Dermatology (Case-Based) Flashcards

1
Q

State the two types of cutaneous adverse drug reactions (CADR)

A
  1. immunologic - type 1 or 4 hypersensitivity
  2. non-immunologic - not related to immune system
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2
Q

State the difference between type 1 and type 4 hypersensitivities. State examples, symptoms and duration.

A

TYPE 1 HS - IgE MEDIATED
- Eg: Urticaria/eczema
- Symptoms - swollen eyes, sausage lips
- Time - occurs within mintues to hours

TYPE 4 HS - T CELL MEDIATED
- Eg: Maculopapular exanthem
- Symptoms - Contact dermatitis, Tuberculin reaction, Autoimmune diseases
- Time - occurs within a few days

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3
Q

State some complications of CADRs

A

skin function compromised (skin failure) when large area of skin is loss
1. loss of barrier function against bacteria
2. volume dysregulation
3. thermodysregulation
4. pain

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4
Q

State whether type 1 or type 4 HS is acute/delayed

A

A - type 1 HS - acute
D - type 4 HS - delayed

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5
Q

Regarding EXANTHEM, state the
- latency
- pathogenesis

A

EXANTHEM
- Latency - 4 days-2 weeks
- Pathogenesis - Keratinocytes at basal layer of epidermis forms adducts with drugs –> body recognises it as foregin –> mounts immune response against the adducts –> basal vacuolar degeneration

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6
Q

Regarding EXANTHEM , state
- Morphology and Histo:
- Drugs indicated:

A

EXANTHEM
- Morpho + histo = Non-scaly erythematous maculopapular rash at trunk and limbs, basal vascuolar degeneration + epidermis otherwise healthy and viable
- Drugs = Antibiotics (beta lactams, sulfonamides), NSAIDs, Antiepileptics (carbamazepine, phenytoin), Allopurinol

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7
Q

Name the drugs indicated for exanthem

A
  1. NSAIDs
  2. Allopurinol - HLA 5801
  3. Antiepileptics (carbamazepine - HLA 1502, phenytoin)
  4. Antibiotics (beta lactams, sulfonamides)
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8
Q

State the presentation of exanthem

A

non-scaly erythematous maculopapular rash over trunk and limbs
- can spread to become patches and plaques
- BSA <30%

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9
Q

Regarding SJS/TEN, state
- latency
- pathogenesis

A

SJS/TEN
- latency - 1-4 weeks
- pathogenesis
Type 4 hypersensitivity reaction mediated by
1. drug-specific CD8+ lymphocytes
2. Fas-FasL pathway of apoptosis
3. Granule-mediated exoctyosis
4. TNF-a
resulting in intense T cell mediated damage to the keratinocytes –> full thickness epidermal necrosis

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10
Q

Regarding SJS/TEN , state
- Morphology and Histo:
- Drugs indicated:

A

SJS/TEN
- Morpho + Histo =
1. Scaly deeply erythematous/violaceous macules and patches
2. Erosions and ulcerations over genitalia, lips and back
3. Necrolytic plaques
4. Nikolsky’s sign - skin falls off with lateral pressure (basal layer of keratinocytes dead)
5. Oedema (resultant inflmmation under dead epidermis)

  • Drugs - NSAIDs, allopurinol, antibiotics (beta-lactams, sulfonamides), antiepileptics (carbamazapine, phenytoin)
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11
Q

State the location of morphology of
- macolopapular exanthem
- SJS/TEN

A

maculopapular exanthem - non-scaly erythematous maculopapular rash on trunk and limbs + basal vacuolar degeneration

SJS/TEN - scaly deeply erythematous/violaceous macules and patches on genitalia, lips and back + necrolytic patches

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12
Q

State the difference percentages of BSA covered in
- SJS
- SJS-TEN
- TEN

A

SJS - <10% BSA
SJS-TEN - 10-30% BSA
TEN - >30% BSA

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13
Q

Recap
State the pathogensis of SJS/TEN

A

SJS/TEN
Type 4 hypersensitivity reaction mediated by
1. drug-specific CD8+ cytotoxic lymphocytes
2. Fas-FasL pathway of apoptosis
3. Granule-mediated apoptosis
4. TNF-a death receptor pathway
Intense T cell mediated damage to the keratinocytes → full thickness epidermal necrosis → forming blisters

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14
Q

State the morphology of SJS/TEN

A
  1. scaly deeply erythematous/violaceous macules and patches
  2. necrolytic patches
  3. erosions and ulcerations over genitalia, lips and back
  4. nikolsky’s sign
  5. oedema
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15
Q

Define AGEP

A

AGEP = acute generalised exanthematous pustulosis
- Acute exanthem with pustulation

