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bioregulatory systems y2 > dermatology > Flashcards

dermatology Flashcards

1
Q

why do we use dermatological diagnostic skills

A

prevent or reduce internal organ damage by early diagnosis
detect internal malignancy

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2
Q

what is an example of a multi organ systemic disease targeting skin

A

sarcoidosis

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3
Q

what is an example of an internal disorder causing flushing in the skin

A

carcinoid syndrome

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4
Q

What underlying skin condition does pyoderma gangrenosum suggest?

A

inflammatory bowel disease

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5
Q

List the 9 different subheadings used when making a differential diagnoses

A

Autoimmune
Idiopathic
Metabolic
Infection
Neoplastic
Genetic
Traumatic
Inflammatory
Drug-induced

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6
Q

List the investigations that are frequently undertaken in dermatology

A

blood tests
microbiology
imaging
skin biopsy
specific

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7
Q

what do you test/look for in blood tests (eg FBC)

A

FBC
renal profile
LFTs
inflammatory markers
autoimmune markers

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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

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9
Q

what do you look for in imaging

A

internal organ involvement
vascular supply

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10
Q

what do you do with skin biopsies

A

look under microscope

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11
Q

what do you do with specific tests

A

urinalysis
nerve conduction studies
endocrine investigations

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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.

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13
Q

what are the 2 main groups of lupus erythematosus

A

Systemic lupus erythematosus

Cutaneous (discoid) lupus erythematosus

(these can overlap)

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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

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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

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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

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17
Q

What haematological findings are a part of the diagnostic criteria of SLE?

A

Haemolytic anaemia

Thrombocytopenia

Leukopenia

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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

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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)

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20
Q

List the skin sign that is present in cutaneous (discoid) lupus erythematosus (CLE)

A

Discoid lupus erythematosus
SCLE

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21
Q

what does Palpable purpura (small vessel cutaneous vasculitis) look like

A

purple splodges on skin area

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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).

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23
Q

which is more common - SLE or CLE

A

CLE (95% of cases)

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24
Q

what organ is affected in CLE

A

only the skin

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25
Q

What is the distinctive feature of CLE?

A

scarring in the ear/cheek /scalp region

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26
Q

what is the underlying condition which affects newborns with lupus

A

neonatal lupus

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27
Q

what AB is positive in neonatal lupus

A

Ro antibodies

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28
Q

what test should be immediately done for neonatal lupus

A

ECG because 50% of neonates with this condition have a risk of heart block and need a pacemaker

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29
Q

What is dermatomyositis?

A

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)

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30
Q

what are some other signs of dermatomyositis

A

ragged cuticles
shawl sign - redness of the trunk
heliotrope rash - erythema of the eyelids
photo distributed redness

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31
Q

what are the clinical features for dermatomyositis with antibody profile Anti Jo-1

A

fever
myositis
gottron’s papules

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32
Q

what are the clinical features for dermatomyositis with antibody profile Anti SRP

A

necrotising myopathy

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33
Q

what are the clinical features for dermatomyositis with antibody profile Anti Mi-2

A

Milde muscle disease

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34
Q

what are the clinical features for dermatomyositis with antibody profile Anti p155

A

associated with malignancy in adults

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35
Q

what are the clinical features for dermatomyositis with antibody profile Anti p140

A

juvenile
associated with calcinosis

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36
Q

what are the clinical features for dermatomyositis with antibody profile Anti SAE

A

+/- amyopathic (lack of muscle weakness)

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37
Q

what are the clinical features for dermatomyositis with antibody profile Anti MDA5

A

increased risk of interstitial lung disease
digital ulcers
ischaemia

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38
Q

A photo-distributed rash with muscle weakness is highly suggestive of what condition?

A

Dermatomyositis

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39
Q

If you suspect dermatomyositis what diagnostic tests should you perform?

A

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

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40
Q

What enzyme is found to be elevated, after LFTs are done, if a patient has dermatomyositis?

A

ALT (alanine transaminase)

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41
Q

What is ALT blood test?

A

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 asjaundice, a condition that causes your skin and eyes to turn yellow.

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42
Q

What is IgA vasculitis?

A

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
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43
Q

What are the 2 classifications of vasculitis affecting small blood vessels

A

Cutaneous small vessel (leukocytoclastic) vasculitis

Small vessel vasculitis - special types

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44
Q

what are the subclassifications for Cutaneous small vessel (leukocytoclastic) vasculitis

A

Idiopathic

Infectious

Inflammatory (connective tissue disease)

Medication exposure

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45
Q

what are the subclassifications for Small vessel vasculitis - special types

A

IgA Vasculitis (Henoch- Scholein)

Urticarial vasculitis

Acute haemorrhagic oedema of infancy

Erythema elevatum diutinum

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46
Q

what is IgA Vasculitis (Henoch- Scholein)

A

IgA collects in small blood vessels which become inflamed and leak blood

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47
Q

what is Urticarial vasculitis

A

eruption of erythematous wheals that clinically resemble uriticaria but histologically shows changes of leukocytoclastic vasculitis

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48
Q

what is Acute haemorrhagic oedema of infancy

A

benign type of leukocytoclastic vasculitis w/ large palpable purpuric skin lesions and oedema

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49
Q

what is Erythema elevatum diutinum

A

chronic form of cutaneous small vessel vasculitis with violaceous red-brown or yellowish papules, plaques or nodules that favour extensor surfaces

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50
Q

What are the 2 classifications of vasculitis that can affect both small and medium blood vessels and their respective subclassifications?

A

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

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51
Q

What is the classification of vasculitis affecting a medium sized blood vessel and its subclassifications?

A

Polyarteritis nodosa (PAN) - fibrinoid necrosis of arterial wall with a leukocytic infiltrate
- benign cutaneous form
- systemic form

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52
Q

What are the classifications of vasculitis affecting a large sized blood vessel?

A

Temporal arteritis

Takayasu - advanced lesions demonstrate a panarteritis with intimal proliferation

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53
Q

What is the difference between macular and papular/palpable?

A

A macule is a flat, reddened area of skin present in a rash

A papule is araisedarea of skin in a rash

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54
Q

what size of blood vessel indicating vasculitis would be affected with purpura

A

small vessel manifestation
- purpura (macular/palpable)

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55
Q

what are some signs in medium vessel manifestations

A

subcutaneous nodules along blood vessels
retiform purpura and ulcers
digital necrosis

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56
Q

A patient presents with cough, dyspnoea, chest pain and ulcerative rash. She also has a saddle nose deformity. What condition does she have?

A

ANCA-associated vasculitis → can be fatal and needs to be treated aggressively

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57
Q

What is sarcoidosis?

A

Systemic granulomatous disorder of unknown origin. Can affect multiple organs.

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58
Q

What organ is most commonly affected in sarcoidosis?

A

lungs

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59
Q

Is the skin involved in most cases of sarcoidosis?

A

No, it is involved in ~33% of cases of sarcoidosis

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60
Q

List the cutaneous manifestations that can occur in sarcoidosis

A

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

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61
Q

If you do the histology of a cutaneous manifestation of sarcoidosis, what would you see

A

Non-caseating epithelioid granulomas (non-caseating = no necrosis)

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62
Q

Is sarcoidosis a diagnosis of exclusion? Explain how.

A

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

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63
Q

What does DRESS stand for?

A

Drug Reaction with Eosinophilia and Systemic Symptoms

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64
Q

Outline the scoring criteria used to diagnose DRESS.

(don’t have to have all of these - just enough to meet the criteria)

A

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

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65
Q

List the internal organs involved in DRESS and the manifestation that occurs in each respective organ.

A

Liver (hepatitis)

Kidneys (interstitial nephritis)

Heart (myocarditis)

Brain

Thyroid (thyroiditis)

Lungs (interstitial pneumonitis)

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66
Q

Which internal organ is most commonly affected in DRESS?

A

Liver - majority of deaths associated with this.

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67
Q

How long after drug exposure does DRESS start?

