HistoPath - General Flashcards
On slide: cell that is 4x RBC size, multi-lobular with lots of granules
Neutrophils
On slide: large cell with lots of cytoplasm
Macrophage
On slide: large cell, purple colour
Lymphocytes
On slide: 4x RBC size, bi-lobed nucleus (blue), red/pink granules
Eosinophils
On slide: 4X RBC size, granules of histamine and heparin
Mast cells
Tumour that produces keratin, has intracellular bridges (prickles), no glands
Squamous cell carcinoma
Tumour that has glandular epithelium and produces mucin
Adenocarcinoma
Tumour found in the bladder, kidney, ureters
Transitional cell carcinoma
Stains Iron in haemochromatosis
Prussian Blue
Stain for amyloid
Congo red → apple green birefringence
Stains melanin
Fontana
Stain used for most histo samples
Haematoxylin (blue nucleus) and eosin (pink/red cytoplasm)
Immunohistochemical marker of the epithelium
Cytokeratin
Immunohistochemical marker of lymphoid tissue
CD45
Immunohistochemical marker of primary bowel cancer
CK20 and CK7
Immunohistochemical marker of neuroendocrine tumours
Chromogranin
70% occlusion of the coronary vessels
Stable angina
> 90% occlusion of the coronary vessels
Unstable angina
Type of flow that predisposes to atheroma
Turbulent
Prinzmetal angina
Coronary artery spasm
Time taken for there to be irreversible damage and myocyte death on MIs
> 20-40mins
Histology for heart tissue <6 hours after MI
No change
Histology for heart tissue 6-24 hours after MI
Myocyte necrotic death
Histology for heart tissue 1-4 days after MI
Inflammatory cell infiltration → macrophages seen
Histology for heart tissues 5-10 days after MI
Removal of debris
Histology for heart tissue 1-2 weeks after MI
Myofibroblasts, new vessels, collagen synthesis, granulation tissue
Histology for heart tissue >2 weeks after MI
Decellularising scarring, strengthening
Heart is pale and oedematous
24h post MI
Heart has haemorrhage, signs of necrosis
3-4 days post MI
Heart is thin an yellow
1-2 weeks post MI
Heart is tough and white
> 3 weeks post MI
complications within 24h of MI
Arrhythmia → VF
Sudden death
cardiogenic shock
Complications of MI 1-3 days after
Fibrinous pericarditis
Complications of MI 3-14 days after
Papillary muscle rupture → mitral regurgitation
LV free wall rupture
Ventricular septal rupture
Complications of MI weeks to months after
Dressler’s syndrome
Heart failure
Reinfarction/recurrence
Aneurysm (atria or ventricles)
Dilated heart, scarring and thinning of the walls with fibrotic replacement of the ventricular myocardium
Heart failure
Boggy and thin heart with systolic dysfunction
Dilated cardiomyopathy
Heart is stiff with a loss of contractility
Restrictive cardiomyopathy
HOCM inheritance
Autosomal dominant
Thickening of valve leaflet, especially along lines of closure and fusion of commissures
Thickening, shortening and fusion of chordae tendineae.
