositis with antibody profile Anti p155
associated with malignancy in adults
35
what are the clinical features for dermatomyositis with antibody profile Anti p140
juvenile
associated with calcinosis
36
what are the clinical features for dermatomyositis with antibody profile Anti SAE
+/- amyopathic (lack of muscle weakness)
37
what are the clinical features for dermatomyositis with antibody profile Anti MDA5
increased risk of interstitial lung disease
digital ulcers
ischaemia
38
A photo-distributed rash with muscle weakness is highly suggestive of what condition?
Dermatomyositis
39
If you suspect dermatomyositis what diagnostic tests should you perform?
Antinuclear antibody (ANA) - positive in a high proportion of cases
Creatine Kinase (CK) - muscles
Skin biopsy - dermatomyositis - AutoAb screen
LFT
EMG - looks at muscles
Screening for internal malignancy - perform imaging and tumour markers to look for this
40
What enzyme is found to be elevated, after LFTs are done, if a patient has dermatomyositis?
ALT (alanine transaminase)
41
What is ALT blood test?
ALT, which stands for alanine transaminase, is an enzyme found mostly in the liver
When liver cells are damaged, they release ALT into the bloodstream
An ALT test measures the amount of ALT in the blood
High levels of ALT in the blood can indicate a liver problem, even before you have signs of liver disease, such as jaundice, a condition that causes your skin and eyes to turn yellow.
42
What is IgA vasculitis?
A type of vasculitis affecting small blood vessels that affects the GI tract causing:
- Abdominal pain
- Bleeding
- Arthralgia - joint stiffness
- Arthritis
- IgA-associated glomerulonephritis - may develop later
43
What are the 2 classifications of vasculitis affecting small blood vessels
Cutaneous small vessel (leukocytoclastic) vasculitis
Small vessel vasculitis - special types
44
what are the subclassifications for Cutaneous small vessel (leukocytoclastic) vasculitis
Idiopathic
Infectious
Inflammatory (connective tissue disease)
Medication exposure
45
what are the subclassifications for Small vessel vasculitis - special types
IgA Vasculitis (Henoch- Scholein)
Urticarial vasculitis
Acute haemorrhagic oedema of infancy
Erythema elevatum diutinum
46
what is IgA Vasculitis (Henoch- Scholein)
IgA collects in small blood vessels which become inflamed and leak blood
47
what is Urticarial vasculitis
eruption of erythematous wheals that clinically resemble uriticaria but histologically shows changes of leukocytoclastic vasculitis
48
what is Acute haemorrhagic oedema of infancy
benign type of leukocytoclastic vasculitis w/ large palpable purpuric skin lesions and oedema
49
what is Erythema elevatum diutinum
chronic form of cutaneous small vessel vasculitis with violaceous red-brown or yellowish papules, plaques or nodules that favour extensor surfaces
50
What are the 2 classifications of vasculitis that can affect both small and medium blood vessels and their respective subclassifications?
Cryoglobulinemia
- type 2 and 3
and
ANCA associated (anti-neutrophil cytoplasm antibodies)
- EGPA (Churg-strauss) - eosinophilic granulomatosis with polyangitis
- microscopic polyangitis
- GPA (Wegener) - granulomatosis with polyangitis
51
What is the classification of vasculitis affecting a medium sized blood vessel and its subclassifications?
Polyarteritis nodosa (PAN) - fibrinoid necrosis of arterial wall with a leukocytic infiltrate
- benign cutaneous form
- systemic form
52
What are the classifications of vasculitis affecting a large sized blood vessel?
Temporal arteritis
Takayasu - advanced lesions demonstrate a panarteritis with intimal proliferation
53
What is the difference between macular and papular/palpable?
A macule is a flat, reddened area of skin present in a rash
A papule is a raised area of skin in a rash
54
what size of blood vessel indicating vasculitis would be affected with purpura
small vessel manifestation
- purpura (macular/palpable)
55
what are some signs in medium vessel manifestations
subcutaneous nodules along blood vessels
retiform purpura and ulcers
digital necrosis
56
A patient presents with cough, dyspnoea, chest pain and ulcerative rash. She also has a saddle nose deformity. What condition does she have?
ANCA-associated vasculitis → can be fatal and needs to be treated aggressively
57
What is sarcoidosis?
Systemic granulomatous disorder of unknown origin. Can affect multiple organs.
58
What organ is most commonly affected in sarcoidosis?
lungs
59
Is the skin involved in most cases of sarcoidosis?
No, it is involved in ~33% of cases of sarcoidosis
60
List the cutaneous manifestations that can occur in sarcoidosis
Red-brown to vivolaceous papules on face, lips, upper back, neck and extremities.
Ulcerative
Lupus pernio - occurs on face
Erythema nodosum - lower leg fat inflammation
Scar sarcoid
61
If you do the histology of a cutaneous manifestation of sarcoidosis, what would you see
Non-caseating epithelioid granulomas (non-caseating = no necrosis)
62
Is sarcoidosis a diagnosis of exclusion? Explain how.
Yes
You have to exclude a microbial infection, so you have to do either TB culture or TB PCR and you should always look for underlying organ involvement, particularly a chest X-ray, for lung involvement
63
What does DRESS stand for?
Drug Reaction with Eosinophilia and Systemic Symptoms
64
Outline the scoring criteria used to diagnose DRESS.
(don't have to have all of these - just enough to meet the criteria)
Fever ≥ 38.5°C
Lymphadenopathy ⩾ 2 sites, > 1cm
Circulating atypical lymphocytes
Peripheral hypereosinophilia >0.7 × 10^9
Internal organs involved - (liver, kidneys, cardiac)
Negative ANA, Hepatitis / mycoplasma, chlamydia
Skin involvement:
- >50% body surface involvement (BSA)
- cutaneous eruption suggestive of DRESS eg facial oedema
- biopsy suggestive of DRESS
65
List the internal organs involved in DRESS and the manifestation that occurs in each respective organ.
Liver (hepatitis)
Kidneys (interstitial nephritis)
Heart (myocarditis)
Brain
Thyroid (thyroiditis)
Lungs (interstitial pneumonitis)
66
Which internal organ is most commonly affected in DRESS?
Liver - majority of deaths associated with this.
67
How long after drug exposure does DRESS start?
2-6 weeks
68
List the drugs that are the most common triggers of DRESS.
Sulfonamides
Anti-epileptics (carbamazepine, phenytoin, lamotrigine)
Allopurinol - treats gout and kidney stones
Antibiotics (vancomycin, amoxicillin, minocycline, piperacillin-tazobactam)
Ibuprofen are common triggers
69
What are the rash morphologies that may manifest in DRESS?
Widespread erythema (Erythroderma)
Head / neck oedema
Urticated papular exanthem - widespread papules
Maculopapular (morbilliform) eruption
Erythema multiforme-like rash
70
What is the treatment of DRESS?
Withdrawal of culprit drug
Corticosteroids are first line treatment - may require months of treatment
(Mortality 5-10%)
71
How can you differentiate if a rash is caused by a drug or by Graft versus Host Disease (GvHD)?
GvHD has:
- Facial involvement
- Acral involvement (acral - distal limbs)
- Diarrhoea
72
What is GvHD?
Multiple-organ disease. Affects ~10-80% of allogenic haematopoetic stem cell transplants (HSCT).
73
Briefly explain the pathogenesis of GvHD.
Donor-derived T-lymphocyte activity against antigens in an immunocompromised recipient.
74
What are the main organs that the GvHD affects?
Skin
Liver
GI tract
75
What is pruritus?
Severe itching of the skin, as a symptom of various ailments.
Itch without a rash.
76
What is itching without a rash suggestive of?
Internal cause
77
What are the haematological causes of pruritus?
Lymphoma and Polycythaemia
78
What are other things can cause pruritus?
HIV / Hepatitis A / B / C
Iron deficiency or iron overload
Cholestasis
Cancer
Uraemia
Psychogenic
Pruritus of old age
Drugs (NB opiates / opioids)
79
List the investigations a patient with pruritus would need
FBC, LDH (for tissue damage)
Renal profile
LFTs
Ferritin
XR chest
HIV/ Hep ABC → Viral screen
80
if a patient with pruritus keeps itching. What is this cutaneous manifestation called?
Nodular prurigo - skin thickening as a manifestation as a defence mechanism from scratch. Actually makes itch worse.
81
What is scurvy?
Vitamin C (ascorbic acid) deficiency
82
What are the cutaneous manifestations of scurvy?
Spongy gingivae with bleeding and erosion
Petechiae, ecchymoses, follicular hyperkeratosis
Corkscrew hairs with perifollicular haemorrhage
83
What is Kwashiorkor?
Protein deficiency
**Severe form of malnutrition**. It's most common in some developing regions where babies and children do not get enough protein or other essential nutrients in their diet.
84
What are the systemic features of Kwashiorkor?
Hepatomegaly
Oedema
Loss of muscle mass
Diarrhoea
Bacterial / fungal infections
Failure to thrive
85
What are the skin signs of Kwashiorkor?