A

2-6 weeks

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68
Q

List the drugs that are the most common triggers of DRESS.

A

Sulfonamides

Anti-epileptics (carbamazepine, phenytoin, lamotrigine)

Allopurinol - treats gout and kidney stones

Antibiotics (vancomycin, amoxicillin, minocycline, piperacillin-tazobactam)

Ibuprofen are common triggers

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69
Q

What are the rash morphologies that may manifest in DRESS?

A

Widespread erythema (Erythroderma)

Head / neck oedema

Urticated papular exanthem - widespread papules

Maculopapular (morbilliform) eruption

Erythema multiforme-like rash

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70
Q

What is the treatment of DRESS?

A

Withdrawal of culprit drug
Corticosteroids are first line treatment - may require months of treatment

(Mortality 5-10%)

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71
Q

How can you differentiate if a rash is caused by a drug or by Graft versus Host Disease (GvHD)?

A

GvHD has:

  • Facial involvement
  • Acral involvement (acral - distal limbs)
  • Diarrhoea
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72
Q

What is GvHD?

A

Multiple-organ disease. Affects ~10-80% of allogenic haematopoetic stem cell transplants (HSCT).

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73
Q

Briefly explain the pathogenesis of GvHD.

A

Donor-derived T-lymphocyte activity against antigens in an immunocompromised recipient.

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74
Q

What are the main organs that the GvHD affects?

A

Skin

Liver

GI tract

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75
Q

What is pruritus?

A

Severe itching of the skin, as a symptom of various ailments.

Itch without a rash.

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76
Q

What is itching without a rash suggestive of?

A

Internal cause

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77
Q

What are the haematological causes of pruritus?

A

Lymphoma and Polycythaemia

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78
Q

What are other things can cause pruritus?

A

HIV / Hepatitis A / B / C

Iron deficiency or iron overload

Cholestasis

Cancer

Uraemia

Psychogenic

Pruritus of old age

Drugs (NB opiates / opioids)

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79
Q

List the investigations a patient with pruritus would need

A

FBC, LDH (for tissue damage)

Renal profile

LFTs

Ferritin

XR chest

HIV/ Hep ABC → Viral screen

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80
Q

if a patient with pruritus keeps itching. What is this cutaneous manifestation called?

A

Nodular prurigo - skin thickening as a manifestation as a defence mechanism from scratch. Actually makes itch worse.

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81
Q

What is scurvy?

A

Vitamin C (ascorbic acid) deficiency

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82
Q

What are the cutaneous manifestations of scurvy?

A

Spongy gingivae with bleeding and erosion

Petechiae, ecchymoses, follicular hyperkeratosis

Corkscrew hairs with perifollicular haemorrhage

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83
Q

What is Kwashiorkor?

A

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.

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84
Q

What are the systemic features of Kwashiorkor?

A

Hepatomegaly

Oedema

Loss of muscle mass

Diarrhoea

Bacterial / fungal infections

Failure to thrive

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85
Q

What are the skin signs of Kwashiorkor?

A

Superficial desquamation large areas of erosion

Sparse, dry hair

Soft, thin nails

Cheilitis - inflammation of the lips

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86
Q

How many enzymes does zinc play a role in?

A

200; includes the regulation of lipid, protein and nucleic acid synthesis.

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87
Q

Does zinc play a role in wound healing and does it act as an oxidant?

A

Plays a role in wound healing

it is an ANTIOXIDANT (not oxidant)

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88
Q

Can zinc deficiency be genetic or acquired?

A

Both (genetic - SLC39A4; acquired - dietary)

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89
Q

What are the triad of symptoms of Zn deficiency?

A

Dermatitis

Diarrhoea

Depression

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90
Q

What are the cutaneous manifestations of Zn deficiency?

A

Perioral, acral and perineal skin in particular is affected with scaly erosive erythema.

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91
Q

What is another name for vitamin B3?

A

Niacin

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92
Q

Is vitamin B3 required for most cellular processes?

A

Yes

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93
Q

What can vitamin B3 deficiency result in?

A

Dermatitis

Diarrhoea

Dementia

Death

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94
Q

What are the cutaneous manifestations of vitamin B3 deficiency?

A

Photo-distributed erythema

‘Casal’s necklace’

Painful fissures of the palms and soles

Peri-anal, genital and perioral inflammation and erosions

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95
Q

A patient with a history of hypertension presents with flushing, diarrhoea, wheezing and dizziness. What do these symptoms indicate the patient has?

A

Carcinoid syndrome

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96
Q

When does carcinoid syndrome develop?

A

When a malignant carcinoid tumour metastasises and secretes 5HT into the systemic circulation.

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97
Q

What are the symptoms of Carcinoid syndrome?

A

Flushing (25% of cases → when it does happen its important to think of Carcinoid syndrome)

Diarrhoea

Bronchospasm

Hypotension

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98
Q

Is Stevens-Johnsons Syndrome/ Toxic Epidermal Necrolysis (SJSTEN) a dermatology emergency?

A

Yes, its rare.

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99
Q

What are the prodromal symptoms of SJSTEN?

A

Flu-like symptoms

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100
Q

What follows the prodromal symptoms of SJSTEN?

A

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

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101
Q

When the body surface area detachment is less than 10% and symptoms of SJSTEN are present, is the disease known as SJS or TEN?

A

SJS

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102
Q

When the body surface area detachment is greater than 30% and symptoms of SJSTEN are present, is the disease known as SJS or TEN?

A

TEN

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103
Q

When the body surface area detachment is between 10-30% what is the disease known as?

A

SJS/ TEN overlap

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104
Q

What is SJS/ TEN caused by?

A

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.

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105
Q

What drugs most commonly cause SJS/ TEN?

A

antibiotics
- beta lactams
- sulphonamides

allopurinol

anti-epileptic drugs
- phenytoin
- carbamazepine
- lamotrigine

NSAIDs

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106
Q

Which other conditions have similar cutaneous manifestations to SJS/TEN?

A

Staphylococcal scalded skin syndrome (SSSS)

Thermal burns

GvHD

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107
Q

What score is used to help assess the severity of SJS/TEN? What are the criteria for this score?

A

SCORTEN – score used to help assess severity

Criteria: age >40, HR, initial % epidermal detachment, serum urea + glucose + bicarbonate, presence of malignancy

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108
Q

What are the complications of SJS/TEN?

A

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.

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109
Q

What is erythroderma?

A

Generalised erythema affecting >90% BSA

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110
Q

List the systemic manifestations reflecting impairment in skin function in erythroderma.

A

Peripheral oedema

Risk of sepsis

Loss of fluid and proteins

Tachycardia

Disturbances in thermoregulation

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111
Q

List some of the aetiologies of erythroderma

A

Cutaneous T-cell lymphoma – Sézary syndrome

Psoriasis

Atopic eczema

Idiopathic (25-30%)

Drug reactions

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112
Q

Outline the management of erythroderma

A

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

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113
Q

cutaneous signs of systemic disease, in particular CKD. Name each of these signs.

A

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

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114
Q

List the features you may see in a patient with CKD.

A

Anaemia - mucosal pallor, hair thinning

Excoriations, prurigo

Calciphylaxis

Half and half nails

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115
Q

In CKD, what signs may you see related to the underlying primary condition causing CKD?

A

Photo-distributed rash of SLE

ANCA-associated vasculitis

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116
Q

In CKD, what signs may you see related the immunosuppression in transplant recipients?

A

Viral warts - infection of HPV → excess keratin on epidermis → wart

Skin cancer

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117
Q

what are some of the cutaneous signs of Chronic Liver Disease. Name them.

A

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

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118
Q

what is necrobiosis lipoidica

A

Necrobiosis Lipoidica - plaques with red-brown raised edge with yellow-brown atrophic centre.

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119
Q

What % of Necrobiosis Lipoidica occurs in DM?

A

20-65%

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120
Q

What is the treatment of Necrobiosis Lipoidica?