Chronic rheumatic valve disease
mid-systolic click + late systolic murmur in middle aged woman with SOB and chest pain
Mitral valve prolapse
Ejection systolic murmur (+ cause)
Aortic stenosis - calcification, bicuspid
Pansystolic murmur (+ cause)
Mitral regurgitation - post MI, RhF, infective endocarditis, connective tissue disease
Mid-diastolic murmur (+ cause)
Mitral stenosis - RhF
Ejection diastolic murmur (+ cause)
Aortic regurgitation - connective tissue disease. aneurysm, IE
Ejection diastolic murmur (+ cause)
Aortic regurgitation - connective tissue disease. aneurysm, IE
Histo: aschoff bodies (Small giant cell granulomas) and Anitschkov mycoytes (Regenerating)
Rheumatic fever
Warty vegetations on valve leaflet
Rheumatic endocarditis
Large irregular masses on valve cusps that extend to the chordae tendinae
Infective endocarditis
Small, bland vegetation on the valves
Non-bacterial thrombotic endocarditis
small, sterile, platelet-rich plaques
Libman Sacks
Cortex forced under the falx cerebri
Subfalcine
Median temporal lobe forced under the tentorial notch
Uncal (transtentorial)
Cerebellum forced through the foramen magnum
Tonsilar
Most likely area for infarction stroke
Basilar artery
Carotid bifurcation
Middle cerebral artery (Emboli from the heart)
Most likely area for haemorrhagic stroke
Basal ganglia
Closely packed vessels with no parenchyma interposed between vascular spaces under low pressure
Cavernous angioma
Target sign on MRI brain
Cavernous angioma
Most common site of sub arachnoid haemorrhage
Internal carotid bifurcation
Bruising behind the mastoid process and around the eyes
Basilar skull fracture
Coup vs Contrecoup
Coup = damage to area of collision
Contrecoup = damage to opposite side of the brain due to rebound
Pick’s bodies
Fronto temporal dementia with tau
unilateral cerebral atrophy and progranulin mutation
Frontotemporal dementia (Tau negative)
alpha synuclein and ubiquitin
Dementia with lewy bodies
Histology of brain: PAPP-LANTOS bodies, glial cells, tufted astrocytes
Progressive supranuclear palsy
Histology of brain: oligodendrocytes containing alpha-synuclein
multiple system atrophy
Presents with aphasia and “alien limb”
Corticobulbar degeneration
Fronto-temporal atrophy, marked gliosis and neuronal loss, balloon neurons, pick bodies
Pick’s disease - Fronto-temporal dementia with Tau
Western blot: 3 dense bands → dephosphorylated to show 3R and 4R tau
Alzheimer’s dementia
Western blot: 2 dense bands → dephosphorylated to show 4R tau
CBD or PSP
Western blot: 2 dense bands → dephosphorylated to show 3R tau
Pick’s (Tau positive fronto-temporal dementia)
protein deposits with spongiform change (lots of vacuoles in the brain)
Prion disease
Mutation 17q11 (NF1)
Pilocytic astrocytoma
Neurofibroma
Mutation 22q12 (NF2)
Schwanomma
Meningioma
MRI: cerebellar lesion, well-circumscribed
Histo: hairy cells, rosenthal fibres, granular bodies
Pilocytic astrocytoma
MRI: hemispheric lesion, non-enhancing
Genetics: IDH1/2 mutation
negligible/absent mitotic activity, vascular proliferation and necrosis absent
Diffuse astrocytoma
MRI: enhancing lesion, heterogenous
Cytology: microvascular proliferation
Histology: high mitotic activity, high cellularity, blood vessel growth
Glioblastoma
MRI: non-enhancing lesion
Cytology: fried egg cells (lots of cytoplasm)
Histology: IDH1/2 codeletion
Oligodendroma
MRI: enhancing lesion
Histology: attaches to the meninges, does not invade it. Globule seen
Meningioma
Histo: small blue round cells and homer-wright rosettes
medulloblastoma
intrepithelial, intracellular oedema
Spongiotic inflammation
epidermal hyperplasia
psoriasiform inflammation
basal cell damage, interface dermatitis
Lichenoid inflammation
purple/red plaques on the wrists and arms with white lines in the mouth (Wickham striae)
Lichen planus
Lichen planus pathophysiology
T cell mediated → basal keratinocytes → loss of difference between epidermis/dermis
Thickened epidermis, disappearance of the stratum granulosum, blood vessel dilation, munro’s abscesses seen
Psoriasis
Sub-epidermal fluid with eosinophils, Anti-hemidesmosome IgG and C3