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16
Q

Regarding AGEP, state
- latency
- pathogenesis

A

AGEP (acute generalised exanthematous pustulosis)
- latency - days-weeks
- pathogenesis - type IV HS reaction with IL8 and CXCL8 as main players

symptoms - systemic symptoms (fever, joint pain, leukocytosis)

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17
Q

Regarding AGEP, state
- morpho + histo
- drugs indicated

A

AGEP
- morpho and histo: scaly erythematous plaques and patches + non-follicular sterile subcorneal pustules (filled with neutrophils and cellular debris)
- drugs - nsaids, antibiotics (beta-lactem, sulfonamide), anticonvulsants, antimalarial, calcium channels blockers

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18
Q

Recap
State the pathogenesis of AGEP

A

AGEP
- Type IV HS with IL8 and CXCL8 as key players
- symptoms - fever, leukocytosis and joint pain
- Acute erythematous oedema followed by formation of many small pustules

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19
Q

Recap
State the morphology of AGEP

A

AGEP
- scaly erythematous plaques and patches
- small non-follicular sterile sub-corneal pustules (filled with neutrophils and cellular debris)

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20
Q

State the drugs indicated in AGEP

A

nsaids
antibiotics (sulfonamides and beta-lactam)
anticonvulsants
antimalarial
calcium channel blockers

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20
Q

Regarding DHS, state
- latency
- pathogenesis

A

DHS = DRUG HYPERSENSITIVITY SYNDROME
- latency - 2-6 weeks (MUCH LONGER)
- pathogenesis - Type IV HS involving drug eruption that involves mutliple other organ systems (liver, LN, kidneys, heart, thyroid) –> systemic symptoms (high fever, creatinine rise in blood, borderline transamninitis)

21
Q

Regarding DHS, state
- morpho + histo
- drugs indicated

A

DHS
- morpho + histo - (BSA >50%) non-scaly deeply erythematous/violaceous oedematous macules, papules and plaques over face and trunk + interface dermatitis
- drugs indicated - nsaids, antiepileptics (carbamazapine, phenytoin), antibiotics (sulfonamides, betalactams), allopurinol

22
Q

State the pathogenesis of DHS

A

type IV HS involving drug eruption involving multiple systems (liver, LN, kidneys, heart, thyroid) –> systemic symptoms (fever, transamninitis, creatinine rise in blood)

23
Q

State the common drugs indicated for DHS

A
  1. allopurinol
  2. nsaids
  3. antibiotics (sulfonamides, beta-lactams)
  4. antiepileptics (carbamazepine, phenytoin)
24
Q

Regarding BULLOUS PEMPHIGOID, state
- latency
- pathogenesis

A

BULLOUS PEMPHIGOID
- latency - unknown
- pathogenesis - Type IV hypersensitivity reaction where autoantibodies target BP180 and BP230 –> blister formation

BP180 - integral protein of the hemidesmosomes (attaches keratinocytes to ECM)

25
Q

Regarding BULLOUS PEMPHIGOID, state
- histo + morpho
- drugs indicated

A

Regarding BULLOUS PEMPHIGOID, state
- histo + morpho - scaly erythematous plaques, erosions, subepidermal blisters (separation between epidermis and dermis), bullae
- drugs indicated:

  1. DPP4 inhibitors - linagliptin
  2. immune checkpoint inhibitors - PD1, PDL1, CTLA4 inhibitors
  3. frusemide
  4. NSAIDs
26
Q

State the risk factors of bullous pemphigoid

A

elderly
neurological diseases (stroke, dementia, parkinson’s)
movement problems

27
Q

State the latency of
1. maculopapular exanthem
2. SJS/TEN
3. AGEP
4. DHS
5. BP

A
  1. maculopapular exanthem - 4 day - 2 weeks
  2. SJS/TEN - 1-4 weeks
  3. AGEP - days - weeks
  4. DHS - 2-6 weeks
  5. BP - unknown
28
Q

State the pathogenesis of
1. maculopapular exanthem
2. SJS/TEN
3. AGEP
4. DHS
5. BP

A

(1) MACULOPAPULAR EXANTHEM
- keratinocytes at basal layer of epidermis form adducts with drugs –> body recognises as foreing and mounts immune response to adduct –> basal vacuolar degeneration (BSA < 30%)

(2) SJS/TEN
Type IV HS reaction mediated by
- drug-specific CD8+ Tc lymphocyte
- granulocyte-mediated exoctyosis
- TNF-a
- fas-fasL pathway of apoptosis
resuls in intense T cell mediated damge to keratinocytes –> full thickness epidermal necrosis –> blister formation