Superficial desquamation large areas of erosion
Sparse, dry hair
Soft, thin nails
Cheilitis - inflammation of the lips
86
How many enzymes does zinc play a role in?
200; includes the regulation of **lipid, protein** and **nucleic acid** synthesis.
87
Does zinc play a role in wound healing and does it act as an oxidant?
Plays a role in wound healing
it is an ANTIOXIDANT (not oxidant)
88
Can zinc deficiency be genetic or acquired?
Both (genetic - SLC39A4; acquired - dietary)
89
What are the triad of symptoms of Zn deficiency?
Dermatitis
Diarrhoea
Depression
90
What are the cutaneous manifestations of Zn deficiency?
Perioral, acral and perineal skin in particular is affected with scaly erosive erythema.
91
What is another name for vitamin B3?
Niacin
92
Is vitamin B3 required for most cellular processes?
Yes
93
What can vitamin B3 deficiency result in?
Dermatitis
Diarrhoea
Dementia
Death
94
What are the cutaneous manifestations of vitamin B3 deficiency?
Photo-distributed erythema
‘Casal’s necklace'
Painful fissures of the palms and soles
Peri-anal, genital and perioral inflammation and erosions
95
A patient with a history of hypertension presents with flushing, diarrhoea, wheezing and dizziness. What do these symptoms indicate the patient has?
Carcinoid syndrome
96
When does carcinoid syndrome develop?
When a malignant carcinoid tumour metastasises and secretes 5HT into the systemic circulation.
97
What are the symptoms of Carcinoid syndrome?
Flushing (25% of cases → when it does happen its important to think of Carcinoid syndrome)
Diarrhoea
Bronchospasm
Hypotension
98
Is Stevens-Johnsons Syndrome/ Toxic Epidermal Necrolysis (SJSTEN) a dermatology emergency?
Yes, its rare.
99
What are the prodromal symptoms of SJSTEN?
Flu-like symptoms
100
What follows the prodromal symptoms of SJSTEN?
Blisters merge – sheets of skin detachment ‘like wet wallpaper’
Abrupt onset of lesions on trunk >face/limbs.
Macules, blisters, erythema – atypical targetoid
Extensive full thickness mucocutaneous (epidermal) necrosis <2-3 days
101
When the body surface area detachment is less than 10% and symptoms of SJSTEN are present, is the disease known as SJS or TEN?
SJS
102
When the body surface area detachment is greater than 30% and symptoms of SJSTEN are present, is the disease known as SJS or TEN?
TEN
103
When the body surface area detachment is between 10-30% what is the disease known as?
SJS/ TEN overlap
104
What is SJS/ TEN caused by?
A cell-mediated cytotoxic reaction against **epidermal** cells
Drugs cause >80% of cases.
May be started up to 3 weeks prior to onset of rash.
105
What drugs most commonly cause SJS/ TEN?
antibiotics
- beta lactams
- sulphonamides
allopurinol
anti-epileptic drugs
- phenytoin
- carbamazepine
- lamotrigine
NSAIDs
106
Which other conditions have similar cutaneous manifestations to SJS/TEN?
Staphylococcal scalded skin syndrome (SSSS)
Thermal burns
GvHD
107
What score is used to help assess the severity of SJS/TEN? What are the criteria for this score?
**SCORTEN** – score used to help assess severity
Criteria: age >40, HR, initial % epidermal detachment, serum urea + glucose + bicarbonate, presence of malignancy
108
What are the complications of SJS/TEN?
Liver and heart failure
Interstitial pneumonitis
Neutropaenia
Kidney failure due to renal tubular necrosis
Eroded GI tract
Dehydration
Hypothermia/hyperthermia
Blindness
Death Overall mortality 30%
Can also have severe psychological sequelae in terms of PTSD.
109
What is erythroderma?
Generalised erythema affecting >90% BSA
110
List the systemic manifestations reflecting impairment in skin function in erythroderma.
Peripheral oedema
Risk of sepsis
Loss of fluid and proteins
Tachycardia
Disturbances in thermoregulation
111
List some of the aetiologies of erythroderma
Cutaneous T-cell lymphoma – Sézary syndrome
Psoriasis
Atopic eczema
Idiopathic (25-30%)
Drug reactions
112
Outline the management of erythroderma
Underlying cause (e.g. treat psoriasis, withdraw drug if drug cause, etc)
Hospitalisation if systemically unwell e.g. sepsis
Restore fluid and electrolyte balance, circulatory status and manage body temperature.
Emollients to support skin barrier
+/- Topical steroids
+/- Antibiotics
113
cutaneous signs of systemic disease, in particular CKD. Name each of these signs.
Calciphylaxis
Half and half nails - white colouring of proximal half nail and red-brown colouring of the distal half of all the nails
Xerosis - dry skin
Excoriations/ prurigo - cannot stop picking at your skin
114
List the features you may see in a patient with CKD.
Anaemia - mucosal pallor, hair thinning
Excoriations, prurigo
Calciphylaxis
Half and half nails
115
In CKD, what signs may you see related to the underlying primary condition causing CKD?
Photo-distributed rash of SLE
ANCA-associated vasculitis
116
In CKD, what signs may you see related the immunosuppression in transplant recipients?
Viral warts - infection of HPV → excess keratin on epidermis → wart
Skin cancer
117
what are some of the cutaneous signs of Chronic Liver Disease. Name them.
clubbing
Porphyria cutaneous tarda - defect in enzyme UROD causing skin lesions on sun-exposed skin
Spider telangiectasia - anomalous dilatation of end vasculature found just beneath the skin surface
Palmar erythema
Terry’s nails - leukonychia, opacification of nearly the entire nail, obliteration of the lunula and a narrow band of normal, pink nail bed at the distal border
Jaundice
Muehrcke’s lines - paired, white, transverse lines that signify an abnoramality in the vascular bed of the nail
118
what is necrobiosis lipoidica
Necrobiosis Lipoidica - plaques with red-brown raised edge with yellow-brown atrophic centre.
119
What % of Necrobiosis Lipoidica occurs in DM?
20-65%
120
What is the treatment of Necrobiosis Lipoidica?
Topical/ intralesional steroids
121
name some cutaneous manifestations of DM
Skin infections
Xanthelesma and xanthomata - yellowish plaque in canthus of eyelid or eyelids themselves due to high cholesterol
Xerosis
Acanthosis nigricans - darker patches or streaks, usually in skin creases or folds due to increased blood insulin
Neuropathic ulcers
Granuloma annulare - rash like ring of small pink, purple bumps usually on back of hands or feet
Terry's nails
122
in what condition might you see cutis gyrata verticis
acromegaly
rare
123
in which endocrinological condition might you see acne
acromegaly
Cushing's syndrome
PCOS
124
in which condition might you see hyperpigmentation
addisons disease
125
in which disease might you see pretibila myxodema
Graves disease
126
what is Bacillary angiomatosis
- form of bartonella infection
causes wart looking spots on face
127
what is Kaposi sarcoma
cancer developed from cells lining lymph or blood vessels
presents with black teeth inside
128
what is Cytomegalovirus (CMV) ulceration
ulcerations of GI tract, most commonly stomach and colon
looks like it has pus in it
129
what is Norwegian scabies
thick crusts of skin that may contain large numbers of scabies mites and eggs and usually in immunocompromised patients
130
what are the warts called on your toes
Extensive viral warts
131
what is Severe seborrhoeic dermatitis
scaly pathces, red skin and stubborn dandrugg usually in scalp or oily surfaces; face, sides of nose, eyebrows, ears, eyelids and chest
132
what condition do you consider for :
extensive viral warts
severe seborrhoeic dermatitis
norwegian scabies
severe psoriasis
CMV ulceration
eosiniphilic folliculitis
kaposi sarcoma
bacillary angiomatosis
HIV
133
In seroconversion of HIV you can get variable manifestations. List them.
Morbilliform rash - fine erythematous macules and papules distributed over the trunk and rash often spreads centripetally from trunk to extremities
Urticaria - hives: appear on skin as welts that are red, very itchy, smoothly elevated areas of skin often with a blanched centre
Erythema multiforme - allergy to medicine or infection adn symmetrical, red, raised skin areas around body and more on fingers and toes
Oral / genital ulceration
134
List things that could lead to underlying HIV being considered as a diagnosis.
Persistent or atypical manifestations or common infections
Opportunistic infections
Severe manifestations of common dermatoses (e.g. psoriasis, seborrheic dermatitis)
Itch
Suggestive dermatoses e.g. eosinophilic folliculitis
135
List the cutaneous diseases associated with IBD.