A

Topical/ intralesional steroids

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121
Q

name some cutaneous manifestations of DM

A

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

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122
Q

in what condition might you see cutis gyrata verticis

A

acromegaly
rare

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123
Q

in which endocrinological condition might you see acne

A

acromegaly
Cushing’s syndrome
PCOS

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124
Q

in which condition might you see hyperpigmentation

A

addisons disease

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125
Q

in which disease might you see pretibila myxodema

A

Graves disease

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126
Q

what is Bacillary angiomatosis

A
  • form of bartonella infection
    causes wart looking spots on face
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127
Q

what is Kaposi sarcoma

A

cancer developed from cells lining lymph or blood vessels
presents with black teeth inside

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128
Q

what is Cytomegalovirus (CMV) ulceration

A

ulcerations of GI tract, most commonly stomach and colon
looks like it has pus in it

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129
Q

what is Norwegian scabies

A

thick crusts of skin that may contain large numbers of scabies mites and eggs and usually in immunocompromised patients

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130
Q

what are the warts called on your toes

A

Extensive viral warts

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131
Q

what is Severe seborrhoeic dermatitis

A

scaly pathces, red skin and stubborn dandrugg usually in scalp or oily surfaces; face, sides of nose, eyebrows, ears, eyelids and chest

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132
Q

what condition do you consider for :
extensive viral warts
severe seborrhoeic dermatitis
norwegian scabies
severe psoriasis
CMV ulceration
eosiniphilic folliculitis
kaposi sarcoma
bacillary angiomatosis

A

HIV

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133
Q

In seroconversion of HIV you can get variable manifestations. List them.

A

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

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134
Q

List things that could lead to underlying HIV being considered as a diagnosis.

A

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

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135
Q

List the cutaneous diseases associated with IBD.

A

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

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136
Q

List the cutaneous manifestation of coeliac disease

A

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.

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137
Q

what are some cutaneous manifestations in GI disorders

A

Panniculitis/ erythema nodosum

Dermatitis herpetiformis

Orofacial granulomatosis

Apthous ulceration

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138
Q

What is hidradenitis suppuritiva?

A

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.

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139
Q

What patients is hidradenitis suppurtiva seen in more commonly?

A

Patients with high BMI

DM

Inflammatory bowel disease

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140
Q

What is pyoderma gangrenosum?

A

Sterile non-infectious pustule on an erythematous base - ulcerates and extends with necrotic undermined border.

Painful

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141
Q

What underlying conditions can pyoderma gangrenosum be associated with?

A

IBD, leukaemia, seronegative arthritis

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142
Q

List the cutaneous signs of malignancy reflecting internal malignancy

A

extramammary pagets disease

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143
Q

list the cutaneous signs of genetic condition predisposing to internal cancer and skin lesions

A

Hereditary leiomyomatosis and renal cell cancer

Peutz–Jeghers syndrome

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144
Q

list the cutaneous signs of skin disease associated with malignancy

A
  • Dermatomyositis
  • Erythema gyratum repens
  • Pyoderma gangrenosum
  • Paraneoplastic pemphigus
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145
Q

list the cutaneous signs associated with non specific skin disease

A

Pruritus

Urticaria

Vasculitis

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146
Q

what is Peau d’Orange associated with

A

breast carcinoma

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147
Q

what are groin metastases associated with

A

prostatic carcinoma

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148
Q

what are haemorrhagic nodules associated with

A

metastatic pancreatic carcinoma

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149
Q

what is pyoderma gangrenosum associated with

A

leukaemia

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150
Q

what are some other cutaneous signs associated with malignancy

A

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)

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151
Q

what is the skin sign for Hereditary leiomyomatosis and renal cell cancer

A

leiomyomas

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152
Q

what is the skin sign for Peutz-Jegher syndrome

A

Mucosal melanosis

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153
Q

What does Staph Aureus express that gives it pathogenic properties?

A

Virulence Factors eg. Haemolysins and PVL

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154
Q

What 6 skin conditions can a Staph Aureus infection cause?

A

Folliculitis (incl Furunculosis and Carbuncles)

Impetigo

Cellulitis

Ecthyma

Staphylococcal scalded skin syndrome

Superinfects other dermatoses ( eg. Atopic Eczema, HSV, leg ulcers)

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155
Q

How does Streptococcus pyogenes attach to epithelial surfaces?

A

Via Lipoteichoic acid portion of its fimbriae

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156
Q

Describe 3 virulence factors produced by Streptococcus pyogenes?

A
  • 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
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157
Q

What 7 skin conditions can a Streptococcus pyogenes infection cause?

A

Impetigo

Scarlet fever

Cellulitis

Ecthyma

Necrotizing fasciitis

Erysipelas

Superinfects other dermatoses (e.g. leg ulcers)

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158
Q

what does the image with what looks like acne - whiteheads and pus filled spots show

A

follicular erythema
sometmes putular (folliculitis)

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159
Q

Where and why might recurrent cases of folliculitis arise?

A

From nasal carriage of Staph Aureus, particularly strains expressing Panton-Valentine Leukocidin (PVL)

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160
Q

What is the treatment for folliculitis?

A

Antibiotics (Flucloxacillin or erythromycin)

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161
Q

What is the difference between a furuncle and a carbuncle?

A

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.

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162
Q

What 2 things do you need to do in case of furunculosis?

A

Incision and drainage

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163
Q

Which one out of furuncle and carbuncle is more likely to lead to cellulitis and septicaemia?

A

carbuncle

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164
Q

Why do some patients develop recurrent Staphylococcal impetigo or recurrent furuncluosis (2 broad categories)

A

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

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165
Q

What is PVL Staph Aureus?

A

β-pore-forming exotoxin

Leukocyte destruction and tissue necrosis

Leads to higher morbidity, mortality and transmissibility

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166
Q

What are the main characteristics of a PVL Staph Aureus infection?

A

Often painful, more than 1 site, recurrent, present in contacts

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167
Q

What 3 effects does PVL Staph Aureus have on the skin?

A

1) Recurrent and painful abscesses

2) Folliculitis

3) Cellulitis

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168
Q

What 3 effects can PVL Staph Aureus have outside the skin?

A

1) Necrotising pneumonia

2) Necrotising fasciitis

3) Purpura fulminans - skin necrosis and DIC (haematological emergency)

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169
Q

What are 5 risk factors for acquiring PVL Staph Aureus (CCCCC)

A

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

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170
Q

Describe treatment for PVL Staph Aureus

A

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

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171
Q

what can you see in someone with pseudomonal folliculitis and what is this condition associated with

A

follicular erythematous papule
Hot tub use, swimming pools and depilatories, wet suit

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172
Q

how do you treat pseudomonal folliculitis

A

most cases don’t require treatment
severe or recurrent cases can be treated with oral ciprofloxacin

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173
Q

What is cellulitis?

A

Infection of lower dermis and subcutaneous tissue

You can see tender swelling with ill-defined blanching erythema or oedema in the images

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174
Q

What are most cases of cellulitis caused by?

A

Streptococcus pyogenes and Staphylococcus aureus

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175
Q

What is a predisposing factor for cellulitis?

A

Oedema

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176
Q

how do you treat cellulitis

A

Systemic antibiotics

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177
Q

describe impetigo

A

Superficial bacterial infection, stuck-on, honey-coloured crusts overlying an erosion

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178
Q

what causes impetigo

A

1) Streptococci (non-bullous)

or

2) Staphylococci (bullous = blistering)→ Caused by exfoliative toxins A & B, split epidermis by targeting desmoglein I

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179
Q

what areas does impetigo most commonly affect

A

face (perioral, ears and nares)

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180
Q

how can impetigo be treated

A

Topical +/- systemic antibiotics

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181
Q

when does impetiginisation occur

A

This condition with its characteristic gold crust is seen following a Staph Aureus infection.