(3) AGEP
- type IV HS reaction involving IL8 and CXCL8 as key players
- systemic symptoms - fever, leukocytosis, joint pain
- acute oedematous erythema followed by formation of sterile pustules

(4) DHS
- type IV HS reaction involving drug eruption involving multiple organ systems (liver, LN, heart, kidneys, thyroid)
- systemic symptoms - fever, creatinine rise in blood, borderline transamninitis

(5) BP
- type IV HS where autoAb targets BP180 and BP230
- BP180 is an integral protein of hemosiderines which anchor epidermis to the dermis –> subepidermal blister formation
- risk factors - elderly, neurological diseases, movement disorders

29
Q

State the morphology of
1. maculopapular exanthem
2. SJS/TEN
3. AGEP
4. DHS
5. BP

A

(1) Maculopapular exanthem
- non-scaly erythematous maculopapular rash on trunk and limbs
- BSA involves < 30%

(2) SJS/TEN
- scaly deeply erythematous/violaceous macules and patches
- erosions and ulcerations over lips, genitalia and back
- necrolytic patches
- nikolsky’s sign - sloughing of the dead epidermal layer (basal layer of keratinocytes dead)
- oedema (inflammation under dead epidermis)

(3) AGEP
- scaly erythematous patches and plaques
- small non-follicular sterile subcorneal pustules

(4) DHS
- non-scaly deeply erythematous/violaceous macules, papules and plaques over face and trunk
- marked interface dermatitis
- BSA involves > 50%

(5) BP
- scaly erythematous plaques
- erosions
- subepidermal blsiters (separation of dermis and epidermis

30
Q

State some causes of blisters

A
  1. SJS/TEN
  2. BP
  3. Disseminated zoster
31
Q

Explain how blisters form in disseminated zoster

A

DISSEMINATED ZOSTER
- viral cytopathic changes –> undergo balloon degeneration
- epidermal cells die but not because of T cells attacking them but because of virus directly attacks them

32
Q

State the risk factors of acne vulgaris

A
  1. family history
  2. cushing’s syndrome
  3. cosmetic usage
  4. high glycemic index foods
  5. low oestrogen
  6. hyperandrogenism
33
Q

State the treatment for acne vulgaris

A

DO NOT ADMINISTER CORTICOSTEROIDS
- topical steroids (retinoids)
- oral antibiotics

34
Q

State the morpholgoical differences between
- non-inflammatory acne
- inflammatory acne

A

NON-INFLAMMATORY ACNE
- closed comedones (whiteheads) - skin covered papules with obvious follicular opening
- open comedones (blackheads) - filled with keratin plug

INFLAMMATORY ACNE
- erythematous papules and pustules
- nodules and cysts with pus or serosanguinous fluid (can coalesce and form sinus tracts)

35
Q

State the pathogenesis of acne vulgaris

A
  1. hyperkeratinisation –> comedones
  2. increased sebum production (seborrhoea) from elevated androgen levels
  3. acute and chronic inflammation
  4. cutibacterium acnes
36
Q

State the retinoids that are contraindicated in pregnant women

A

pregnancy category c - tretinoin and adapalene

pregnancy category x - tazarotene

37
Q

Name the preferred choice of systemic oral antibiotics

A

**tetracycline class of antibiotics **(doxycyline, minocycline) - 1st line therapy in moderate to severe acne
- MOA = inhibits protein synthesis by binding the 30S subunit of bacterial ribosome
- anti-inflammaotry effect - inhibits chemotaxis, inhibits metalloproteinase activity

38
Q

NEUROFIBROMA
- ____ peripheral nerve tumour
- Cell of origin =
- ____ patients
- ____ solitary and not associated with ____

A

NEUROFIBROMA
- BENIGN peripheral nerve tumour
- Cell of origin = SCHWANN CELLS
- YOUNG patients
- 90% solitary and not associated with NEUROFIBROMATOSIS 1

39
Q

NEUROFIBROMATOSIS 1
- Benign/Malignant
- Autosomal ____ mutation of ____ gene (____)
- Presentation
- Increased risking of developing ____

A

NEUROFIBROMATOSIS 1
- Benign
- Autosomal DOMINANT mutation of NF-1 gene (NEUROFIBROMIN)
- Presentation =
1. F - fibrosis
2. I - iris hamartoma (lisch nodules)
3. B - bone lesions (sphenoid dysplasia)
4. R - relatives
5. O - optic glioma
6. M - macules (cafe au lait macules)
7. A - axillary freckling
8. N - neurologic abnormalities
- Increased risking of developing PHEOCHROMOCYTOMA