Pyoderma gangrenosum - painful sores on skin and mainly legs
Orofacial granulomatosis - lip swelling and sometimes of face, inner cheeks and gums
Panniculitis (erythema nodosum) - reddish, painful, tender lumps most commonly in front of legs below knees
Aphthous ulceration - small, shallow lesions that develop on soft tissues in mouth or at base of gums
Association with psoriasis, pemphigoid - large fluid filled blisters
136
List the cutaneous manifestation of coeliac disease
**Dermatitis herpetiformis** (because of homology of the antigens of tTG (tissue transglutaminase) and antigens in the skin) → patients need SI biopsy
Very non-specific as the blisters are so itchy they get scratched away leaving scratch marks.
137
what are some cutaneous manifestations in GI disorders
Panniculitis/ erythema nodosum
Dermatitis herpetiformis
Orofacial granulomatosis
Apthous ulceration
138
What is hidradenitis suppuritiva?
Condition that causes **inflamed nodules and sterile abscesses**, which can rupture into tunnels or sinus tracks.
Extensive scarring
Favouring intertriginous zones especially axillary, anogenital and inframmary area.
Causes pain, body image issues, discharge and death.
139
What patients is hidradenitis suppurtiva seen in more commonly?
Patients with high BMI
DM
Inflammatory bowel disease
140
What is pyoderma gangrenosum?
Sterile non-infectious pustule on an erythematous base - ulcerates and extends with necrotic undermined border.
Painful
141
What underlying conditions can pyoderma gangrenosum be associated with?
IBD, leukaemia, seronegative arthritis
142
List the cutaneous signs of malignancy reflecting internal malignancy
extramammary pagets disease
143
list the cutaneous signs of genetic condition predisposing to internal cancer and skin lesions
Hereditary leiomyomatosis and renal cell cancer
Peutz–Jeghers syndrome
144
list the cutaneous signs of skin disease associated with malignancy
- Dermatomyositis
- Erythema gyratum repens
- Pyoderma gangrenosum
- Paraneoplastic pemphigus
145
list the cutaneous signs associated with non specific skin disease
Pruritus
Urticaria
Vasculitis
146
what is Peau d'Orange associated with
breast carcinoma
147
what are groin metastases associated with
prostatic carcinoma
148
what are haemorrhagic nodules associated with
metastatic pancreatic carcinoma
149
what is pyoderma gangrenosum associated with
leukaemia
150
what are some other cutaneous signs associated with malignancy
leukaemia cutis
metastatic oesophageal carcinoma
metastatic bronchial carcinoma
extramammary - Paget’s disease
acanthosis nigricans - internal malignancy
Paget’s disease of the nipple
erythema gyratum repens secondary to bronchial carcinoma
dermatomyositis
paraneoplastic pemphigus - autoimmune blistering condition
chilblain like lesions
itch
vasculitis
urticaria (hives)
151
what is the skin sign for Hereditary leiomyomatosis and renal cell cancer
leiomyomas
152
what is the skin sign for Peutz-Jegher syndrome
Mucosal melanosis
153
What does Staph Aureus express that gives it pathogenic properties?
Virulence Factors eg. Haemolysins and PVL
154
What 6 skin conditions can a Staph Aureus infection cause?
Folliculitis (incl Furunculosis and Carbuncles)
Impetigo
Cellulitis
Ecthyma
Staphylococcal scalded skin syndrome
Superinfects other dermatoses ( eg. Atopic Eczema, HSV, leg ulcers)
155
How does Streptococcus pyogenes attach to epithelial surfaces?
Via Lipoteichoic acid portion of its fimbriae
156
Describe 3 virulence factors produced by Streptococcus pyogenes?
- Has M protein (anti-phagocytic) & hyaluronic acid capsule
- Produces erythrogenic exotoxins
- Produces streptolysins S and O - proteins involved in the breakdown of host tissues and cells
157
What 7 skin conditions can a Streptococcus pyogenes infection cause?
Impetigo
Scarlet fever
Cellulitis
Ecthyma
Necrotizing fasciitis
Erysipelas
Superinfects other dermatoses (e.g. leg ulcers)
158
what does the image with what looks like acne - whiteheads and pus filled spots show
follicular erythema
sometmes putular (folliculitis)
159
Where and why might recurrent cases of folliculitis arise?
From nasal carriage of Staph Aureus, particularly strains expressing Panton-Valentine Leukocidin (PVL)
160
What is the treatment for folliculitis?
Antibiotics (Flucloxacillin or erythromycin)
161
What is the difference between a furuncle and a carbuncle?
A furuncle is a deep infection of the hair follicle leading to abscess formation with accumulation of pus and necrotic tissue whereas a Carbuncle is where there is involvement with adjacent connected follicles.
162
What 2 things do you need to do in case of furunculosis?
Incision and drainage
163
Which one out of furuncle and carbuncle is more likely to lead to cellulitis and septicaemia?
carbuncle
164
Why do some patients develop recurrent Staphylococcal impetigo or recurrent furuncluosis (2 broad categories)
1) Establishment of Staph aureus as part of the resident microbial flora (particularly nasal flora)
2) Immune deficiency
- chronic granulomatous disease
- hypogammaglobulinaemia
- AIDS
- DM
- hyperIgE syndrome deficiency
165
What is PVL Staph Aureus?
β-pore-forming exotoxin
Leukocyte destruction and tissue necrosis
Leads to **higher morbidity, mortality and transmissibility**
166
What are the main characteristics of a PVL Staph Aureus infection?
Often painful, more than 1 site, recurrent, present in contacts
167
What 3 effects does PVL Staph Aureus have on the skin?
1) Recurrent and painful abscesses
2) Folliculitis
3) Cellulitis
168
What 3 effects can PVL Staph Aureus have outside the skin?
1) Necrotising pneumonia
2) Necrotising fasciitis
3) Purpura fulminans - skin necrosis and DIC (haematological emergency)
169
What are 5 risk factors for acquiring PVL Staph Aureus (CCCCC)
Close Contact – e.g. hugging, contact sports
Contaminated items , e.g. gym equipment, towels or razors.
Crowding –crowded living conditions such as e.g. military accommodation, prisons and boarding schools.
Cleanliness (of environment) - lack thereof
Cuts and grazes – having a cut or graze will allow the bacteria to enter the body
170
Describe treatment for PVL Staph Aureus
Consult local microbiologist / guidelines
Antibiotics (often tetracycline)
Decolonisation – *often*:
- Chlorhexidine (disinfectant) body wash for 7 days
- Nasal application of mupirocin (blocks isoleucyl-tRNA synthetase so prevents bacterial protein production) ointment 5 days
Treatment of close contacts
171
what can you see in someone with pseudomonal folliculitis and what is this condition associated with
follicular erythematous papule
Hot tub use, swimming pools and depilatories, wet suit
172
how do you treat pseudomonal folliculitis
most cases don't require treatment
severe or recurrent cases can be treated with oral ciprofloxacin
173
What is cellulitis?
Infection of lower dermis and subcutaneous tissue
You can see tender swelling with ill-defined blanching erythema or oedema in the images
174
What are most cases of cellulitis caused by?
Streptococcus pyogenes and Staphylococcus aureus
175
What is a predisposing factor for cellulitis?
Oedema
176
how do you treat cellulitis
Systemic antibiotics
177
describe impetigo
Superficial bacterial infection, stuck-on, honey-coloured crusts overlying an erosion
178
what causes impetigo
1) Streptococci (non-bullous)
or
2) Staphylococci (bullous = blistering)→ Caused by exfoliative toxins A & B, split epidermis by targeting desmoglein I
179
what areas does impetigo most commonly affect
face (perioral, ears and nares)
180
how can impetigo be treated
Topical +/- systemic antibiotics
181
when does impetiginisation occur
This condition with its characteristic gold crust is seen following a Staph Aureus infection.
182
Describe Ecythyma and where in the body does it usually occur
Severe form of streptococcal impetigo
Thick crust overlying a punch out ulceration surrounded by erythema
Usually on lower extremities
183
what causes Staphylococcal Scaled skin syndrome
Exfoliative toxin (same one that causes bullous impetigo)
184
What age category is SSSS condition mainly seen in?
Neonates, infants or immunocompromised adults
185
Why can’t the organism causing SSSS be cultured from denuded skin?
Infection occurs at a distant site ( i.e conjunctivitis or abscess)
186
Why does Staphylococcal Scaled skin syndrome only mainly affect neonates?
As neonates kidneys cannot excrete the exfoliative toxin quickly
187
Describe the progression of Staphylococcal scalded skin syndrome
→ Diffuse tender erythema that
→ Rapid progression to flaccid bullae
→ Wrinkle and exfoliate, leaving oozing erythematous base
188
What is the difference between SSSS and Stevens-Johnson syndrome/toxic epidermal necrolysis
SSSS Only penetrates stratum corneum
189
what is toxic shock syndrome (TSS)
Febrile illness due to Group A Staphylococcus aureus strain that produces pyrogenic exotoxin TSST-1
190
What are the main clinical features of TSS?
