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Dermatology (Case-Based) Flashcards

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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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
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

Study These Flashcards
A
  1. allopurinol
  2. nsaids
  3. antibiotics (sulfonamides, beta-lactams)
  4. antiepileptics (carbamazepine, phenytoin)
24
Regarding **BULLOUS PEMPHIGOID**, state - latency - pathogenesis
**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
Regarding **BULLOUS PEMPHIGOID**, state - histo + morpho - drugs indicated
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
State the risk factors of bullous pemphigoid
elderly neurological diseases (stroke, dementia, parkinson's) movement problems
27
State the latency of 1. maculopapular exanthem 2. SJS/TEN 3. AGEP 4. DHS 5. BP
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
State the pathogenesis of 1. maculopapular exanthem 2. SJS/TEN 3. AGEP 4. DHS 5. BP
**(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
State the morphology of 1. maculopapular exanthem 2. SJS/TEN 3. AGEP 4. DHS 5. BP
**(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
State some causes of blisters
1. SJS/TEN 2. BP 3. Disseminated zoster
31
Explain how blisters form in disseminated zoster
**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
State the risk factors of acne vulgaris
1. family history 2. cushing's syndrome 3. cosmetic usage 4. high glycemic index foods 5. low oestrogen 6. hyperandrogenism
33
State the treatment for acne vulgaris
DO NOT ADMINISTER CORTICOSTEROIDS - topical steroids (retinoids) - oral antibiotics
34
State the morpholgoical differences between - non-inflammatory acne - inflammatory acne
**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
State the pathogenesis of acne vulgaris
1. **hyperkeratinisation** --> comedones 2. **increased sebum production** (seborrhoea) from **elevated androgen levels** 3. **acute** and **chronic inflammation** 4. **cutibacterium acnes**
36
State the retinoids that are contraindicated in pregnant women
pregnancy category c - tretinoin and adapalene pregnancy category x - tazarotene
37
Name the preferred choice of systemic oral antibiotics
**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
**NEUROFIBROMA** - ____ peripheral nerve tumour - Cell of origin = - ____ patients - ____ solitary and not associated with ____
**NEUROFIBROMA** - **BENIGN** peripheral nerve tumour - Cell of origin = **SCHWANN CELLS** - **YOUNG** patients - **90%** solitary and not associated with **NEUROFIBROMATOSIS 1**
39
**NEUROFIBROMATOSIS 1** - Benign/Malignant - Autosomal ____ mutation of ____ gene (____) - Presentation - Increased risking of developing ____
**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
State the neurologic abnormalities in neurofibromatosis 1
**NEUROFIBROMATOSIS 1** 1. cognitive deficits and learning difficulties 2. headaches 3. seizures 4. gross and fine motor developmental delays 5. macrocephaly
41
**EPIDERMAL CYST** - Most common skin cyst - ____ lesion made up of a ____ filled with ____ - Common sites = - Can be ____, ____, ____, ____, ____ - Treatment =
**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
**IMPETIGO** - Causative agent = - Common demographic = - Compare primary and secondary impetigo - Manifestations (3)
**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
State the treatment of impetigo
**limited impetigo** - topcial therapy - mupirocin, fusidic acid x5 days **extension impetigo** - systemic antibiotics - cloxacillin + cephalexin x7 days
44
**INFANTILE HEMANGIOMA** - Proliferative ____ of ____ endothelium - Common sites = - Latency = - Morphology =
**INFANTILE HEMANGIOMA** - Proliferative **HAMARTOMAS** of **VASCULAR** endothelium - Common sites = **HEAD AND NECK** - Latency = **Appears in first few weeks of life** - Morphology = **Raised plaque**
45
Regarding ATOPIC DERMATITIS, **(1) ACUTE PHASE OF ATOPIC DERMATITIS** - ____ driven - Cytokines produced by ____ = **(2) CHRONIC PHASE OF ATOPIC DERMATITIS** - ____ driven
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
State the histological features of SPONGIOTIC DERMATITIS
**SPONGIOTIC DERMATITIS = eczematous dermatitis** - slightly thickened epidermis - intercellular oedema gross - Little vesicles forming on skin of palm and sole for acute dermatitis
47
State the distribution of eczema in infants, children and adults
infants - face, scalp, neck - extremities - knees, elbows (extensor surfaces) children and adults - face and neck - extremities and flexor surfaces
48
State the presentation of chronic plaque psoriasis
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
State the risk factors of psoriasis
**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
State the histological features of PSORIASIS
1. Parakeratosis 2. Aggregates of neutrophils - munroabscesses 3. Predominantly lymphocytes and eosinophils
51
State the treatment of psoriasis
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

M2 Pathology (26 decks)

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