Bullous pemphigoid
IgG anti-desmosomes → loss of intracellular connections
Chicken-wire pattern
Pemphigus vulgaris
IgG against desmoglein-1 of the stratum corneum
Pemphigus foliaceus
acanthosis, hyperparakeratosis, lichenification, crusting, scaling, T cells, eosinophil
Chronic eczema
Auspitz’ sign and Koebner phenomenon
Auspitz’ sign: rubbing the skin causes pin-point bleeding
Koebner phenomenon: lesions form at the site of trauma
Psoriasis
Dysplastic change affecting the bottom keratinocytes with no BM mutation, PCTH mutation
Basal cell carcinoma
Pearly lesion, rolled edges, central ulceration, telengiectasia
Basal cell carcinoma
Pleomorphic squamous epithelial cells arising from the epidermis and extending into the dermis
Squamous cell carcinoma
Junctional melanocytes move up through the dermis (vertical growth) instead of maturing and dropping out the dermis (pagetoid spread)
Atypical Melanocytes with mitotic figures
Melanoma
Lots of growth and ordered proliferation
Ordered and benign growth
“Horn cysts” – epidermis entrapping keratin
Seborrheic keratosis
Cyst surrounded by squamous epithelium
Sebaceous cyst
Cytology of breast shows increased neutrophils
Mastitis
Cytology of breast shows empty fat spaces, neutrophilia and giant cells
Fat necrosis
Cytology of the breast shows macrophages and proteinaceous material, histology shows duct dilatation and inflammation
Duct ectasia
Peri-menopausal woman presents with thick yellow discharge from the nipples
Duct ectasia
Multiple layers of cells with a regular lumen in the breast
Multiple layers of epithelial cells
Cytology: Spindle stromal and glandular cells, naked nuclei, epithelium in antler horn clusters or honeycomb sheets
Histology: branching sheaths of epithelial cells
Fibroadenoma
Lumpiness of the breast that correlates with the menstrual cycle, histology shows dilated cystic ducts
Fibrocystic disease
Blood discharge from nipple
Intraductal papilloma
Cytology: branching papillary group of epithelium
Histology: papillary mass in a dilated duct
Intraductal papilloma
Mammogram shows stellate pattern
Radial scar
Histology: peripheral proliferation of ducts and acini, central stellate pattern
Radial scar
Histology: leaf like epithelial pattern
Phyllodes tumour
breast cancer screening
47-73 years of age every 3 years
Histology of breast: uniform cells with calcification
Ductal carcinoma in situ (Low grade)
Histology of breast: microcalcifications, larger cells with fewer lumens
Ductal carcinoma in situ (high grade)
Proliferation of malignant glandular epithelial cells in the nipple areolar epidermis
Paget’s disease of the breast
Sheets of atypical cells, triple receptor negative
Basal-like cancer carcinoma
Extracellular mucin
Mucinous carcinoma
Elongated tubules invading stroma in the breast
Tubular carcinoma
Linear arrangement, in single files
Monomorphic
lobular carcinoma
Big pleomorphic cells, E cadherin -ve
Ductal carcinoma
Most important prognostic factor for breast cancer
Status of axillary lymph node
Treatment for breast cancer according to receptor presence
Oestrogen → tamoxifen, SERMs
HER2 → herceptin
Staghorn calculi
Magnesium ammonium phosphate stones
Common areas of stones
Pelvo-ureteric junction
Pelvic brim
Vesico-ureteric junction
Histology: nodules, prostatic epithelial ducts with duct spaces
benign prostatic hyperplasia
Most common prostate cancer
Adenocarcinoma
Most common testicular tumours
Germ cell tumours
Histology of the kidney: bland epithelial cells growing in a papillary/tubopapillary pattern. well-circumscribed cortical nodules
Papillary adenoma
Histology of the kidney: sheets of oncolytic cells, pink cytoplasm and nests of cells
(macroscopically = mahogany brown)
Oncocytoma
Histology of the kidney: fat spaces, blood vessels, spindle cell components
Angiomyolipoma
Golden yellow kidney with haemorrhages
Micro: nests of epithelium with clear cytoplasm
Clear cell carcinoma (RCC)
Fragile, friable brown kidney
Papillary/tubopapillary pattern >15mm
Papillary renal cell carcinoma
Solid brown kidney, well-circumscribed
Sheets of large cells with distinct borders