Mucous membranes (erythema)
Hematologic (platelets <100 000/mm3)
Involvement of ≥ systems:
- Gastrointestinal
- Muscular
- CNS, Renal and Hepatic
Diffuse erythema
Fever >38.9°C
Hypotension
191
what occurs after resolution of TSS
Desquamation predominantly of palms and soles 1-2 weeks after resolution of erythema
192
what causes erythrasma
Infection of Corynebacterium Minutissimum
193
how does the patch in erythrasma evolve over time
Well demarcated patches in intertriginous areas
- initially pink
- become brown and scaly
194
what is pitted keratolysis caused by
Corynebacteria
195
how is pitted keratolysis treated
Topical Clindamycin
196
what causes erysipeloid and how can you be exposed to it
*Erysipelothrix rhusiopathiae*
Erythema and oedema of the hand after handling **contaminated raw fish or meat**
Extends slowly over weeks.
197
what causes bacillus anthracis (finger ulcer that looks circular with purple outline and yucky middle)
Painless necrotic ulcer with surrounding oedema and regional lymphadenopathy (with pain in lymph nodes) at the site of contact with hides, bone meal or wool infected with Bacillus anthracis
198
what causes Blistering Distal Dactylitis
Streptococcus Pyogenes or Staphylococcus aureus
199
what parts of the body are affected by Blistering Distal Dactylitis
1 or more tender superficial bullae on erythematous base on the volar **fat pad of a finger**
**Toes** may rarely be affected
200
What is Erysipelas and what microorganisms can cause it?
- Infection of deep dermis and subcutis
- Caused by β-haemolytic streptococci or *Staphylococcus aureus*
201
what are the early clinical signs and symptoms of erysipelas
Malaise, fever and headache
202
What does Erysipelas present as?
Presents as erythematous indurated plaque with a sharply demarcated border and a cliff-drop edge +/- blistering
**Face or limb**
+/- red streak of lymphangitis and local lymphadenopathy.
203
What can the portal of entry be for erysipelas?
Tinea Pedis - foot infection due to a dermatophyte fungus
204
how do we treat erysipelas
IV Antibiotics
205
what causes scarlet fever
Caused by upper respiratory tract infection with erythrogenic toxin-producing Streptococcus pyogenes
206
what are the skin symptoms in scarlet fever preceded by
Sore throat, Headache, Malaise, Chills, Anorexia and fever
207
Describe the skin symptoms seen in a child with scarlet fever?
Eruption begins 12-48 hours later
- Blanchable tiny pinkish-red spots on chest, neck and axillae
- Spread to whole body within 12 hours
- Sandpaper-like texture
208
What are potential complications of scarlet fever?
Otitis, mastoiditis, sinusitis, pneumonia, myocarditis, hepatitis, meningitis, rheumatic fever, acute glomerulonephritis
209
Describe progression of necrotising fasciitis.
Initial dusky induration (usually of a limb), followed by rapid painful necrosis of skin, connective tissue and muscle.
210
What 4 organisms can potentially cause necrotising fasciitis
Streptococci, Staphylococci, Enterobacteriaceae and anaerobes
211
What are investigations performed to confirm necrotising fasciitis?
MRI, blood and tissue cultures
212
What is the treatment of necrotising fasciitis?
Broad spectrum parenteral antibiotics
Surgical debridement - removal of dead (necrotic) or infected skin tissue to help a wound heal. It's also done to remove foreign material from tissue
213
What is the name given to necrotising fasciitis affecting the scrotum?
Fournier’s gangrene
214
describe the ulcer seen and spread by mycobacterium marinum
Mycobacterium marinum causes indolent granulomatous ulcers (fish-tank granuloma) in healthy people
Sporotrichoid spread - **linear ascending extension along lymphatic chains, generally found with deep fungal infections but can also be present in other organisms**
215
when can infection by mycobacterium chelonae occur (yellowy dented holes)
Puncture wounds, tattoos, skin trauma or surgery
216
What organism is an important cause of ulceration in Africa and Australia?
Mycobacterium ulcerans
Africa - Buruli ulcer
Australia - Searle’s ucler
217
what is Lyme disease and what is it caused by
Annular erythema develops at site of the bite of a Borrelia-infected tick - Borreliosis (Lyme Disease)
Bite from Ixodes tick infected with Borrelia burgdorferi
218
Describe what you would seen on the skin as time passes in someone with lyme disease
Initial cutaneous manifestation: Erythema migrans (only in 75%)
- Erythematous papule at the bite site
- Progression to annular erythema of >20cm
219
What are the secondary lesions seen in Lyme Disease and when do they occur?
1. Neuroborreliosis
- Facial palsy / other CN palsies
- Aseptic meningitis
- Polyradiculitis
2. Arthritis – painful and swollen large joints (knee is the most affected join)
3. Carditis
220
what is Tularaemia caused by
Francisella tularensis
221
how can you acquire tularaemia (3 ways)
1) Handling infected animals (squirrels and rabbits)
2) Tick bites
3) Deerfly bites
222
Describe the primary skin lesion seen in patients who have Tularemia?
Small papules at inoculation site that rapidly necroses - leading to painful ulceration.
+/- local cellulitis
Painful regional lymphadenopathy
223
Describe systemic symptoms of Tularemia?
Fever, chills, headache and malaise
224
what does Pseudomonas aeruginosa cause
Embolic lesion from ecthyma gangreosum on central chest. Note the necrotic centre and inflammatory border
225
in which type of patients do you usually see pseudomonas aeruginosa
Usually occurs in neutropenic patients.
-
226
Describe the progression of the lesion in Ecthyma Gangrenosum
Red macule(s) → oedematous → haemorrhagic bullae.
May ulcerate in late stages or form an eschar surrounded by erythema
227
What are some differentials for Escharotic Lesions?
Pseudomonas
*Aspergillosis
*Leishmaniasis
*Cryptococcosis
*Lues maligna
*Rickettsial infections
*Cutaneous anthrax
*Tularaemia
*Necrotic arachnidism (brown recluse spider bite)
*Scrub typhus (Orientia tsutsugamushi)
*Rat bite fever (Spirillum minus)
*Staphylococcal or streptococcal
*Ecthyma
*Lyme disease
228
What is the causative agent of syphilis?
Treponema Pallidum
229
Describe the skin lesion seen in a primary syphilis infection
Primary infection Chancre -painless ulcer with a firm indurated border
Painless regional lymphadenopathy one week after the primary chancre
Chancre appears within 10-90 days
230
When does secondary syphilis begin?
Begins ~50 days after chancre
231
What are some symptoms of secondary syphilis
- Malaise, fever, headache, pruritus, loss of appetite, iritis
- Alopecia (‘moth-eaten’)
- Residual primary chancre
- Condylomata lata
- Hepatosplenomegaly
- Lymphadenopathy
- Rash (88-100%) -Pityriasis rosea-like rash
- Mucous patches
232
what is the presentation of syphilis on the skin
Widespread exanthem of pink papules ( Syphilis)
233
what would show in a man positive with HIV
Pityriasis rosea like lesions localised to arms in an HIV positive man
234
what is a rare manifestation of secondary syphilis
Lues maligna - Rare manifestation of secondary syphilis
235
Describe Lues maligna and what manifestation is it more common in?
Pleomorphic skin lesions with pustules, nodules and ulcers with necrotising vasculitis
More frequent in HIV manifestation
236
Describe the skin lesions seen in tertiary syphillis?
Gumma Skin lesions - nodules and plaques
Extend peripherally while central areas heal with scarring and atrophy
Mucosal lesions extend to and destroy the nasal cartilage
237
What are two general morbidities seen in patients with tertiary syphilis?
Cardiovascular disease
Neurosyphilis (general paresis or tabes dorsalis)
238
What is the treatment for syphilis?
IM Benzylpenicillin or oral tetracycline
239
what organism causes leprosy
Mycobacterium leprae → Obligate intracellular bacteria - predominantly affects skin & nerves, but can affect any organ
240
Give the 2 broad categories seen in the clinical spectrum of leprosy?
A) Lepromatous leprosy
B) Tuberculoid leprosy
241
Describe Lepromatous leprosy.
***Multiple*** lesions: macules, papules,nodules
Sensation and sweating normal (early on
242
Describe Tuberculoid leprosy.
Solitary or few lesions: elevated borders – atrophic center, sometimes annular
243
How do the 2 categories of leprosy differ from each other?
Tuberculoid leprosy is hairless, anhidrotic and numb
244
What are the 3 ways in which cutaneous TB may be acquired?
1. **Exogenously** (primary-inoculation TB and tuberculosis verrucosa cutis)
2. **Contiguous endogenous spread** – (scrofuloderma )or autoinoculation – periorificial tuberculosis
3. **Haematogenous/lymphatic endogenous spread** –dissemination (lupus vulgaris, military tuberculosis, gummas)
245
What are the 3 top investigations to do if you suspect TB?
A) Interferon-γ release assay (Quantiferon-TB)
B) Histology – ZN stain
C) Culture / PCR
246
what presentation could you see with TB
Endogenous spread of TB - Scrofluoderma : subcutaneous nodule with necrotic material - becomes fluctuant and drains, with ulceration and sinus tract formation.