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182
Q

Describe Ecythyma and where in the body does it usually occur

A

Severe form of streptococcal impetigo

Thick crust overlying a punch out ulceration surrounded by erythema

Usually on lower extremities

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183
Q

what causes Staphylococcal Scaled skin syndrome

A

Exfoliative toxin (same one that causes bullous impetigo)

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184
Q

What age category is SSSS condition mainly seen in?

A

Neonates, infants or immunocompromised adults

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185
Q

Why can’t the organism causing SSSS be cultured from denuded skin?

A

Infection occurs at a distant site ( i.e conjunctivitis or abscess)

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186
Q

Why does Staphylococcal Scaled skin syndrome only mainly affect neonates?

A

As neonates kidneys cannot excrete the exfoliative toxin quickly

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187
Q

Describe the progression of Staphylococcal scalded skin syndrome

A

→ Diffuse tender erythema that

→ Rapid progression to flaccid bullae

→ Wrinkle and exfoliate, leaving oozing erythematous base

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188
Q

What is the difference between SSSS and Stevens-Johnson syndrome/toxic epidermal necrolysis

A

SSSS Only penetrates stratum corneum

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189
Q

what is toxic shock syndrome (TSS)

A

Febrile illness due to Group A Staphylococcus aureus strain that produces pyrogenic exotoxin TSST-1

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190
Q

What are the main clinical features of TSS?

A

Mucous membranes (erythema)

Hematologic (platelets <100 000/mm3)

Involvement of ≥ systems:

  • Gastrointestinal
  • Muscular
  • CNS, Renal and Hepatic

Diffuse erythema

Fever >38.9°C

Hypotension

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191
Q

what occurs after resolution of TSS

A

Desquamation predominantly of palms and soles 1-2 weeks after resolution of erythema

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192
Q

what causes erythrasma

A

Infection of Corynebacterium Minutissimum

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193
Q

how does the patch in erythrasma evolve over time

A

Well demarcated patches in intertriginous areas

  • initially pink
  • become brown and scaly
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194
Q

what is pitted keratolysis caused by

A

Corynebacteria

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195
Q

how is pitted keratolysis treated

A

Topical Clindamycin

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196
Q

what causes erysipeloid and how can you be exposed to it

A

Erysipelothrix rhusiopathiae

Erythema and oedema of the hand after handling contaminated raw fish or meat

Extends slowly over weeks.

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197
Q

what causes bacillus anthracis (finger ulcer that looks circular with purple outline and yucky middle)

A

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

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198
Q

what causes Blistering Distal Dactylitis

A

Streptococcus Pyogenes or Staphylococcus aureus

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199
Q

what parts of the body are affected by Blistering Distal Dactylitis

A

1 or more tender superficial bullae on erythematous base on the volar fat pad of a finger

Toes may rarely be affected

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200
Q

What is Erysipelas and what microorganisms can cause it?

A
  • Infection of deep dermis and subcutis
  • Caused by β-haemolytic streptococci or Staphylococcus aureus
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201
Q

what are the early clinical signs and symptoms of erysipelas

A

Malaise, fever and headache

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202
Q

What does Erysipelas present as?

A

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
Q

What can the portal of entry be for erysipelas?

A

Tinea Pedis - foot infection due to a dermatophyte fungus

204
Q

how do we treat erysipelas

A

IV Antibiotics

205
Q

what causes scarlet fever

A

Caused by upper respiratory tract infection with erythrogenic toxin-producing Streptococcus pyogenes

206
Q

what are the skin symptoms in scarlet fever preceded by

A

Sore throat, Headache, Malaise, Chills, Anorexia and fever

207
Q

Describe the skin symptoms seen in a child with scarlet fever?

A

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
Q

What are potential complications of scarlet fever?

A

Otitis, mastoiditis, sinusitis, pneumonia, myocarditis, hepatitis, meningitis, rheumatic fever, acute glomerulonephritis

209
Q

Describe progression of necrotising fasciitis.

A

Initial dusky induration (usually of a limb), followed by rapid painful necrosis of skin, connective tissue and muscle.

210
Q

What 4 organisms can potentially cause necrotising fasciitis

A

Streptococci, Staphylococci, Enterobacteriaceae and anaerobes

211
Q

What are investigations performed to confirm necrotising fasciitis?

A

MRI, blood and tissue cultures

212
Q

What is the treatment of necrotising fasciitis?

A

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
Q

What is the name given to necrotising fasciitis affecting the scrotum?

A

Fournier’s gangrene

214
Q

describe the ulcer seen and spread by mycobacterium marinum

A

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
Q

when can infection by mycobacterium chelonae occur (yellowy dented holes)

A

Puncture wounds, tattoos, skin trauma or surgery

216
Q

What organism is an important cause of ulceration in Africa and Australia?

A

Mycobacterium ulcerans

Africa - Buruli ulcer

Australia - Searle’s ucler

217
Q

what is Lyme disease and what is it caused by

A

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
Q

Describe what you would seen on the skin as time passes in someone with lyme disease

A

Initial cutaneous manifestation: Erythema migrans (only in 75%)

  • Erythematous papule at the bite site
  • Progression to annular erythema of >20cm
219
Q

What are the secondary lesions seen in Lyme Disease and when do they occur?

A
  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
Q

what is Tularaemia caused by

A

Francisella tularensis

221
Q

how can you acquire tularaemia (3 ways)

A

1) Handling infected animals (squirrels and rabbits)

2) Tick bites

3) Deerfly bites

222
Q

Describe the primary skin lesion seen in patients who have Tularemia?

A

Small papules at inoculation site that rapidly necroses - leading to painful ulceration.

+/- local cellulitis

Painful regional lymphadenopathy

223
Q

Describe systemic symptoms of Tularemia?

A

Fever, chills, headache and malaise

224
Q

what does Pseudomonas aeruginosa cause

A

Embolic lesion from ecthyma gangreosum on central chest. Note the necrotic centre and inflammatory border

225
Q

in which type of patients do you usually see pseudomonas aeruginosa

A

Usually occurs in neutropenic patients.

-

226
Q

Describe the progression of the lesion in Ecthyma Gangrenosum

A

Red macule(s) → oedematous → haemorrhagic bullae.

May ulcerate in late stages or form an eschar surrounded by erythema

227
Q

What are some differentials for Escharotic Lesions?

A

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
Q

What is the causative agent of syphilis?

A

Treponema Pallidum

229
Q

Describe the skin lesion seen in a primary syphilis infection

A

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
Q

When does secondary syphilis begin?

A

Begins ~50 days after chancre

231
Q

What are some symptoms of secondary syphilis

A
  • 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
Q

what is the presentation of syphilis on the skin

A

Widespread exanthem of pink papules ( Syphilis)

233
Q

what would show in a man positive with HIV

A

Pityriasis rosea like lesions localised to arms in an HIV positive man

234
Q

what is a rare manifestation of secondary syphilis

A

Lues maligna - Rare manifestation of secondary syphilis

235
Q

Describe Lues maligna and what manifestation is it more common in?

A

Pleomorphic skin lesions with pustules, nodules and ulcers with necrotising vasculitis

More frequent in HIV manifestation

236
Q

Describe the skin lesions seen in tertiary syphillis?

A

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
Q

What are two general morbidities seen in patients with tertiary syphilis?

A

Cardiovascular disease

Neurosyphilis (general paresis or tabes dorsalis)

238
Q

What is the treatment for syphilis?

A

IM Benzylpenicillin or oral tetracycline

239
Q

what organism causes leprosy

A

Mycobacterium leprae → Obligate intracellular bacteria - predominantly affects skin & nerves, but can affect any organ

240
Q

Give the 2 broad categories seen in the clinical spectrum of leprosy?

A

A) Lepromatous leprosy

B) Tuberculoid leprosy

241
Q

Describe Lepromatous leprosy.

A

Multiple lesions: macules, papules,nodules

Sensation and sweating normal (early on

242
Q

Describe Tuberculoid leprosy.

A

Solitary or few lesions: elevated borders – atrophic center, sometimes annular

243
Q

How do the 2 categories of leprosy differ from each other?

