Histopath - Skin & Breast Flashcards
Pathophysiology of Pemphigus vulgaris
IgG binds to desmosome proteins 1,3 Intraepidermal bullae (flaccid blisters)
- Histology = acantholysis, suprabasal blistering
- Direct immunofluorescence = chicken wire pattern of intercellular deposits of IgG ?
Invasive squamous cell carcinoma histology
Perineural invasion
Increased mitotic activity
Keratin ‘pearls’
Other:
Irregular aggregates of pink tumour cels
Infiltrative nests in dermis
Basal cell carcinoma histology
Basaloid tumour
Peripheral palisading
Clefting
Mitotic activity
Immunohistochemical stains for Malignant melanoma
Melan A
S100
HMB45
Vesicobullous inflammatory reaction pattern
Within epidermis
Forms bullae
Spongiotic inflammatory reaction pattern
Within epidermis
Becomes oedematous
Psoriaform inflammatory reaction pattern
Within epidermis
Becomes thickened
Lichenoid inflammatory reaction pattern
Within epidermis
Forms sheeny plaque?
Vasculitic inflammatory reaction pattern
Within dermis
Associated with vasculitis
Granulmatous inflammatory reaction pattern
Within dermis
Associated with (mainly non caseating) granuloma
Subcutis inflammatory reaction patterns?
Panniculitis e.g. erythema nodosum
Key histology of eczema / dermatitis
Acute = spongiotic pattern
- fluid / oedema around keratinocytes
- inflammatory infiltrate in dermis
- dilated dermal capillaries
Chronic
- acanthosis
- hyper parakeratosis
- T cells, eosinophils
Key histology of Lichen Planus
Flat epidermis
Basement membrane obscured by T cells
Colloid bodies (dead looking keratinocytes)
Koebner’s phenomenon
Psoriatic reaction at site of injury/irritation
Mechanism of psoriasis
Abnormally rapid turnover of epidermis (6 days vs 56 days normally)
Accumulation of thick scale over sites of frequent trauma/irritation
Key histology of psoriasis
Parakeratosis (remnants of nuclei indead keratinocytes - not time to be lost)
Hypogranulosis / Loss of stratum granulosum - no time for granular layer to form
Clubbing of rete ridges
Munro’s micro-abscesses (neutrophil recruitment) in stratum corneum
Dilated blood vessels
Pathophysiology of Dermatitis herpetiformis
Associated with coeliac disease
IgA abs bind to basement membrane –> sub epidermal bullae
Pathophysiology of Bullous pemphigoid
- IgG binds to hemidesmosomes (of basement membrane)
- Subepidermal large + tense blister (bullae)
- Eosinophils - release elastase
Direct immunofluorescence: linear IgG along basement membrane
Indirect: raised serum IgG
Pathophysiology of Pemphigus foliaceous
IgG (/ IgE?) Ab against desmoglein 1 within desmosomes
Inter-epidermal blister - not intact, appear excoriated
- Histology = acantholysis, subcorneal blistering
- Direct immunofluorescence = chicken wire pattern of intercellular deposits of IgG ?
Seborrheic keratosis features
Keratin horns
Olderly proliferation
Acanthosis (thickening of epidermis)
Clinical features of Basal cell carcinoma
Pearly lesion
Rolled edge
Central ulceration
Cause of BCC
PTCH mutation Usually somatic (UV exposure), rarely inherited (Gallin syndrome)
Histology of actinic keratosis
atypia of epidermis (basal)
Abnormal stratum corneum (parakeratosis)
Basement membrane NOT lost
Bowen’s disease (SCC in situ) histology
Pleiomorphic cells
Hyperchromatic nuclei
Disorderd maturation
Increased mitotic activity, atypical mitotic figures
Full thickness atypia BUT basement membrane intact
Types of benign naevi (moles)
Junctional: melanocyte nests in epidermis, young people, well circumscribed, uniform pigment, flat.
Compound: nests of melanocytes within epidermis + dermis, can be very large, may need multiple excisions.
Intradermal: melanocytes within dermis, older patient.