Exogenous spread : Tuberculosis verrucosa cutis
Orifical TB - non-healing ulcer of the nasal mucosa that is painful
247
Describe what a Tuberculous chancre looks like?
Painless, firm, reddish-brown papulonodule that forms an ulcer
248
Describe what tuberculosis verrucosa cutis looks like?
Wart-like papule that evolves to form redbrown plaque
249
Describe what Military TB looks like?
Pinhead-sized, bluish-red papules capped by minute vesicles
250
Describe what Tuberculosis gumma looks like?
Firm subcutaneous nodule - later ulcerates
251
what is the differential for molluscum contagiosum
Verrucae
Condyloma acuminata
Basal cell carcinoma
Pyogenic granuloma
252
What are 3 treatment options for Molluscum Contagiosum?
Curettage, Imiquimod, Cidofovir
253
What are the two types of HSV and how do they spread?
HSV-1 – direct contact with contaminated saliva / other infected secretions
HSV-2 - sexual contact
254
How does HSV replicate and travel in the body?
Replicates at mucocutaneous site of infection
Travels by retrograde axonal flow to dorsal root ganglia
255
When do HSV symptoms start and what are they preceded by?
Symptoms with 3-7 days of exposure
Preceded by tender lymphadenopathy, malaise, anorexia ± Burning, tingling
256
Describe the skin lesions seen due to HSV infection
●Painful rouped vesicles on erythematous base → ulceration / pustules / erosions with scalloped border
●Crusting and resolution within 2-6 weeks
●Orolabial lesions – often asymptomatic
257
What are some systemic manifestations of HSV?
Genital Involvement : Painful and leads to urinary retention.
Aseptic meningitis occurs in up to 10% of women
258
When can reactivation of HSV occur and why
Occurs spontaneously, can be associated with UV, fever, local tissue damage and stress
259
why is Eczema hercepticum causing monomorphic, punched out erosions ( excoriated vesicles)
an emergency
Can lead to HSV encephalitis which can be fatal
260
What is the treatment for eczema herpeticum?
IV Acyclovir + antibiotics if there is a superinfection with Staph A or Strep
261
what is Herpetic whitlow
HSV (1>2) infection of digits - pain, swelling and vesicles
262
what is Herpes gladitorum
HSV 1 involvement of cutaneous site reflecting sites of contact with another athletes lesions. Seen in contact sports eg. wrestling.
263
what is Neonatal HSV infection
Exposure to HSV during vaginal delivery – risk higher when HSV acquired near time of delivery
Affects scalp or trunk and onset is from birth to 2 weeks
264
What can neonatal HSV infection lead to?
Encephalitis —> mortality >50% without tx, 15% with tx —> neurological deficits.
265
How do you treat neonatal HSV infection
IV antivirals
266
what is the presentation of severe/chronic HSV
Most commonly : chronic, enlarging ulceration.
Multiple sites or disseminated
Often atypical eg. verrucous, exophytic or pustular lesions
267
What is the diagnostic test for HSV?
Swab for PCR
268
What is the treatment for HSV
Oral valacyclovir or acyclovir 200mg five times daily in immunocompetent localised infection
Intravenous 10mg/kg TDS X 7-19 days
269
what can Varicella Zoster Virus affect
can affect a single dermatome or multiple dermatomes
270
what organism can cause hand foot and mouth disease
- Coxsackie A16, Echo 71
- An acute self-limiting coxsackievirus infection
- Echo 71 (associated with a higher incidence of neurological involvement included fatal cases of encephalitis)
271
What are early symptoms of HFAM Disease?
Fever, malaise and a sore throat
272
Describe the skin lesion seen in HFAM
Red macules, vesicles (typically gray and eliiptical), and ulcers develop on buccal mucosa, tongue, palate and pharynx, and may also develop on hands and feet (acral and volar surfaces).
273
How does HFAM spread?
Via Oral-oral route or oral-faecal route
274
Which viruses cause morbilliform (measles-like) eruptions?
Measles, Rubella, EBV, CMV, HHV6 & HHV7 cause morbilliform (measles-like) eruptions
275
What other agents cause morbilliform rashes?
Leptospirosis
Rickettsia
276
What causes petechial/purpuric eurptions
Coagulation abnormalities - TTP, ITP, DIC
*Vasculitis
*Infections
*Viruses - Hepatitis B, CMV, Rubella, Yellow fever, Dengue fever, West nile virus
*Bacterial (BREN) - Borrelia, Rickettsia, Neisseria, Endocarditis
*Other infections - Plasmodium falciparum, Trichinella
*Other - TEN, Ergot poisoning, Raynauds
277
what is Gianottic Crosti syndrome ( aka papular acrodermatitis of childhood)
A viral eruption that causes and acute symmetrical erythematous papular eruption on face, extremities and buttocks – usually in children aged 1-3 years
278
what are 5 potential causes for Gianottic Crosti syndrome ( aka papular acrodermatitis of childhood)
- EBV (most common)
- CMV
- HHV6
- Coxsackie viruses A16, B4 and B5
- Hepatitis B
279
what causes Erythema Infectiosum
Parvovirus B19
280
what is the progression of erythema infectiosm
Initially: mild fever and headache → A few days later – ‘slapped cheeks’ for 2-4 days → then reticulated (lacy) rash of chest and thighs in 2nd stage of disease
281
what causes Exanthem Subitum aka 6th disease
hhv6 and hhv7
282
describe the progression for exanthem Subitum aka 6th disease
2-5 days of high fever → followed by appearance of small pale pink papules on the trunk and head → lasts hours to 2 days.
283
what is Orf caused by
Direct exposure to sheep or goats
284
what is the skin lesion seen in orf
Dome-shaped, firm bullae that develop an umbilicated crust
285
Where does the lesion develop in orf
Hands and forearms
286
How do you treat the skin lesions in orf
Generally resolve without therapy within 4-6 weeks.
287
what causes Pityriasis versicolor
Malassezia spp.
288
what is the skin lesion in Pityriasis versicolor
Hypopigmented, hyperpigmented or erythematous macular eruption +/- fine scale
289
when do flares occur in Pityriasis versicolor
When temp + humidity is high ( immunosupression)
290
What is the treatment for Pityriasis versicolor
Topical azole
291
what is Tinea faciei
superficial fungal infection
An area of erythema and scale
292
What is a kerion?
**Kerion** – an inflammatory fungal infection that may mimic a bacterial folliculitis or an abscess of the scalp; scalp is tender and patient usually has posterior cervical lymphadenopathy
- Frequently secondarily infected with *Staphylococcus aureus*
293
what superficial fungal infection is associated with the scalp
Kerion formation due to T. tonsurans
294
what is Onychomycosis
superficial fungal infection causing white fungal toes
295
What organism is responsible for the most superficial fungal infections?
Trichophyton rubrum
296
what does Trichophyton rubrum cause at the plantar surface of the foot
Scaling and hyperkeratosis
297
What does Trichophyton mentagrophytes sometimes cause?
Vesiculobullous reaction on arch or side of foot
298
what is an ID reaction ( aka Dermatophytid reactions)
Inflammatory reactions at sites distant from the associated dermatophyte infection
May include urticaria, hand dermatitis, or erythema nodosum
Likely secondary to a strong host immunologic response against fungal antigens
299
what are Majocchi granuloma
Follicular abscess produced when dermatophyte infection penetrates the follicular wall into surrounding dermis; tender
300
what organisms cause Majocchi granuloma
Trichophyton rubrum
Mentagrophytes
301
what is Candidiasis predisposed by
Occlusion, moisture, warm temperature and DM
302
what features do most sites show with candidiasis
Erythema oedema and thin purulent discharge
303
which areas of the body does candidiasis affect
Usually an intertriginous infection (affecting the axillae, submammary folds, crurae and digital clefts) or of oral mucosa.
304
What is Candidiasis a common cause of
Vulvovaginitis
305
what is sporotrichosis
deep fungal infection
306
what is Chromomycosis
deep fungal infection
307
what is Madura foot
a deep fungal infection
308
what is Blastomycosis
systemic fungal infection
309
what is Coccidiodomycosis
a systemic fungal infection
310
what is Histoplasmosis
systemic fungal infection
311
Describe the clinical manifestation of Aspergillosis
Primary cutaneous aspergillosis characterized by hyperpigmented plaques with brown–black scale-crusts at the site of intravenous catheters on the arm
or
Necrotic hemorrhagic bulla due to embolus of Apergillus flavus
312
describe the lesions seen in aspergillosis
Cutaneous lesions being as well-circumscribed papule with necrotic base and surrounding erythematous halo,
*Propensity to invade blood vessels causing thrombosis and infarction
*Lesions destructive – may extend into cartilage, bone and fascial planes
313
How do people with Mucormycosis present
fever, headache, facial oedema, proptosis, facial pain, orbital cellulitis ± cranial nerve dysfunction
hole in body
314
what does Muromycosis associate with
Diabetes mellitus (1/3 of patients - DKA very high risk
Malnutrition
Uraemia
Neutropaenia
Medications: Steroids / antibiotics / desferoxamine
Burns
HIV
315
What is the treatment for muromycosis?