A

Tuberculoid leprosy is hairless, anhidrotic and numb

244
Q

What are the 3 ways in which cutaneous TB may be acquired?

A
  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
Q

What are the 3 top investigations to do if you suspect TB?

A

A) Interferon-γ release assay (Quantiferon-TB)

B) Histology – ZN stain

C) Culture / PCR

246
Q

what presentation could you see with TB

A

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
Q

Describe what a Tuberculous chancre looks like?

A

Painless, firm, reddish-brown papulonodule that forms an ulcer

248
Q

Describe what tuberculosis verrucosa cutis looks like?

A

Wart-like papule that evolves to form redbrown plaque

249
Q

Describe what Military TB looks like?

A

Pinhead-sized, bluish-red papules capped by minute vesicles

250
Q

Describe what Tuberculosis gumma looks like?

A

Firm subcutaneous nodule - later ulcerates

251
Q

what is the differential for molluscum contagiosum

A

Verrucae

Condyloma acuminata

Basal cell carcinoma

Pyogenic granuloma

252
Q

What are 3 treatment options for Molluscum Contagiosum?

A

Curettage, Imiquimod, Cidofovir

253
Q

What are the two types of HSV and how do they spread?

A

HSV-1 – direct contact with contaminated saliva / other infected secretions

HSV-2 - sexual contact

254
Q

How does HSV replicate and travel in the body?

A

Replicates at mucocutaneous site of infection

Travels by retrograde axonal flow to dorsal root ganglia

255
Q

When do HSV symptoms start and what are they preceded by?

A

Symptoms with 3-7 days of exposure

Preceded by tender lymphadenopathy, malaise, anorexia ± Burning, tingling

256
Q

Describe the skin lesions seen due to HSV infection

A

●Painful rouped vesicles on erythematous base → ulceration / pustules / erosions with scalloped border

●Crusting and resolution within 2-6 weeks

●Orolabial lesions – often asymptomatic

257
Q

What are some systemic manifestations of HSV?

A

Genital Involvement : Painful and leads to urinary retention.

Aseptic meningitis occurs in up to 10% of women

258
Q

When can reactivation of HSV occur and why

A

Occurs spontaneously, can be associated with UV, fever, local tissue damage and stress

259
Q

why is Eczema hercepticum causing monomorphic, punched out erosions ( excoriated vesicles)
an emergency

A

Can lead to HSV encephalitis which can be fatal

260
Q

What is the treatment for eczema herpeticum?

A

IV Acyclovir + antibiotics if there is a superinfection with Staph A or Strep

261
Q

what is Herpetic whitlow

A

HSV (1>2) infection of digits - pain, swelling and vesicles

262
Q

what is Herpes gladitorum

A

HSV 1 involvement of cutaneous site reflecting sites of contact with another athletes lesions. Seen in contact sports eg. wrestling.

263
Q

what is Neonatal HSV infection

A

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
Q

What can neonatal HSV infection lead to?

A

Encephalitis —> mortality >50% without tx, 15% with tx —> neurological deficits.

265
Q

How do you treat neonatal HSV infection

A

IV antivirals

266
Q

what is the presentation of severe/chronic HSV

A

Most commonly : chronic, enlarging ulceration.

Multiple sites or disseminated

Often atypical eg. verrucous, exophytic or pustular lesions

267
Q

What is the diagnostic test for HSV?

A

Swab for PCR

268
Q

What is the treatment for HSV

A

Oral valacyclovir or acyclovir 200mg five times daily in immunocompetent localised infection

Intravenous 10mg/kg TDS X 7-19 days

269
Q

what can Varicella Zoster Virus affect

A

can affect a single dermatome or multiple dermatomes

270
Q

what organism can cause hand foot and mouth disease

A
  • 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
Q

What are early symptoms of HFAM Disease?

A

Fever, malaise and a sore throat

272
Q

Describe the skin lesion seen in HFAM

A

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
Q

How does HFAM spread?

A

Via Oral-oral route or oral-faecal route

274
Q

Which viruses cause morbilliform (measles-like) eruptions?

A

Measles, Rubella, EBV, CMV, HHV6 & HHV7 cause morbilliform (measles-like) eruptions

275
Q

What other agents cause morbilliform rashes?

A

Leptospirosis

Rickettsia

276
Q

What causes petechial/purpuric eurptions

A

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
Q

what is Gianottic Crosti syndrome ( aka papular acrodermatitis of childhood)

A

A viral eruption that causes and acute symmetrical erythematous papular eruption on face, extremities and buttocks – usually in children aged 1-3 years

278
Q

what are 5 potential causes for Gianottic Crosti syndrome ( aka papular acrodermatitis of childhood)

A
  • EBV (most common)
  • CMV
  • HHV6
  • Coxsackie viruses A16, B4 and B5
  • Hepatitis B
279
Q

what causes Erythema Infectiosum

A

Parvovirus B19

280
Q

what is the progression of erythema infectiosm

A

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
Q

what causes Exanthem Subitum aka 6th disease

A

hhv6 and hhv7

282
Q

describe the progression for exanthem Subitum aka 6th disease

A

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
Q

what is Orf caused by

A

Direct exposure to sheep or goats

284
Q

what is the skin lesion seen in orf

A

Dome-shaped, firm bullae that develop an umbilicated crust

285
Q

Where does the lesion develop in orf

A

Hands and forearms

286
Q

How do you treat the skin lesions in orf

A

Generally resolve without therapy within 4-6 weeks.

287
Q

what causes Pityriasis versicolor

A

Malassezia spp.

288
Q

what is the skin lesion in Pityriasis versicolor

A

Hypopigmented, hyperpigmented or erythematous macular eruption +/- fine scale

289
Q

when do flares occur in Pityriasis versicolor

A

When temp + humidity is high ( immunosupression)

290
Q

What is the treatment for Pityriasis versicolor

A

Topical azole

291
Q

what is Tinea faciei

A

superficial fungal infection
An area of erythema and scale

292
Q

What is a kerion?

A

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
Q

what superficial fungal infection is associated with the scalp

A

Kerion formation due to T. tonsurans

294
Q

what is Onychomycosis

A

superficial fungal infection causing white fungal toes

295
Q

What organism is responsible for the most superficial fungal infections?

A

Trichophyton rubrum

296
Q

what does Trichophyton rubrum cause at the plantar surface of the foot

A

Scaling and hyperkeratosis

297
Q

What does Trichophyton mentagrophytes sometimes cause?

A

Vesiculobullous reaction on arch or side of foot

298
Q

what is an ID reaction ( aka Dermatophytid reactions)

A

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
Q

what are Majocchi granuloma

A

Follicular abscess produced when dermatophyte infection penetrates the follicular wall into surrounding dermis; tender

300
Q

what organisms cause Majocchi granuloma

A

Trichophyton rubrum

Mentagrophytes

301
Q

what is Candidiasis predisposed by

A

Occlusion, moisture, warm temperature and DM

302
Q

what features do most sites show with candidiasis

A

Erythema oedema and thin purulent discharge

303
Q

which areas of the body does candidiasis affect

A

Usually an intertriginous infection (affecting the axillae, submammary folds, crurae and digital clefts) or of oral mucosa.

304
Q

What is Candidiasis a common cause of

A

Vulvovaginitis

305
Q

what is sporotrichosis

A

deep fungal infection

306
Q

what is Chromomycosis

A

deep fungal infection

307
Q

what is Madura foot

A

a deep fungal infection

308
Q

what is Blastomycosis

A

systemic fungal infection

309
Q

what is Coccidiodomycosis

A

a systemic fungal infection

310
Q

what is Histoplasmosis

A

systemic fungal infection

311
Q

Describe the clinical manifestation of Aspergillosis

A

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
Q

describe the lesions seen in aspergillosis

A

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
Q

How do people with Mucormycosis present

A

fever, headache, facial oedema, proptosis, facial pain, orbital cellulitis ± cranial nerve dysfunction
hole in body

314
Q

what does Muromycosis associate with

A

Diabetes mellitus (1/3 of patients - DKA very high risk

Malnutrition

Uraemia

Neutropaenia

Medications: Steroids / antibiotics / desferoxamine

Burns

HIV

315
Q

What is the treatment for muromycosis?