Subtypes of melanoma
Lentigo maligna
Superficial spreading
Nodular
Acral lentiginous
Histology of melanoma
Atypical melanocytes
Cellular atypia in dermis
Pagetoid spread of melanocytes (ascend into epidermis)
Radial growth phase - horizontal in epidermis THEN vertical growth into dermis
Breslow thickness
Most important prognostic factor for melanoma
Measures from granular layer –> deepest abnormal melanocyte
<0.8mm = stage 1a
C1 breast cytopathology - meaning
Inadequate sample
- RBC, neutrophils
- Debris
- Cannot see cells clearly
C2 breast cytopathology - meaning
Benign
Glandular proliferation
- branching, staghorn clefts
- possible benign tumour
C3 breast cytopathology - meaning
Atypia, likely benign
C4 breast cytopathology - meaning
Atypia, likely malignant
C5 breast cytopathology - meaning
Malignant
Current gold standard for diagnosing breast ca.
Histopathology
Clinical features of duct ectasia
Nipple discharge
breast pain
mass
Nipple retraction
Histology of duct ectasia
Duct distension - proteinaceous maternal inside
Foamy macrophages
Cytology of fat necrosis
Fat cells surrounded by macrophages (histiocytes)
Clinical features of acute mastitis
Painful, red breast
Cytology of acute mastitis
Acute inflammatory cells - neutrophils
Foamy macrophages
Usual causative organism of acute mastitis
Staphylococcus
Usual epithelial hyperplasia - histological features
Increased cell proliferation causing multilayering
Clefts + empty spaces
Contained within duct
Flat epithelial atypia / atypical ductal carcinoma - histology
Punched out margins
+/- calcification
In situ lobular neoplasia - histology
Monomorphic
Fibrocystic disease - histology
Dilated + calcified ducts
Fibroadenoma - histology
Well circumscribed
Glands compressed
Phyllodes’ tumour - histology
‘Leaf-like’ - broad based papillae, long clefts
High cellularity + Stromal overgrowth = more malignant
Intraductal papilloma - histology
Dilated ducts
Polypoid mass in centre
Fibrovascular core
Blood vessels within stroma
Radial scar - histology
2 distinct areas:
- central stellate scar
- peripheral proliferation of ducts/acini
Tx of radial scar
Removal
Can contain malignant cells
Tx of intraductal papilloma
Removal = curative
Tx of Phyllodes’ tumour
Removal
Benign, borderline + malignant types
What benign lesion can resemble ca. on imaging?
Radial scar
mobile breast lump in 28 yo woman?
Fibroadenoma
Most common ca. in women
Invasive breast carcinoma
- ductal most common within this
Features of low grade Ductal carcinoma in situ
Lumens compact + regular
calcification
overlapping clls
Features of high grade ductal carcinoma in situ
Central lumen necrotic material
Pleiomorphic cells occlude duct
RF for invasive breast carcinoma
Early menarche Late menopause Increased BMI EtOH COCP \+ve family Hx
Malignant breast cancer that does not produce mammographic densities
Invasive lobular carcinoma
is picked up incidentally on biopsy
Invasive ductal carcinoma - histology
Pleimorphic cells
Large nuclei, little cytoplasm
E-cadherin +ve
Invasive lobular carcinoma - histology
Linear ‘Indian file’ pattern
Monomorphic
No calcification or stromal reaction?
Invasive tubular carcinoma - histology
Elongated tubules invading stroma
Associated with radial scar
Invasive mucinous carcinoma - histology
Nests of tumour cels
Extravasated mucin pools
Basal like carcinoma - histology
Sheets of atypical cells
Prominent lymphocytic infiltrate
Central necrosis common
+ve for cytokeratins CK5/6 and 14
Nottingham grading for breast ca.
Graded histologically looking at:
- tubule formation
- nuclear pleomorphism
- mitotic activity
each scored 1-3 then totals added
Receptors checked in breast ca.
Oestrogen receptor (ER) Progesterone receptor (PR) Her2 status
Receptor status of low grade tumours
ER/PR +
HER2-
Receptor status of high grade tumours
ER/PR -
HER2+
Receptor status of basal like carcinoma
Triple negative
ER-, PR-. HER2-
Most important prognostic factor in breast ca
Axillary lymph node status