40
Q

State the neurologic abnormalities in neurofibromatosis 1

A

NEUROFIBROMATOSIS 1
1. cognitive deficits and learning difficulties
2. headaches
3. seizures
4. gross and fine motor developmental delays
5. macrocephaly

41
Q

EPIDERMAL CYST
- Most common skin cyst
- ____ lesion made up of a ____ filled with ____
- Common sites =
- Can be ____, ____, ____, ____, ____
- Treatment =

A

EPIDERMAL CYST
- Most common skin cyst
- ROUND lesion made up of a CAPSULE filled with KERATIN
- Common sites = FACE + UPPER TRUNK
- Can be INFLAMED, RED, SWOLLEN, PAINFUL, OOZE A WHITE CHEESY SMELLY MATERIAL
- Treatment = Observation + Surgery

42
Q

IMPETIGO
- Causative agent =
- Common demographic =
- Compare primary and secondary impetigo
- Manifestations (3)

A

IMPETIGO
- Causative agent = STAPH AUREUS
- Common demographic = Children 2-5 years old
- Primary impetigo = direct bacterial invasion into previously normal skin
- Secondary impetigo = infections at skin of minor skin trauma
- Manifestations (3)

  1. non-bullous impetigo - golden crust appearnace, papules that progress to vesicles surrounded by erythema
  2. bullous impetigo - young children, vesicles form flaccid bullae with clear yellow fluid –> rupture to leave thin brown crust
  3. ecthyma - punched out ulcers covered with yellow crust surrounded by violaceous margins, lesions extend through epidermis deep into dermis
43
Q

State the treatment of impetigo

A

limited impetigo
- topcial therapy - mupirocin, fusidic acid x5 days

extension impetigo
- systemic antibiotics - cloxacillin + cephalexin x7 days

44
Q

INFANTILE HEMANGIOMA
- Proliferative ____ of ____ endothelium
- Common sites =
- Latency =
- Morphology =

A

INFANTILE HEMANGIOMA
- Proliferative HAMARTOMAS of VASCULAR endothelium
- Common sites = HEAD AND NECK
- Latency = Appears in first few weeks of life
- Morphology = Raised plaque

45
Q

Regarding ATOPIC DERMATITIS,

(1) ACUTE PHASE OF ATOPIC DERMATITIS
- ____ driven
- Cytokines produced by ____ =

(2) CHRONIC PHASE OF ATOPIC DERMATITIS
- ____ driven

A

Regarding ATOPIC DERMATITIS,

(1) ACUTE PHASE OF ATOPIC DERMATITIS
- Th2 driven
- Cytokines produced by Th2 = IL-4, IL-5, IL-13, IL-31

(2) CHRONIC PHASE OF ATOPIC DERMATITIS
- Th1 driven

46
Q

State the histological features of SPONGIOTIC DERMATITIS

A

SPONGIOTIC DERMATITIS = eczematous dermatitis
- slightly thickened epidermis
- intercellular oedema

gross
- Little vesicles forming on skin of palm and sole for acute dermatitis

47
Q

State the distribution of eczema in infants, children and adults

A

infants
- face, scalp, neck
- extremities - knees, elbows (extensor surfaces)

children and adults
- face and neck
- extremities and flexor surfaces

48
Q

State the presentation of chronic plaque psoriasis

A
  1. Psoriatic plaque around the umbilicus,
  2. Affecting hairline, nape of the neck - a lot of plaques and scales, flaking away
  3. Nail changes common
49
Q

State the risk factors of psoriasis

A

GENETIC
- HLACW6 - early onset psoriasis
- HLAB27 - psoriasis and psoriatic arthritis
- Genes encoding TNFa and IL23

ENVIRONMENT
- Metabolic syndrome (DM, osteoporosis. HTN, non-alcoholic fatty liver, hyperlipidemia)
- Smoking
- Obesity
- Alcohol use
- Drugs - lithium blockers, beta-blockers, anti-malarials, non-steroidal anti-inflammatory drugs, immune-checkpoint inhibitors
- Infections - bacterial and viral
- Stress

50
Q

State the histological features of PSORIASIS

A
  1. Parakeratosis
  2. Aggregates of neutrophils - munroabscesses
  3. Predominantly lymphocytes and eosinophils
51
Q

State the treatment of psoriasis

A
  1. Topical medications
    - Glucocorticoids and corticosteroids
    - Calcineurin inhibitors
    - PDE-4 inhibitros
    - Vitamin D analogues
  2. Phototherapy
  3. Systemic retinoid
  4. Systemic immunosuppression
    - Methotrexate
    - Cyclosporine
  5. Biologics
    - TNFa inhibitors - infliximab, adalimumab
    - IL-17 inhibitors
    - IL-12 inhibitors
    - IL-23 inhibitors