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Year 5 > Histopathology > Flashcards

Histopathology Flashcards

1
Q

Lymphocytes are seen in

A
  • Chronic inflammation

- Sheets of lymphocytes - think lymphoma

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2
Q

Eosinophils are seen in

A
  • Allergy
  • Parasitic infection
  • Hodgkin Lymphoma
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3
Q

Macrophages are seen in

A
  • Late stages of acute inflammation

- Granulomas

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4
Q

Non-caseating granuloma

A

Sarcoidosis

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5
Q

Caseating granuloma

A

TB - stains positive on Ziehl-Neelsen staining

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6
Q

Tumours from epithelial cells

A

CARCINOMAS
- These express cytokeratins

Squamous cell carcinoma
- intercellular bridges and keratin

Adenocarcinoma - from glandular epithelium
- goblet cells and glands

Transitional cell carcinoma

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7
Q

Histological staining types

A

Histochemical - chemical reaction to specific tissue components

Immunohistochemical - antibodies which bind to specific antigens present in the cell

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8
Q

Congo red stain

A

Amyloidosis

Congo red positive and shows apple-green birefringence under polarised light

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9
Q

Prussian blue stain

A

Haematochromatosis (iron overload)

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10
Q

Ziehl-Neelsen staining

A
  • Acid-fast bacilli

- Goes bright red

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11
Q

Imunohistochemical markers

A
  • Cytokeratin - epithelial marker. NO CYTROKERATINS MEANS IT IS NOT A CARCINOMA!
  • CD45 - lymphoid marker
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12
Q

Fontana stain

A

Positive for melanin (turns brown-black)

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13
Q

Differences between parts of stomach

A

The fundus and body have specialised glands which secrete acid and enzymes

the antrum and pylorus have non-specialised glands (gastric pits)

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14
Q

Duodenum - crypts and villi

A
  • The cells proliferate in the crypts and midrate up to the villi
  • Villous:crypt ratio 2:!
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15
Q

Barrett’s oesophagus

A
  • Squamous epithelium of the oesophagus can become relines with metaplastic columnar epithelium (gastric-type epithelium)
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16
Q

Eosophagus - progression to adenocarcinoma

A
  • Barret’s oesophagus is gastric-type epithelium
  • This can go one step further to intestinal-type metaplasia (contains goblet cells)
  • Intestinal type metaplasia carries high risk of cancer BUT it is reversible with the treatment of GORD
  • If there are cytological and histological features of malignancy, but DM not involved, it is dysplasia
  • If there is invasion of the BM, it is adenocarcinoma
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17
Q

Commonest types of oesophageal cancers

A

UK - adenocarcinoma (GORD)

Globally - SCC (smoking, alcohol)

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18
Q

Causes of chronic gastritis

A

ABC

  • Auto-immune (e.g. pernicious anaemia)
  • Bacterial - H. pylori
  • Chemicals - NSAIDs, bile reflux
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19
Q

What feature on stomach biopsy would indicate H.pylori infection?

A

Lymphoid follicles - indicates patient has had H. pylori infection at SOME POINT

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20
Q

Effect of H. pylori on stomach cells

A

Binds to epithelial cell surfaces
injects toxins into cells (such as urease)
These lower the pH in the stomach

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21
Q

Different strains of H. pylori

A

Cag A +ve – needle-like appendage injects toxins into intercellular junctions, so organism can attach more easily

Cag A -ve – associated with severe chronic inflammation

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22
Q

What is the risk of cancer with chronic H. pylori infection?