A

Aggressive debridement and antifungal therapy

316
Q

what is scabies caused by

A
  • Contagious infestation caused by Sarcoptes species
  • Female mates, burrows into upper epidermis, lays her eggs and dies after one month.
317
Q

what is the onset of scabies like

A

Insidious onset of red to flesh-coloured pruritic papules

318
Q

what parts of the body are affected by scabies

A

Affects interdigital areas of digitis, volar wrists, axillary areas and genitalia

319
Q

what is a characteristic feature of scabies

A

A diagnostic burrow consisting of fine white scale is often seen

320
Q

What is Norwegian Scabies?

A

Hyperkeratosis : Often asymptomatic, found in immunocompromised individuals

321
Q

What is the treatment for scabies?

A

Permethrin, Oral ivermectin ( two cycles of treatment are required)

322
Q
  • What are 3 types of lice
A

head lice
body lice
pubic lice

323
Q

how is head lice treated

A

Malathion, Permethrin or oral ivermectin

324
Q

how does body louse present and how is it treated

A

Pruritic papules and hyperpigmentation.

Eliminated through cleaning and discarding clothes

325
Q

how are pubic lice treated

A

Malathion/Permethrin, oral ivermectin

326
Q

what causes an itchy weal around a central punctum?

A

Bedbugs (fumigate home and tx is only needed if patient is symptomatic)

327
Q

What is meant by a melanoma?

A

Malignant tumour arising from melanocytes

328
Q

What percentage of skin cancer deaths does melanoma lead to?

A

> 75%

329
Q

Melanomas can arise on mucosal surfaces and what tract within the eye?

A

Uveal tract of the eye

Mucosal surfaces - oral, conjunctival, vaginal

330
Q

What is the central depigmented zone in the melanoma below due to?
- image shows An asymmetric, irregularly pigmented melanocytic lesion -

A

The central depigmented zone is due to tumour regression
host immunity

331
Q

What genetic risk factors are there for melanomas?

A

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
Q

What environmental factors are there for melanomas?

A

Intense intermittent sun exposure

Chronic sun exposure

Residence in equatorial latitudes

Sunbeds

Immunosuppression

333
Q

What is a melanocytic nevus?

A

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
Q

More than how many melanocytic nevi are a risk factor for melanomas?

A

> 100

Or Atypical melanocytic nevi

335
Q

What does the Mitogen-activated protein kinase (MAPK) [RAS-RAf-MEK-ERK] pathway mediate?

A

Cellular proliferation, growth and migration

-

336
Q

Mutations of what gene account for 20-40% of acral and mucosal melanomas?

A

KIT - proto-oncogene so overexpression can lead to cancers

Makes receptor tyrosine kinases

337
Q

Activation mutations are present in which genes during melanomas?

A

NRAS gene (15-20% of melanomas)
BRAF gene (50-60%)

338
Q

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

A

High in melanomas of skin with intermittent UV exposure, yet low in melanomas of skin with high cumulative UV exposure

339
Q

How can mutations in CDK2NA lead to MAPK pathway disruption?

A

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
Q

What is the function of the Cyclin D1-CDK4/6 complex?

A

Phosphorylates Rb, inactivating it, leading to E2F release - E2F promotes cell cycle progression

341
Q

Which T cell is able to kill tumour cells?

A

CD8+ T-cell recognise melanoma-specific antigens and if activated appropriately, are able to kill tumour cells

342
Q

Are CD4+ helper T-cells and antibodies involved in host response to melanoma?

A

Yes, they play a critical role

343
Q

What antigen is a natural inhibitor of T-cell activation and how does it do this?

A

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
Q

How does Ipilimumab work?

A

Binds to CTLA-4, blocking the inhibitory signal, which allows the CTLs to destroy the cancer cells.

345
Q

How do checkpoint inhibitors work?

A

Prevent PD-1 to PDL1 binding to allow T cell killing of tumour cell

346
Q

In what populations are melanomas developing predominantly in?

A

Caucasian populations

347
Q

Is the incidence of melanomas low in fairer or darker pigmented populations?

A

Darkly pigmented populations

348
Q

What is the rate of melanoma occurrence per year in Europe and Australia respectively?

A

10-19/100,000 per year in Europe

60/100,000 per year in Australia / NZ

3x more in Australia

349
Q

What are the 5 subtypes of melanoma

A

Superficial spreading

Nodular

Lentigo maligna

Acral lentiginous

Unclassifiable

350
Q

Which subtypes makes 60-70% of all melanomas and is it the most common type in darker or fairer skinned individuals?

A

Superficial

Fair-skinned

351
Q

In which areas of the body are superficial melanomas found most commonly in men and women respectively?

A

Men - trunk

Women - legs

352
Q

Superficial melanomas arise only de novo, is this true?

A

No, can be from pre-existing nevus

353
Q

In up to 2/3 of superficial tumours, regression is visible, what does this signify and how does it present visibly?

A

Reflects interaction of host immune system with the tumour

Grey, hypo- or depigmentation

354
Q

Superficial melanomas only have radial growth, is this true?

A

No there is first radial (horizontal) growth and then vertical

355
Q

What is the second most common type of melanoma in fair skinned individuals?

A

Nodular melanoma

356
Q

Most commonly, nodular melanomas affect the head, neck and what other structure?

A

Trunk

357
Q

Is nodular melanoma a more common occurence in males or females?

A

Males

358
Q

What colour may nodular melanoma usually present with?

A

Usually present as blue to black, but sometimes pink to red, nodule – may be ulcerated, bleeding

359
Q

Nodular melanomas only have a vertical growth phase is this true?

A

Yes (only)

360
Q

Which melanoma subtype accounts for around 10% of the cutaneous melanomas?

A

Lentigo maligna

361
Q

what age group is Lentigo maligna common in

A

> 60 years old

362
Q

Which areas of the body does this occur most in?

A

Occurs in chronically sun-damaged skin, most commonly on the face

363
Q

How does lentigo maligna usually present visually?

A

Slow growing, asymmetric brown to black macule with colour variation and an irregular indented border

364
Q

What percentage of lentigo maligna lesions progress to invasive melanoma?

A

5%

365
Q

Which melanoma subtype makes up around 5% of all melanomas?

A

Acral lentiginous

366
Q

In which decade of life is acral lentiginous melanoma most frequently diagnosed?

A

7th decade

367
Q

In which parts of the body does acral lentiginous melanoma most commonly occur?

A

Typically occurs on palms and soles or in and around the nail apparatus

368
Q

Acral lentiginous melanomas occur more in darker pigmented individuals, is this true?

A

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
Q

what is Melanonychia

A

Pigmented line in the nail

370
Q

What is an amelanotic melanoma

A

Type of skin cancer in which the cells do not make melanin

It has an asymmetrical shape, and an irregular faintly pigmented border

371
Q

What does ABCDE stand for in the self-detection public awareness campaign

A

asymmetry
border
colour
diameter
evolution

372
Q

What is Garbe’s rule when patients self-detect a skin lesion?

A

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
Q

What are the differential diagnoses for melanomas?

A

Basal cell carcinoma

Seborrhoeic keratosis - proliferation of epidermal keratinocytes

Dermatofibroma - overgrowth of mixture of different cel types in dermis of skin

374
Q

What are 6 of the poor prognostic features of melanoma?

A

Increased Breslow thickness >1mm

Ulceration

Age

Male gender

Anatomical site – trunk, head, neck

Lymph node involvement

375
Q

How does the prognosis change, the worse the stage of the melanoma is?

A

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
Q

What is meant by Breslow thickness?

A

Description of how deeply tumour cells have invaded

377
Q

What is dermoscopy?