Chromophobe
Small round blue cells
Epithelium trying to differentiate → primitive renal tubules
Wilm’s tumour
Frond like growths projecting from the bladder wall, often multifocal
Non-invasive transitional cell carcinoma
Bladder cancer in a pt from an endemic country for schistosomiasis
Squamous cell carcinoma
Most common bladder tumour
Transitional cell tumour
Loss of cancellous bone
Osteoporosis
Excess unmineralised bone (osteoid)
Osteomalacia
Multinucleate giant cell tumours (brown tumours) and fibrosis of bone
hyperparathyroidism
Huge osteoclasts with >100 nuclei, mosaic pattern (lamellar)
Paget’s disease
Cotton wool skull appearance, picture frame vertebrae, ivory vertebrae, sclerosis and lucency of pelvis
Paget’s disease of the bone
Rat bite erosions on x ray
Gout
chondrocalcinosis (white lines) on x ray
pseudogout
Subperiosteal new bone in early disease → lytic bone destruction 10 days after
Osteomyelitis
X-ray: loss of joint space, osteophytes, subchondral scerlosis, subchondral cysts
Osteoarthritis
O/E: nodules at the PIPJ and DIPJ
PIPJ = bouchard’s nodes
DIPJ = heberden’s nodes
Osteoarthritis
Joint swelling and pain (wrists, elbows, ankles, knees) with synovial swelling, pulmonary fibrosis, vasculitis, amyloidosis, pericarditis, SC nodules and DVT Hx
Rheumatoid arthritis
O/E either: extension of the PIPJ and flexion of the DIPJ OR flexion of the PIPJ and extension of the DIPJ
extension of the PIPJ and flexion of the DIPJ = swan neck deformity
flexion of the PIPJ and extension of the DIPJ = boutonnieres deformity
rheumatoid arthritis
X ray: lengthening of synovial membranes, surface synoviocyte hyperplasia, inflammatory cell infiltration, fibrin deposition, necrosis
Rheumatoid arthritis
No periosteal reaction with thick endosteal reaction
Regular bone and calcification
Intraosseous
Benign bone neoplasm
Acute periosteal reaction with varied bone formation
Extraosseous
Irregular calcification
Malignant bone neoplasm
Cartilage tumour of the hands with either multiple enchondromas or with haemangiomas
Enchondroma
X-ray: lytic lesions with cotton wool calcification, expansile, O ring sign
Histology: NORMAL cartilage, calcified matrix
Enchondroma
Fibrous dysplasia, cafe au lait spots, precocious puberty, hyperthyroidism, cushing’s. acromegaly
McCune Albright syndrome
Histology: Chinese letters
X ray: soap bubble osteolysis, sheperd’s crook deformity
Fibrous dysplasia
Histo: normal bone
X-ray: speckled mineralisation
Osteoblastoma
X-ray: normal bone
Histo: central nidus (luscent) with sclerotic rim (opaque) = bulls eye appearance
osteoid osteoma
X-ray: normal bone
Multiple polyps
Osteoma
X-ray: well-define bony protuberance from the bone, cartilage capped bone spur on the surface of bone (mushroom)
Histo: cartilage capped mushroom bony outgrowth
osteochondroma
X-ray: lytic well defined bone
Simply cyst
X-ray: Codman’s triangle, sunburst appearance
ALP raised
Histo: trabecular bone
Osteosarcoma
X-ray: lytic lesion with fluffy calcification
Chondrosarcoma
X-ray: onion skin appearance
Histo: small blue round cells
C99 +ve
t (11;22)
Ewing’s sarcoma
X-ray: lytic/luscent lesions
Histo: soap bubble appearance, giant multinuclear osteoclasts
Giant cell bone malignancy
Light microscopy: no change
Electron microscopy: loss of podocyte foot processes
Minimal change disease
Light microscopy: diffuse thickening of the glomerular basement membrane
Electron microscopy: spiky subepithelial deposits and loss of podocyte foot processes
Membranous glomerular disease
Light microscopy: focal and segmental scarring and consolidation, hyalinolysis
Electron microscopy: loss of podocyte foot processes
Focal segmental glomerulosclerosis
Diffuse glomerular basement membrane thickening
Mesangial matrix nodules (Kimmelstiel-Wilson nodules)
Diabetic nephropathy
Urine dip: proteinuria
Urine Protein: creatinine ratio >300
serum albumin: low
total cholesterol: high
Immunoglobulins: low
Nephrotic syndrome
Light microscopy: hypercellularity of the glomeruli
Fluorescence microscopy: granular deposits of IgG and C3
Electron microscopy: subepithelial humps