A

8x increased risk of gastric cancer

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23
Q

Types of cancer that chronic H. pylori can cause

A
  • adenocarcinoma

- lymphoma (MALT)

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24
Q

Causes of gastritis is an immunosuppressed patient

A
  • CMV

- Strongyloides

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25
Q

Definitions:

  • Gastric ulcer
  • Gastric erosion
  • Chronic ulcer
A

Ulcer - loss of epithelial tissue extending deeper than muscularis mucosae

Erosion - loss of epithelial tissue extending up to the lamina propria

Chronic ulcers - have fibrosis

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26
Q

Classification of stomach adenocarcinomas

A
  • Intestinal type - well differentiated, large mucin-containing glands
  • Diffuse type - poorly differentiated cells, not producing glands

SIGNET CELL IS HALLMARK (diffuse type)

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27
Q

Causes of duodenitis

A
  • H. pylori - leading cause (spills over from gastritis)
  • Giardiasis
  • CMV (in immunosuppressed)
  • Cryptosporydiosis
  • Whipple’s disease - very rare
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28
Q

Histological features of coeliac disease

A
  • villous atrophy (damage from T-cell response to gliadin)
  • crypt hyperplasia (to try and replace villi)
  • increased numbers of intraepithelial lymphocytes
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29
Q

Lymphocytic duodenitis

A
  • lymphocytic infiltration of duodenum without architectural changes
  • may cause mild coeliac disease
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30
Q

Duodenal MALToma

A
  • associated with coeliac disease
  • very aggressive lymphoma
  • can manage by treating H. pylori infection and abiding to gluten-free diet
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31
Q

Hirschsprung disease - gene

A

RET proto-oncogene Cr10

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32
Q

Diagnosis of Hirschsprung disease

A

Full thickness biopsy shows hypertrophies nerve fibres with no ganglia

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33
Q

Volvulus sites by age

A

Small children - small bowel

Old people - sigmoid colon

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34
Q

Pseudomembranous colitis

A
  • Acute colitis caused by enterotoxins of C. difficile
  • Associated with antibiotic use
  • There is pseudomembrane formation
  • Histology shoes volcano-like epithelial surface, these are the necrotic pseudomembranous regions filled with pus and inflammatory cells
  • Detection of C. diff on toxin stool assay
  • Tx - metronidazole or vancomycin
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35
Q

Risk of adenocarcinoma with UC?

A

20-30x increased risk

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36
Q

Neoplastic polyps of the colon

A

3 types of neoplastic polyps:

  • Tubular
  • Tubovillous
  • Villous adenoma

With villous adenoma you can get hypoproteinaemic hypokalaemia

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37
Q

Risk factors for polyp - cancer

A
  • Size of polyp
  • Proportion of villous component
  • degree of dysplastic change within a polyp
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38
Q

Familial Adenomatous Polyps

A
  • Autosomal dominant
  • large numbers (min 100) of adenomatous polyps
  • APC gene mutation
  • 100% risk cancer in 10-15 years

Features
- Retinal pigment epithelium hypertrophy at birth

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39
Q

Gardner’s Syndrome

A
  • Same as FAP but with significant extra-intestinal manifestations
  • Osteomas of skull and mandible
  • Epidermoid cysts
  • Desmoid tumours
  • Dental caries, unerupted teeth
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40
Q

Hereditary Non-Polyposis Hereditary Cancer

A
  • Autosomal Dominant
  • Mutation in DNA repair gene, so there are DNA replication erroris
  • High frequency of early onset carcinomas proximal to the splenic flexure
  • There can be extra-colonic cancers
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41
Q

Dukes staging for Bowel Cancer

A

A - confined to bowel wall
B - through the bowel wall
C - lymph node metastases
D - distant metastases

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42
Q

Renal stones

A

75% calcium oxalate - associated with hypercalcURIA

10% triple stones (magnesium ammonium phosphate) - associated with Proteus infection and staghorn calculi

5% uric acid stones - associated with gout and high cell turnover e.g. chemotherapy

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43
Q

Benign renal tumours

A
  1. Papillary adenoma
    - Formed of papillary cells ± tubules
    - <15mm by definition
  2. Renal oncocytoma
    - PINK oncocytic cells
    - Naked eye - mahogany brown with central scar
  3. Renal angiomyolipoma
    - Made of blood vessels, smooth muscle and fat
    - Can be seen in tuberous sclerosis
    - Remove if >4cm
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44
Q