Aggressive debridement and antifungal therapy
316
what is scabies caused by
- Contagious infestation caused by *Sarcoptes* species
- Female mates, burrows into upper epidermis, lays her eggs and dies after one month.
317
what is the onset of scabies like
Insidious onset of red to flesh-coloured pruritic papules
318
what parts of the body are affected by scabies
Affects interdigital areas of digitis, volar wrists, axillary areas and genitalia
319
what is a characteristic feature of scabies
A diagnostic burrow consisting of fine white scale is often seen
320
What is Norwegian Scabies?
Hyperkeratosis : Often asymptomatic, found in immunocompromised individuals
321
What is the treatment for scabies?
Permethrin, Oral ivermectin ( two cycles of treatment are required)
322
- What are 3 types of lice
head lice
body lice
pubic lice
323
how is head lice treated
Malathion, Permethrin or oral ivermectin
324
how does body louse present and how is it treated
Pruritic papules and hyperpigmentation.
Eliminated through cleaning and discarding clothes
325
how are pubic lice treated
Malathion/Permethrin, oral ivermectin
326
what causes an itchy weal around a central punctum?
Bedbugs (fumigate home and tx is only needed if patient is symptomatic)
327
What is meant by a melanoma?
Malignant tumour arising from melanocytes
328
What percentage of skin cancer deaths does melanoma lead to?
>75%
329
Melanomas can arise on mucosal surfaces and what tract within the eye?
Uveal tract of the eye
Mucosal surfaces - oral, conjunctival, vaginal
330
What is the central depigmented zone in the melanoma below due to?
- image shows An asymmetric, irregularly pigmented melanocytic lesion -
The central depigmented zone is due to **tumour regression**
host immunity
331
What genetic risk factors are there for melanomas?
Family history (CDKN2A mutations), MC1R (key protein in skin and hair colour in melanocytes) variants
Lightly pigmented skin
Red hair
DNA repair defects (e.g. xeroderma pigmentosum - inherited condition with extreme sensitivity to UV from sunlight)
332
What environmental factors are there for melanomas?
Intense intermittent sun exposure
Chronic sun exposure
Residence in equatorial latitudes
Sunbeds
Immunosuppression
333
What is a melanocytic nevus?
**Abnormally dark, noncancerous skin patch** (nevus) that is composed of pigment-producing cells called melanocytes.
Usually present from birth or noticeable soon after birth.
334
More than how many melanocytic nevi are a risk factor for melanomas?
>100
Or Atypical melanocytic nevi
335
What does the Mitogen-activated protein kinase (MAPK) [RAS-RAf-MEK-ERK] pathway mediate?
Cellular proliferation, growth and migration
-
336
Mutations of what gene account for 20-40% of acral and mucosal melanomas?
KIT - proto-oncogene so overexpression can lead to cancers
Makes receptor tyrosine kinases
337
Activation mutations are present in which genes during melanomas?
NRAS gene (15-20% of melanomas)
BRAF gene (50-60%)
338
In melanomas of skin with intermittent UV exposure are you likely to see high or low BRAF mutations and how does this change if there is high cumulative UV exposure
High in melanomas of skin with intermittent UV exposure, yet low in melanomas of skin with high cumulative UV exposure
339
How can mutations in CDK2NA lead to MAPK pathway disruption?
CDK2NA encodes P16 which is a tumour suppressor
P16 would normally bind to CDK4/6, and prevent formation of cyclin D1-CDK4/6 complex
340
What is the function of the Cyclin D1-CDK4/6 complex?
Phosphorylates Rb, inactivating it, leading to E2F release - E2F promotes cell cycle progression
341
Which T cell is able to kill tumour cells?
CD8+ T-cell recognise melanoma-specific antigens and if activated appropriately, are able to kill tumour cells
342
Are CD4+ helper T-cells and antibodies involved in host response to melanoma?
Yes, they play a critical role
343
What antigen is a natural inhibitor of T-cell activation and how does it do this?
Cytotoxic T-lymphocyte-associated antigen-4 (**CTLA-4**) is natural inhibitor of T-cell activation
By **removing the costimulatory** signal (B7 on APC to CD28 on T-Cell)
344
How does Ipilimumab work?
Binds to CTLA-4, blocking the inhibitory signal, which allows the CTLs to destroy the cancer cells.
345
How do checkpoint inhibitors work?
Prevent PD-1 to PDL1 binding to allow T cell killing of tumour cell
346
In what populations are melanomas developing predominantly in?
Caucasian populations
347
Is the incidence of melanomas low in fairer or darker pigmented populations?
Darkly pigmented populations
348
What is the rate of melanoma occurrence per year in Europe and Australia respectively?
10-19/100,000 per year in Europe
60/100,000 per year in Australia / NZ
3x more in Australia
349
What are the 5 subtypes of melanoma
Superficial spreading
Nodular
Lentigo maligna
Acral lentiginous
Unclassifiable
350
Which subtypes makes 60-70% of all melanomas and is it the most common type in darker or fairer skinned individuals?
Superficial
Fair-skinned
351
In which areas of the body are superficial melanomas found most commonly in men and women respectively?
Men - trunk
Women - legs
352
Superficial melanomas arise only de novo, is this true?
No, can be from pre-existing nevus
353
In up to 2/3 of superficial tumours, regression is visible, what does this signify and how does it present visibly?
Reflects interaction of host immune system with the tumour
Grey, hypo- or depigmentation
354
Superficial melanomas only have radial growth, is this true?
No there is first radial (horizontal) growth and then vertical
355
What is the second most common type of melanoma in fair skinned individuals?
Nodular melanoma
356
Most commonly, nodular melanomas affect the head, neck and what other structure?
Trunk
357
Is nodular melanoma a more common occurence in males or females?
Males
358
What colour may nodular melanoma usually present with?
Usually present as blue to black, but sometimes pink to red, nodule – may be ulcerated, bleeding
359
Nodular melanomas only have a vertical growth phase is this true?
Yes (only)
360
Which melanoma subtype accounts for around 10% of the cutaneous melanomas?
Lentigo maligna
361
what age group is Lentigo maligna common in
>60 years old
362
Which areas of the body does this occur most in?
Occurs in chronically sun-damaged skin, most commonly on the face
363
How does lentigo maligna usually present visually?
Slow growing, asymmetric brown to black macule with colour variation and an irregular indented border
364
What percentage of lentigo maligna lesions progress to invasive melanoma?
5%
365
Which melanoma subtype makes up around 5% of all melanomas?
Acral lentiginous
366
In which decade of life is acral lentiginous melanoma most frequently diagnosed?
7th decade
367
In which parts of the body does acral lentiginous melanoma most commonly occur?
Typically occurs on palms and soles or in and around the nail apparatus
368
Acral lentiginous melanomas occur more in darker pigmented individuals, is this true?
Incidence similar across all racial and ethnic groups
As more darkly pigmented Africans and Asians do not typically develop sun-related melanomas, ALM represents disproportionate percentage of melanomas diagnosed in Afro-Caribbean (up to 70%) or Asians (up to 45%)
369
what is Melanonychia
Pigmented line in the nail
370
What is an amelanotic melanoma
**Type of skin cancer in which the cells do not make melanin**
It has an asymmetrical shape, and an irregular faintly pigmented border
371
What does ABCDE stand for in the self-detection public awareness campaign
asymmetry
border
colour
diameter
evolution
372
What is Garbe’s rule when patients self-detect a skin lesion?
If a patient is worried about a single skin lesion, do not ignore their suspicion and have a low threshold for performing a biopsy
373
What are the differential diagnoses for melanomas?
Basal cell carcinoma
Seborrhoeic keratosis - proliferation of epidermal keratinocytes
Dermatofibroma - overgrowth of mixture of different cel types in dermis of skin
374
What are 6 of the poor prognostic features of melanoma?
Increased Breslow thickness >1mm
Ulceration
Age
Male gender
Anatomical site – trunk, head, neck
Lymph node involvement
375
How does the prognosis change, the worse the stage of the melanoma is?
Stage 1A melanoma have 10 year survival of >95%
Whereas
Thick melanomas >4mm and ulceration pT4b have a 10 year survival rate of 50%
376
What is meant by Breslow thickness?
Description of how deeply tumour cells have invaded
377
What is dermoscopy?
Shining a UV light that penetrates the **stratum corneum** by **negating refraction** and so you can see the melanoma in more detail than with the naked eye or microscopy
Can improve correct diagnosis of melanoma by nearly **50%**
378
What are the global features of melanomas?
Asymmetry
Presence of multiple colours
Reticular, globular, reticular-globular, homogenous
Starburst
379
What are some of the non-global features of melanomas?
Atypical networks
Streaks
Atypical dots
Globules
Irregular blood vessels
Regression structures
Blue-white veil as seen below
380
What is the significance of the blue-white veil in melanomas?