A

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
Q

What are the global features of melanomas?

A

Asymmetry

Presence of multiple colours

Reticular, globular, reticular-globular, homogenous

Starburst

379
Q

What are some of the non-global features of melanomas?

A

Atypical networks

Streaks

Atypical dots

Globules

Irregular blood vessels

Regression structures

Blue-white veil as seen below

380
Q

What is the significance of the blue-white veil in melanomas?

A

Significantly associated with BRAF mutations

381
Q

If globules are present in regular formation as opposed to irregular distribution, what can this imply?

A

Regular distribution → Benign melanocytic lesion

Irregular distribution → Malignant melanocytic lesion

382
Q

if there is any doubt, should you excise a lesion?

A

Yes, excise the lesion for histological assessment

383
Q

How would you excise the lesion?

A

Primary excision down to subcutaneous fat

2mm peripheral margin

384
Q

If it is deep, what could you risk doing?

A

Excising the mole rather than the melanoma

385
Q

What is the margin of incision determined by and what does this method prevent?

A

Breslow depth

Margin should be 5mm for in situ

Margin should be 10mm for ≤ 1mm deep

Prevents local recurrence or persistent disease

386
Q

When is sentinel lymphoma node biopsy offered?

A

For pTb1 or more advanced only

387
Q

What is sentinel lymphoma node biopsy?

A

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
Q

What does extracapsular spread then require if present on lymph node biopsy?

A

Needs lymph node dissection

389
Q

When would you conduct imaging in a melanoma?

A

Stage III, IV

And stage IIc without SLNB

390
Q

What imaging could you conduct in a melanoma?

A

PET-CT

MRI Brain

391
Q

What is a major prognostic factor in metastatic melanoma?

A

LDH

392
Q

If the melanoma is unresectable or metastatic, what 2 types of therapy could be done in management?

A

Immunotherapy

Mutated oncogene targeted therapy

393
Q

In unresectable or metastatic BRAF negative melanoma, what immunotherapy is given?

A

Ipilimumab - CTLA-4 inhibtion

394
Q

What other immunotherapy is commonly given in combination to Ipilimumab?

A

PD-L1 (Programmed cell death ligand) inhibitors (Nivolumab)

395
Q

Is combination immunotherapy better than single agent?

A

Not much better than single agent

Combination immunotherapy leads to 60% response vs 20% monotherapy alone

396
Q

In BRAF positive melanoma, which management is given?

A

Mutated oncogene targeted therapy

397
Q

What is the mutated oncogene targeted therapy a combination of?

A

BRAF inhibitor - encorafenib, vemurafenib, dabrafenib

MEK inhibitor - trametinib

398
Q

Keratinocyte Dysplasia/Carcinoma is most common in paler or fairer skin types?

A

Pale

399
Q

What are the 4 subtypes of Keratinocyte Dysplasia/Carcinoma?

A

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
Q

What is a significant risk factor for Basal Cell Carcinoma?

A

UV radiation

401
Q

Basal cell carcinoma is dependent on what?

A

Stroma (provides oncogenic signals) produced by dermal fibroblasts

402
Q

Cross talk between which two cell types upregulates receptors for PDGF in Stroma?

A

Tumour cells and mesenchymal cells of stroma

403
Q

If receptors for PDGF are upregulated in the stroma, what is upregulated in the tumour cells?

A

PDGF

404
Q

What is the function of PDGF in basal cell carcinoma?

A

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
Q

What enables the proteolytic activity in BCC?

A

Metalloproteinases and collagenases – degrade pre-existing dermal tissue and facilitate spread of tumour cells

406
Q

Loss of function of what gene in chromosome 8q enables Sonic Hedgehog-Patched signalling pathway?

A

PTCH gene

407
Q

What is the function of Sonic Hedgehog-Patched signalling pathway?

A

Growth of established BCCs

408
Q

What type of mutations are the majority of P53 mutations?

A

Missense mutations that carry a UV signature

409
Q

Describe the pathogenesis of squamous cell carcinomas?

A

Normal skin → Epidermal p53 clone → Squamous cell dysplasia → Squamous cell carcinoma in situ → Invasive squamous cell carcinoma → Metastasis of squamous cell carcinoma

410
Q

What is the function of the NOTCH1 or NOTCH2 signalling pathway?

A

Regulator of self-renewal and differentiation in several cell types

Hyperactivation has been implicated as oncogenic

411
Q

What is the function of the Wnt/B-catenin signalling pathway?

A

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
Q

What is the most common skin cancer?

A

Basal cell carcinoma

413
Q

What is the ratio of prevalence of BCC to SCC?

A

BCC:SCC → 4:1

414
Q

Are BCC and SCC more common in men or women?

A

Both more common in men vs women

2-3:1

415
Q

What is the median age at diagnosis of BCC?

A

68

416
Q

What genetic syndromes are risk factors for keratinocyte carcinomas?

A

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 syndromeand 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
Q

What is nevus sebaceous?

A

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
Q

What are some of the other risk factors for keratinocyte carcinomas?

A

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
Q

Do actinic keratoses pass the epidermis?

A

No, they are confined to the epidermis

420
Q

How do actinic keratoses present visually?

A

Erythematous macule or scale or both-> thick papules or hyperkeratosis or both

Sometimes cutaneous horn

421
Q

What is required when it is difficult to distinguish between SCC and actinic keratoses?

A

Biopsy

422
Q

What is the risk of progression of actinic keratoses to SCC per year for any single lesion?

A

0.025–16% per year for any single lesion

423
Q

What is Bowen’s disease?

A

SCC in situ

424
Q

How does Bowen’s disease present visually?

A

Erythematous scaly patch or slightly elevated plaque

425
Q

Can Bowen’s disease only arise de novo?

A

No, can arise from pre-existing AK

426
Q

What else might Bowen’s disease resemble?

A

AK, Psoriasis, Chronic eczema

427
Q

What 6 treatment methods are there for AK or Bowen’s disease?

A

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
Q

How can SCC present visually?

A

Erythematous to skin coloured
Papule
Plaque-like
Exophytic
Hyperkeratotic
Ulceration

429
Q

What areas of the body are high risk for SCC?

A

Localisation: Trunk and limbs > 2cm; Head / neck > 1cm; Periorificial zones

430
Q

Are the margins well-defined for SCC?

A

No, they are ill-defined

431
Q

Are SCC fast or slow growing?

A

Rapidly growing

432
Q

What are 2 other risk factors for SCC?

A

Immunosuppressed patients - immune system less able to destroy cancer cells

Previous radiotheapy or site of chronic inflammation

433
Q

How would you describe the histology of SCC?

A

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
Q

What is the controversy around keratoacanthoma?

A

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
Q

What does a keratoacanthoma look like?

A

Rapidly enlarging papule that evolves into a sharply circumscribed, crateriform nodule with keratotic core

436
Q

After resolving slowly over months, what does the keratoacanthoma leave behind?

A

Atrophic scar

437
Q

What parts of the body does keratoacanthoma usually occur on?

A

Mostly on head or neck / sun exposed areas

438
Q

What is a keratoacanthoma difficult to distinguish clinically and histologically from?

A

Squamous Cell Carcinoma

-

439
Q

Is a clinical diagnoses sufficient or is a diagnositc biopsy always required in SCC?

A

Often clinical diagnoses sufficient

Diagnostic biopsy may be taken if diagnostic uncertainty

440
Q

If there are concerns regarding regional lymph node metastases in SCC, what investigations should be done?

A

Ultrasound of regional lymph nodes with/without Fine Needle Aspiration

441
Q

What are the differential diagnoses of SCC?

A

Basal Cell Carcinoma

Viral Wart

Merkel Cell Carcinoma

442
Q

If the SCC is resectable, after examination of the rest of skin and regional lymph nodes, what treatment should be done?

A

Excision

443
Q

If the SCC is unresectable and there are high risk features such as perineural invasion, what should be done?

A

Radiotherapy

444
Q

For metastatic SCC, what should be given?