Post-streptococcal glomerulonephritis
Immunofluorescence: granular deposition of IfA and C3 in mesangium
IgA nephropathy (berger)
Light microscopy: crescents in the glomeruli
Electron microscopy: Linear deposition of IgG in the GBM
Goodpasture’s disease (Crescenteric) glomerulonephritis
Light microscopy: crescents in the glomeruli
Electron microscopy: IgG immune complex deposition in the GBM/mesangium, granular (lumpy /bumpy) appearance
Immune complex mediated (crescenteric) glomerulonephritis
Light microscopy: crescents in the glomeruli
Electron microscopy: scanty/lack of immune complex deposition
Pauci-immune (GwP or microscopic polyangiitis)
Nephritic syndrome, sensorineural deafness, cataracts
Alport’s (XLR, Type IV collagen alpha-5)
asymptomatic haematuria that runs in the family
Thin basement membrane / benign familial haematuria (AutDom, type IV collagen alpha-4)
Differentials for asymptomatic haematuria
Thin basement membrane/benign familial haematuria
IgA nephropathy (more common in asians, more likely to have a change in renal function e.g. Cr)
Alport syndrome
Most common cause of renal AKI
acute tubular necrosis/acute tubular injury
Pt with AKI and hypovolaemia, hypovolaemia is corrected but the AKI still persists
Acute tubular injury/necrosis
Histo: necrosis of short segments of tubules
acute tubular injury/necrosis
Histo: inflammatory infiltrate with tubular injury, eosinophils and granulomas
Acute interstitial nephritis
Pt has taken NSAIDs or diuretics → day after they have fever, skin rash, haematuria, proteinuria and eosinophilia
Acute interstitial nephritis
↓Hb ↓plt
↑bilirubin, ↑reticulocytes, ↑LDH
Fragmented RBCs (schistocytes) on blood smear
Coomb’s test negative
HUS or TTP (TTP = more CNS involvement, no renal failure)
Most common cause of chronic renal failure
Diabetes
(2 = glomerulonephritis, 3 = HTN, vascular disease)
US ovaries: ring of fire
Corpus luteal cysts
HISTO: Psammoma bodies
BRCA +ve
Serous epithelial cystadenoma
Histo: mucin secretion
Pseudomyxoma peritonei
Mucinous cystadenoma
Histo: hobnail appearance, clear cells
PMHx: DES exposure in pregnancy, endometriosis
Clear cell epithelial adenoma
testicular seminoma in women
Dysgerminoma
Sex cord ovarian tumour not producing hormones
Fibroma
Fibroma, pleural effusion, ascites
Meig’s syndrome
Raised oestrogen, precocious puberty
Histo: call exner bodies
Granulosa cell tumour
Mucin producing signet cells that affect both ovaries
Mets from GI → krunkenberg tumour
Anti-dsDNA, anti-Sm, anti-smith (most specific)
If drug induced: anti-histone
SLE
Histology: LE bodies, wire loop appearance of the glomeruli, onion skin lesions in the spleen, Libman-Sack endocarditis, small vessel angiopathy
SLE
Histology: raised collagen in the skin and organs, onion skin thickening of arterioles
Limited cutaneous systemic sclerosis
Histo: inflammation within or around muscle fibres with anti-topoisomerase II (Scl-70)
Diffuse cutaneous systemic sclerosis
Histology: endomysial inflammatory infiltrate
Anti-Jo-1 positive
Raised CK
Increased risk of NHL, ovarian, pancreatic malignancy
Dermatomyositis
Histology: “drop out” of capillaries and myofibre damage
Anti-Jo1 positive
Raised CK
Increased risk of NHL, lung and bladder malignancy
Polymyositis
Angiogram: corkscrew appearance from segmental occlusive lesions
Buerger’s disease
Angiography: microaneurysms (string of pearls/rosary bead)
Histology: fibrinoid necrosis and neutrophil infiltration
Hep B +ve
Polyarteritis nodosa
(1) Upper resp tract: sinusitis, epistaxis, saddle nose
(2) Lower resp tract: cavitation, pulmonary haemorrhage
(3) Kidneys: crescentic glomerulonephritis → haematuria & proteinuria
Granulomatosis with polyangiitis
Asthma, allergic rhinitis
Eosinophilia
Later systemic involvement
Eosinophilic granulomatosis with polyangiitis
Pulmonary renal syndrome:
(a) Pulmonary haemorrhage
(b) Rapidly progressive glomerulonephritis
pANCA positive
Microscopic polyangiitis
Histology: non-caseating granulomas, schaumann and asteroid bodies
Sarcoidosis
Raised calcium, raised ECR, raised ACE, restrictive picture on spirometry
Sarcoidosis