Significantly associated with BRAF mutations
381
If globules are present in regular formation as opposed to irregular distribution, what can this imply?
Regular distribution → Benign melanocytic lesion
Irregular distribution → Malignant melanocytic lesion
382
if there is any doubt, should you excise a lesion?
Yes, excise the lesion for histological assessment
383
How would you excise the lesion?
Primary excision down to subcutaneous fat
2mm peripheral margin
384
If it is deep, what could you risk doing?
Excising the mole rather than the melanoma
385
What is the margin of incision determined by and what does this method prevent?
Breslow depth
Margin should be 5mm for in situ
Margin should be 10mm for ≤ 1mm deep
Prevents local recurrence or persistent disease
386
When is sentinel lymphoma node biopsy offered?
For pTb1 or more advanced only
387
What is sentinel lymphoma node biopsy?
Lymphatic drainage of finite regions of skin drained specifically to an initial node within a given nodal basin - the ‘sentinel node’
It represents most likely nodes to contain metastatic disease
388
What does extracapsular spread then require if present on lymph node biopsy?
Needs lymph node dissection
389
When would you conduct imaging in a melanoma?
Stage III, IV
And stage IIc without SLNB
390
What imaging could you conduct in a melanoma?
PET-CT
MRI Brain
391
What is a major prognostic factor in metastatic melanoma?
LDH
392
If the melanoma is unresectable or metastatic, what 2 types of therapy could be done in management?
Immunotherapy
Mutated oncogene targeted therapy
393
In unresectable or metastatic BRAF negative melanoma, what immunotherapy is given?
Ipilimumab - CTLA-4 inhibtion
394
What other immunotherapy is commonly given in combination to Ipilimumab?
PD-L1 (Programmed cell death ligand) inhibitors (Nivolumab)
395
Is combination immunotherapy better than single agent?
Not much better than single agent
Combination immunotherapy leads to 60% response vs 20% monotherapy alone
396
In BRAF positive melanoma, which management is given?
Mutated oncogene targeted therapy
397
What is the mutated oncogene targeted therapy a combination of?
BRAF inhibitor - encorafenib, vemurafenib, dabrafenib
MEK inhibitor - trametinib
398
Keratinocyte Dysplasia/Carcinoma is most common in paler or fairer skin types?
Pale
399
What are the 4 subtypes of Keratinocyte Dysplasia/Carcinoma?
**Actinic keratoses**
- Dysplastic keratinocytes
**Bowen’s disease** (Squamous cell carcinoma *in situ*)
**Squamous cell carcinoma**
- Potential for metastasis/ death
**Basal cell carcinoma**
- (Virtually) ***never metastasises***
- Locally invasive
400
What is a significant risk factor for Basal Cell Carcinoma?
UV radiation
401
Basal cell carcinoma is dependent on what?
Stroma (provides oncogenic signals) produced by dermal fibroblasts
402
Cross talk between which two cell types upregulates receptors for PDGF in Stroma?
Tumour cells and mesenchymal cells of stroma
403
If receptors for PDGF are upregulated in the stroma, what is upregulated in the tumour cells?
PDGF
404
What is the function of PDGF in basal cell carcinoma?
Potent mitogen in mesenchymal and glial cells and it regulates cell morphology and cell movement such as **chemotaxis**
PDGF signalling is involved in embryogenesis, carcinogenesis, atherosclerosis and wound healing
405
What enables the proteolytic activity in BCC?
Metalloproteinases and collagenases – degrade pre-existing dermal tissue and facilitate spread of tumour cells
406
Loss of function of what gene in chromosome 8q enables Sonic Hedgehog-Patched signalling pathway?
PTCH gene
407
What is the function of Sonic Hedgehog-Patched signalling pathway?
Growth of established BCCs
408
What type of mutations are the majority of P53 mutations?
Missense mutations that carry a UV signature
409
Describe the pathogenesis of squamous cell carcinomas?
Normal skin → Epidermal p53 clone → Squamous cell dysplasia → Squamous cell carcinoma in situ → Invasive squamous cell carcinoma → Metastasis of squamous cell carcinoma
410
What is the function of the NOTCH1 or NOTCH2 signalling pathway?
Regulator of self-renewal and differentiation in several cell types
Hyperactivation has been implicated as oncogenic
411
What is the function of the Wnt/B-catenin signalling pathway?
Wnt pathway causes accumulation of B-catenin in cytoplasm and its eventual translocation into nucleus to act as transcriptional coactivator of transcription factors
Wnt signalling is an important pathway for **immune cell maintenance and cell renewal**
412
What is the most common skin cancer?
Basal cell carcinoma
413
What is the ratio of prevalence of BCC to SCC?
BCC:SCC → 4:1
414
Are BCC and SCC more common in men or women?
Both more common in men vs women
2-3:1
415
What is the median age at diagnosis of BCC?
68
416
What genetic syndromes are risk factors for keratinocyte carcinomas?
Xeroderma pigmentosum - inherited condition characterized by an extreme sensitivity to ultraviolet (UV) rays ****from sunlight
Oculocutaneous albinism - Affected individuals typically have very fair skin and white or light-colored hair
Muir Torre syndrome - form of Lynch syndrome and is characterized by sebaceous (oil gland) skin tumors in association with internal cancers. The most common internal site involved is the gastrointestinal tract, followed by the genitourinary tract
Nevoid basal cell carcinoma syndrome
417
What is nevus sebaceous?
Risk factor for keratinocyte carcinomas
Type of birthmark usually on scalp - made of **extra oil glands** in the skin and hair does not grow here
418
What are some of the other risk factors for keratinocyte carcinomas?
Porokeratosis - abnormal keratinisation - dry and atrophic with well-defined ridge-like hyperkeratotic border
Organ transplantation (immunosuppressive drugs)
Chronic non-healing wounds
Ionising radiation
Airline pilots
Occupational chemical exposures
Tar, polycyclic aromatic hydrocarbons
419
Do actinic keratoses pass the epidermis?
No, they are confined to the epidermis
420
How do actinic keratoses present visually?
Erythematous macule or scale or both-> thick papules or hyperkeratosis or both
Sometimes cutaneous horn
421
What is required when it is difficult to distinguish between SCC and actinic keratoses?
Biopsy
422
What is the risk of progression of actinic keratoses to SCC per year for any single lesion?
0.025–16% per year for any single lesion
423
What is Bowen’s disease?
SCC in situ
424
How does Bowen’s disease present visually?
Erythematous scaly patch or slightly elevated plaque
425
Can Bowen’s disease only arise de novo?
No, can arise from pre-existing AK
426
What else might Bowen’s disease resemble?
AK, Psoriasis, Chronic eczema
427
What 6 treatment methods are there for AK or Bowen’s disease?
5-fluorouracil cream - inhibts thymidylate synthase to give anti-cancer effects
Cryotherapy - destroys targeted cells in quick transfer of heat from skin to heat sink
Imiquimod cream - triggers immune system to target cancerous cells
Photodynamic therapy - porphorin induced apoptosis
Curettage and cautery - scrape off skin lesion with sharp blade called curette, cautery is method used to stop bleeding and seal wound
Excision
428
How can SCC present visually?
Erythematous to skin coloured
Papule
Plaque-like
Exophytic
Hyperkeratotic
Ulceration
429
What areas of the body are high risk for SCC?
Localisation: Trunk and limbs > 2cm; Head / neck > 1cm; Periorificial zones
430
Are the margins well-defined for SCC?
No, they are ill-defined
431
Are SCC fast or slow growing?
Rapidly growing
432
What are 2 other risk factors for SCC?
Immunosuppressed patients - immune system less able to destroy cancer cells
Previous radiotheapy or site of chronic inflammation
433
How would you describe the histology of SCC?
Grade of differentiation: poorly differentiated
Acantholytic, adenosquamous, demosplastic subtypes
Tumour thickness - Clark level: >6mm, Clark IV, V
Invasion beyond subcutaneous fat
Perineural, lymphatic or vascular invasion
434
What is the controversy around keratoacanthoma?
Whether it is a Pseudo-malignancy vs Variant of SCC
Psueudo-malignancy - Benign tumor that appears, clinically or histologically, to be a malignant neoplasm
435
What does a keratoacanthoma look like?
Rapidly enlarging papule that evolves into a sharply circumscribed, crateriform nodule with keratotic core
436
After resolving slowly over months, what does the keratoacanthoma leave behind?
Atrophic scar
437
What parts of the body does keratoacanthoma usually occur on?
Mostly on head or neck / sun exposed areas
438
What is a keratoacanthoma difficult to distinguish clinically and histologically from?
Squamous Cell Carcinoma
-
439
Is a clinical diagnoses sufficient or is a diagnositc biopsy always required in SCC?
Often clinical diagnoses sufficient
Diagnostic biopsy may be taken if diagnostic uncertainty
440
If there are concerns regarding regional lymph node metastases in SCC, what investigations should be done?