Malignant renal tumours

A
  1. Clear cell renal carcinoma
    - Most common type
    - Clear cells = small round blue cells
    - LEIBOVICH RISK MODEL (risk progression index)
  2. Renal papillary carcinoma
    - Papillary cells
    - >15mm by definition
  3. Chromophobe renal cell carcinoma
    - Different coloured cells
  4. Nephroblastoma
    - Made of 3 layers of tissue: stromal, epithelial and blastoma
    - Children
    - Good prognosis
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45
Q

Bladder cancers

A

Transitional cell carcinomas

  • Most common bladder cancer
  • Associated with smoking and aromatic amines
  • Painless haematuria
  • 3 subtypes: Clear cell transitional carcinoma, Infiltrations transitional carcinoma and flat epithelial carcinoma in situ

SCC
- Associated with Schistosomiasis

Adenocarcinoma
- Rare

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46
Q

Prostate pathology

A

Benign Prostate Hyperplasia

  • Increase in the numbers of cells in the prostate
  • Very common, aetiology unknown
  • Presents with LUTS
  • Mx - alpha-blockers (tamsulosin), 5a=reductase inhibitors (finasteride), TURP

Prostate cancer

  • Develops from prostate intraepithelial neoplasia
  • Risk factors = smoking, FHx, red meat consumption
  • Prognosis - GLEASON SCORE
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47
Q

Testicular pathology

A

Testicular tumours

  • 95% are germ cell tumours and 5% are non-germ cell tumours
  • Most germ cell tumours are seminomas (clear cells)

Other germ cell tumours;

  • Teratoma - can occur at any age, but always pathological in post-pubertal males
  • Embryonal carcinoma
  • Yolk sac tumour
  • Choriocarcinoma

Non-germ cell tumours

  • Leydig cell tumour - precocious puberty
  • Sertoli cell tumours

Epididymitis

  • Associated with N gonorrhoea/C. trachomatis in men <35
  • Men >35 - E. coli
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48
Q

Gold standard for diagnosing breast cancer?

A

Histopathology, because you can see cellular detail AND cellular architecture.

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49
Q

What’s the terminal duct lobular unit?

A

Duct + acinar tissue

All breast cancers arise from here

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50
Q

What are the two layers of epithelium in breast tissue?

A
  • Outer layer = myoepithelium

- Inner layer = luminal cells

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51
Q

Inflammatory breast disease

A

DUCT ECTASIA

  • Inflammation and dilation of breast duct
  • Smoking = biggest risk factor
  • Lump with thick white nipple secretions
  • There can be slit-like nipple retraction
  • Cytology of nipple discharge = proteinaceous material, inflammatory cells

ACUTE MASTITIS

  • Inflammation of breast tissue
  • Associated with lactation(Staphyloccal infection)
  • If not lacating - keratinising squamous metaplasia
  • Painful tender breast
  • Neutrophils
  • Incision & drainage + Abx

FAT NECROSIS

  • Inflammatory reaction to adipose injury e.g. radiotherapy
  • PAINLESS breast lump
  • Giant multinucleate cells
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52
Q

Benign Breast Disease

A

Fibrocystic breast disease

  • Fibrous and cystic changes to breast tissue
  • Changes with cycle
  • Calcification may be seen

Fibroadenoma

  • Fibrosis of stroma and glandular tissue
  • Mouse
  • Generally self-resolving

Phyllodes tumour

  • Leaf-like
  • Malignant potential
  • Pink = benign, purple = malignant

Duct papilloma

  • NO LUMP!!!
  • Central papillomas - arise from large lactiferous ducts
  • Perpheral papillomas - arise from small terminal ductules
  • Central papillomas can give bloody discharge

Radial scar

  • Central scarring surrounded by proliferating glandular mesenchyme
  • Excise, because there can be malignancy at the edges
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53
Q

Proliferative breast disease

A

Usual epithelial neoplasia

  • Proliferation of the epithelial cells
  • No direct increase risk in malignancy
  • Serrated lumen

Atypical ductal hyperplasia

  • Epithelial proliferation - multiple layers of cells
  • Rounded lumen

Atypical lobular hyperplasia

  • Proliferation into the acinar space
  • May not be able to see lumen
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54
Q