A

Cemiplimab - G4 mAbx binding to PD-1 to potentiate T cell killing of tumour cell

445
Q

What 2 secondary prevention measures should be in place for SCC?

A

Skin monitoring advice

Sun protection advice

446
Q

What are the 6 subtypes of Basal Cell Carcinoma?

A

Nodular

Superficial

Morpheic

Infiltrative

Basisquamous

Micronodular

447
Q

What is the most common subtype for BCC?

A

Nodular

Accounts for aprox. 50% of all BCC

448
Q

How does Nodular BCC typically present?

A

Shiny, pearly papule or nodule

449
Q

How would you describe the visual presentation of Superficial BCC?

A

Well-circumscribed, erythematous, macule / patch or thin papule /plaque

450
Q

Is Morpheic BCC common, and if so, how common?

A

less common

451
Q

How would you describe the visual presentation of Morpheic BCC?

A

Slightly elevated or depressed area of induration (process of or condition produced by growing hard specifically)

Usually light-pink to white in colour

452
Q

What type of growth behaviour does Morpheic BCC have?

A

More aggressive - extensive local destruction

453
Q

Basisquamous BCC has the histological features of which 2 types of carcinomas?

A

Basal Cell Carcinoma

Squamous Cell Carcinoma

454
Q

Micronodular BCC resembles which other type of BCC clinically?

A

Nodular Basal Cell Carcinoma

455
Q

What is the difference between Micronodular and Nodular BCC?

A

More destructive behaviour

Higher rates of recurrence and subclincal spread

456
Q

Is clinical diagnoses sufficient or is a diagnostic biopsy always required in BCC?

A

Often clinical diagnoses sufficient

Diagnostic biopsy may be taken if doubt

457
Q

What are 3 differential diagnoses for Basal Cell Carcinomas?

A

Squamous cell carcinoma

Adnexal (sebaceous) carcinoma

Merkel Cell Carcinoma

458
Q

What are the standard treatments options for BCC?

A

Standard surgical excision

Mohs Micrographic surgery

459
Q

When would Mohs Micrographic surgery be preferred?

A

Recurrent basal cell carcinoma

Aggressive subtype (morpheic / infiltrative / micronodular)

Critical site for example, cannot excise whole nose

460
Q

How does Mohs Micrographic surgery work?

A
  1. Thin layer removed
  2. Another thin layer removed
  3. Another thin layer removed
  4. Final layer of cancer removed
461
Q

What are some of the other options for BCC treatment?

A

Topical therapy e.g. 5-Fluorouracil, Imiquimod

Photodynamic therapy

Curettage

Radiotherapy

Vismodegib - selectively inhibits abnormal signalling in Hedgehog (Hh) pathway

462
Q

What percentage of cutaneous lymphomas are T-cell?

A

75%

463
Q

Cutaneous T-cell lymphomas are homogenous group of neoplasms of skin-homing T-cells, is this true?

A

No, they are heterogenous group of neoplasms of skin-homing T-cells

464
Q

What are the 2 most common subtypes of Cutaneous T-cell lymphomas?

A

Sezary syndrome

Mycosis fungoides

465
Q

What is the underlying molecular pathogenesis of CTCL?

A

Unknown - Inactivation of genes controlling cell cycle and apoptosis has been identified

466
Q

What is the prevalence of Mycosis Fungoides?

A

0.4/100,000

467
Q

What age group is CTCL most common in?

A

Median age of diagnosis 55-60

468
Q

What percentage of all CTCL is Sezary syndrome?

A

It is rare - <5% of all CTCL

469
Q

How much of primary Cutaneous Lymphoma does MF make up?

A

50%

470
Q

Can you have diagnoses of MF solely on clinical observation?

A

No, skin biopsy required

-

471
Q

Why might diagnoses of MF take years?

A

Skin lesions may be present that are neither clinically nor histologically diagnostic for many years

Patch stage → Plaque stage → Tumour stage disease

472
Q

What might be found in lymphomatoid drug eruptions?

A

Atypical T-Cell infiltrates

473
Q

Does the clinical course of MF cause pain?

A

No it has an indolent clinical course

474
Q

Does MF have many years of non-specific eczematous or psoriasiform skin lesions?

A

Mycosis Fungoides
Yes

475
Q

What is the median duration of onset of skin lesions to diagnosis of MF?

A

4-6 years

But may vary from several months to more than 5 decades

476
Q

What is the early patch stage of MF characterised by?

A

Variably sized erythematous, finely scaling lesions which may be mildly pruritic

477
Q

Describe the main pathogenesis of MF?

A

Stepwise accumulation of genetic abnormalities → clonal proliferation → malignant transformation → progressive and widely disseminated disease

478
Q

What are the molecular events in the pathogenesis of MF?

A

Unidentified

479
Q

What genes so far have been identified in advanced MF?

A

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
Q

Are there antigens known in MF and if so, which ones?

A

Persistent antigenic stimulation plays a crucial role in various lymphomas but no antigens known in MF

481
Q

Evaluation of MF requires examination with attention to what?

A

Type and extent of skin lesions

Presence of palpable lymph nodes

Skin biopsies

Complete blood counts and serum chemistries

482
Q

What 4 categories is staging of MF therefore due to?

A

Tumour stage

Node involvement

Metastasis

Blood count abnormalities

483
Q

How do you treat plaque/patch stage MF?

A

Topical corticosteroids

Phototherapy

Radiotherapy

484
Q

When is systemic chemotherapy given as treatment for MF?

A

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
Q

What is an example of immunotherapy in MF?

A

Brentuximab vedotin - anti-CD30

486
Q

How does the prognosis change in MF?

A

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
Q

What are 3 differential diagnoses for MF?

A

Psoriasis

Eczema (discoid)

Parapsoriasis

488
Q

Sezary syndrome has a triad of what?

A

Presence of neoplastic T-Cells (Sezary cells) in the skin, lymph nodes and peripheral blood

Erythroderma

Generalised lymphadenopathy

489
Q

What are the criteria for diagnoses of Sezary syndrome?

A

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
Q

What are the treatment options for Sezary syndrome?

A

Systemic treatment is required

Extracorporeal photophoresis - combination of 8-MOP and UVA radiation causes apoptosis of treated leukocytesand 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
Q

Which Human Herpesvirus plays a role in the aetiology of Kaposi Sarcoma?

A

HHV8

492
Q

Is aetiology of Kaposi Sarcoma only related to immunosuppression?

A

No, can also be endemic

-

493
Q

How does Kaposi Sarcoma present visually?

A

Cutaneous lesions can vary from pink patches to dark violet plaques, nodules or polyps

494
Q

What treatment of Kaposi Sarcoma is preferred over surgery?

A

Chemotherapy - vincristine, doxorubicin, etoposide, bleomycin

Radiotherapy

495
Q

What is Merkel Cell Carcinoma?

A

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
Q

80% of Merkel Cell Carcinomas are associated with what?

A

Polyomavirus

497
Q

Is UV exposure an aetiological factor for Merkel Cell Carcinoma?

A

Yes

498
Q

A preference of presentation on what body part is most common in Merkel Cell Carcinoma?

A

Head and Neck region of Older Adults

499
Q

How would you visually describe the Merkel Cell Carcinoma?

A

Solitary, rapidly growing nodule- pink-red to violaceous, firm, dome shaped

500
Q

Can ulceration occur in Merkel Cell Carcinoma?

A

Yes

501
Q

Does Merkel Cell Carcinoma have non-invasive properties?

A

No, it is aggressive and exhibits malignant behaviour

502
Q

What percentage of Merkel Cell Carcinoma develop advanced disease?

A

Over 40%

503
Q

What are the treatment options for Merkel Cell Carcinoma?

A

Surgery

Radiation Therapy

504
Q

What chemotherapy can be given in Merkel Cell Carcinoma?

A

Pembrolizumab - anti-PD1

Avelumab - anti-PDL1

bioregulatory systems y2 (6 decks)

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