Ultrasound of regional lymph nodes with/without Fine Needle Aspiration
441
What are the differential diagnoses of SCC?
Basal Cell Carcinoma
Viral Wart
Merkel Cell Carcinoma
442
If the SCC is resectable, after examination of the rest of skin and regional lymph nodes, what treatment should be done?
Excision
443
If the SCC is unresectable and there are high risk features such as perineural invasion, what should be done?
Radiotherapy
444
For metastatic SCC, what should be given?
Cemiplimab - G4 mAbx binding to PD-1 to potentiate T cell killing of tumour cell
445
What 2 secondary prevention measures should be in place for SCC?
Skin monitoring advice
Sun protection advice
446
What are the 6 subtypes of Basal Cell Carcinoma?
Nodular
Superficial
Morpheic
Infiltrative
Basisquamous
Micronodular
447
What is the most common subtype for BCC?
Nodular
Accounts for aprox. 50% of all BCC
448
How does Nodular BCC typically present?
Shiny, pearly papule or nodule
449
How would you describe the visual presentation of Superficial BCC?
Well-circumscribed, erythematous, macule / patch or thin papule /plaque
450
Is Morpheic BCC common, and if so, how common?
less common
451
How would you describe the visual presentation of Morpheic BCC?
Slightly elevated or depressed area of induration (process of or condition produced by growing hard specifically)
Usually light-pink to white in colour
452
What type of growth behaviour does Morpheic BCC have?
More aggressive - extensive local destruction
453
Basisquamous BCC has the histological features of which 2 types of carcinomas?
Basal Cell Carcinoma
Squamous Cell Carcinoma
454
Micronodular BCC resembles which other type of BCC clinically?
Nodular Basal Cell Carcinoma
455
What is the difference between Micronodular and Nodular BCC?
More destructive behaviour
Higher rates of recurrence and subclincal spread
456
Is clinical diagnoses sufficient or is a diagnostic biopsy always required in BCC?
Often clinical diagnoses sufficient
Diagnostic biopsy may be taken if doubt
457
What are 3 differential diagnoses for Basal Cell Carcinomas?
Squamous cell carcinoma
Adnexal (sebaceous) carcinoma
Merkel Cell Carcinoma
458
What are the standard treatments options for BCC?
Standard surgical excision
Mohs Micrographic surgery
459
When would Mohs Micrographic surgery be preferred?
Recurrent basal cell carcinoma
Aggressive subtype (morpheic / infiltrative / micronodular)
Critical site for example, cannot excise whole nose
460
How does Mohs Micrographic surgery work?
1. Thin layer removed
2. Another thin layer removed
3. Another thin layer removed
4. Final layer of cancer removed
461
What are some of the other options for BCC treatment?
Topical therapy e.g. 5-Fluorouracil, Imiquimod
Photodynamic therapy
Curettage
Radiotherapy
Vismodegib - selectively inhibits abnormal signalling in Hedgehog (Hh) pathway
462
What percentage of cutaneous lymphomas are T-cell?
75%
463
Cutaneous T-cell lymphomas are homogenous group of neoplasms of skin-homing T-cells, is this true?
No, they are heterogenous group of neoplasms of skin-homing T-cells
464
What are the 2 most common subtypes of Cutaneous T-cell lymphomas?
Sezary syndrome
Mycosis fungoides
465
What is the underlying molecular pathogenesis of CTCL?
Unknown - Inactivation of genes controlling cell cycle and apoptosis has been identified
466
What is the prevalence of Mycosis Fungoides?
0.4/100,000
467
What age group is CTCL most common in?
Median age of diagnosis 55-60
468
What percentage of all CTCL is Sezary syndrome?
It is rare - <5% of all CTCL
469
How much of primary Cutaneous Lymphoma does MF make up?
50%
470
Can you have diagnoses of MF solely on clinical observation?
No, skin biopsy required
-
471
Why might diagnoses of MF take years?
Skin lesions may be present that are neither clinically nor histologically diagnostic for many years
Patch stage → Plaque stage → Tumour stage disease
472
What might be found in lymphomatoid drug eruptions?
Atypical T-Cell infiltrates
473
Does the clinical course of MF cause pain?
No it has an indolent clinical course
474
Does MF have many years of non-specific eczematous or psoriasiform skin lesions?
Mycosis Fungoides
Yes
475
What is the median duration of onset of skin lesions to diagnosis of MF?
4-6 years
But may vary from several months to more than 5 decades
476
What is the early patch stage of MF characterised by?
Variably sized erythematous, finely scaling lesions which may be mildly pruritic
477
Describe the main pathogenesis of MF?
Stepwise accumulation of genetic abnormalities → clonal proliferation → malignant transformation → progressive and widely disseminated disease
478
What are the molecular events in the pathogenesis of MF?
Unidentified
479
What genes so far have been identified in advanced MF?
P53 - growth arrest, DNA repair and apoptosis
CDK2NA - transcribes p16 which is a tumour suppressor
PTEN - produces enzyme that acts as part of a chemical pathway to signal cells to stop dividing
STAT3 - helps control cell growth and proliferation, migration and apoptosis
480
Are there antigens known in MF and if so, which ones?
Persistent antigenic stimulation plays a crucial role in various lymphomas but no antigens known in MF
481
Evaluation of MF requires examination with attention to what?
Type and extent of **skin lesions**
Presence of palpable **lymph nodes**
**Skin biopsies**
Complete **blood counts** and **serum** chemistries
482
What 4 categories is staging of MF therefore due to?
Tumour stage
Node involvement
Metastasis
Blood count abnormalities
483
How do you treat plaque/patch stage MF?
Topical corticosteroids
Phototherapy
Radiotherapy
484
When is systemic chemotherapy given as treatment for MF?
Only indicated in advanced stage when there is nodal or visceral involvement or in patients with rapidly progressive tumours unresponsive to less aggressive therapies
485
What is an example of immunotherapy in MF?
Brentuximab vedotin - anti-CD30
486
How does the prognosis change in MF?
Depends on stage
10 year survival rates are:
>95% in limited patch / plaque disease
85% in generalised patch / plaque disease
42% in tumour stage disease
20% in those with histological lymph node involvement
487
What are 3 differential diagnoses for MF?
Psoriasis
Eczema (discoid)
Parapsoriasis
488
Sezary syndrome has a triad of what?
Presence of neoplastic T-Cells (Sezary cells) in the skin, lymph nodes and peripheral blood
Erythroderma
Generalised lymphadenopathy
489
What are the criteria for diagnoses of Sezary syndrome?
Demonstration of a **T-cell clone** in peripheral blood by molecular or cytogenetic methods
Demonstration of immunophenotypical abnormalities an **expanded CD4+ T-cell** population
Resulting in a CD4/ CD8 ratio of greater than 10 and / or aberrant expression of **pan-T-cell antigens**
An absolute Sézary cell count of at least **1000 cells per microlitre**
490
What are the treatment options for Sezary syndrome?
Systemic treatment is required
**Extracorporeal photophoresis** - combination of 8-MOP and UVA radiation causes apoptosis of treated leukocytes and may cause preferential **apoptosis of activated or abnormal T cells**
Skin-directed therapies like **PUVA** or potent **topical corticosteroids** may be used as adjuvant
491
Which Human Herpesvirus plays a role in the aetiology of Kaposi Sarcoma?
HHV8
492
Is aetiology of Kaposi Sarcoma only related to immunosuppression?
No, can also be endemic
-
493
How does Kaposi Sarcoma present visually?
Cutaneous lesions can vary from pink patches to dark violet plaques, nodules or polyps
494
What treatment of Kaposi Sarcoma is preferred over surgery?
Chemotherapy - vincristine, doxorubicin, etoposide, bleomycin
Radiotherapy
495
What is Merkel Cell Carcinoma?
Malignant proliferation of highly anaplastic (lost mature or specialised features) cells which share structural and immunohistochemical features with various neuroectodermally derived cells, including Merkel cells
They are not carcinomas of Merkel Cells
496
80% of Merkel Cell Carcinomas are associated with what?
Polyomavirus
497
Is UV exposure an aetiological factor for Merkel Cell Carcinoma?
Yes
498
A preference of presentation on what body part is most common in Merkel Cell Carcinoma?
Head and Neck region of Older Adults
499
How would you visually describe the Merkel Cell Carcinoma?
Solitary, rapidly growing nodule- pink-red to violaceous, firm, dome shaped
500
Can ulceration occur in Merkel Cell Carcinoma?
Yes
501
Does Merkel Cell Carcinoma have non-invasive properties?
No, it is aggressive and exhibits malignant behaviour
502
What percentage of Merkel Cell Carcinoma develop advanced disease?
Over 40%
503
What are the treatment options for Merkel Cell Carcinoma?
Surgery
Radiation Therapy
504
What chemotherapy can be given in Merkel Cell Carcinoma?
Pembrolizumab - anti-PD1
Avelumab - anti-PDL1