Breast cancer - carcinoma in situ

A

30% of breast cancer
- Can be DUCTAL (DCIS) or LOBULAR (LCIS)

Lobular CIS
- Loss of E-adherin

Ductal CIS

  • Areas of calcification
  • Proliferation along the length of the duct
  • Low-grade - cribriform appearance
  • High-grade - only one central lumen, containing necrotic material
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55
Q

Invasive breast cancer

A
  • Invasion through the BM and into the stromal tissue
  • Associated with high lifetime oestrogen exposure and BRCA mutation

Types of invasive breast cancer

  • Ductal
  • Tubular - elongated tubules of cells
  • Lobular - linear arrangement of cells in Indian file pattern
  • Mucinous - lots of mucin production
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56
Q

Breast basal-like carcinoma

A
  • Sheets of atypical cells with predominantly lymphocytic infiltration
  • Associated with BRCA mutations
  • Positive staining for CK5/6, CK14
  • Usually triple-negative
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57
Q

Breast cancer screening

A
  • All women aged 47-73, every 3 years
  • Looks for masses and abnormal calcification
  • If mammogram is abnormal, may need to be recalled for further investigation
  • Triple assessment = examination + USS + FNA/core biopsy
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58
Q

Prognostic factors in breast cancer

A

ER or PR positive - good prognosis (tamoxifen responsive)

Her2 positive - poor prognosis

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59
Q

Hyperpituitarism

A
  • Functional adenoma
  • Most common is prolactinoma
  • Others are GH adenoma (gigantism/acromegaly) or CRH adenoma (Cushing’s syndrome)
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60
Q

Hypopituitarism

A

Causes:

  • Non-secretory adenomas
  • Ischaemic necrosis e.g. Sheehan’s)
  • DIC/shock etc

Clinical manifestations in adults:

  1. Gonadotrophin deficiency - low libido, low fertility, amenorrhea
  2. TSH and ACTH deficiency
  3. Prolactin deficiency - rarely
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61
Q

Thyroid physiology

A

Usual thyroid stuff but also

PARAFOLLICULAR CELLS

  • These produce CALCITONIN
  • Promotes absorption of calcium to increase serum calcium
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62
Q

Hashimoto’s thyroiditis - histology

A
  • Painless enlargement of the thyroid

- There is massive lymphocytic infiltration with HURTHLE CELLS

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63
Q

Thyroid cancer - histology

A

PAPILLARY CARCINOMA

  • Optically clear nuclei
  • Intranuclear inclusions
  • Psammoma bodies

MEDULLARY CARCINOMA

  • Arises from parafollicular C-cells
  • Secretion of calcitonin and CEA
  • AMYLOID DEPOSITION IN THE TUMOUR
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64
Q

3 layers of skin?

A

Top layer = Epidermis (keratinocytes)

Middle layer = dermis (connective tissue and macrophages, mast cells and fibroblasts - fibroblasts produce ECM)

Bottom layer - = subcutaneous fat

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65
Q

6 inflammatory reactions (rashes) of skin?

A
  • Pemphigoid
  • Spngiotic
  • Psoriaform
  • Lichenoid
  • Vasculitis
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66
Q

Vesicobullous skin disease

A

Bullous Pemphigoid

  • DEEP = tense bullae, don’t rupture
  • Complement-driven attack on the BM
  • IgG binds to hemidesmosomes of the BM
  • IgG and C3 along the dermal-epidermal junction

Pemphigus vulgaris

  • SUPERFICIAL = these rupture
  • IgG=mediated damage to keratinocytes with intact BM (acantholysis)
  • Intercellular IgG deposits

Pemphigus foliaceous

  • Thin blister which may not be visible if they have burst
  • IgG-mediated damage to stratum corneum
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67
Q

Spongiotic skin disease

A

Eczema

  • T-cell mediated recruitment of eosinophils
  • Hyperkeratosis with oedema between keratinocytes
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68
Q

Psoriaform skin disease

A

Plaque psoriasis

- Munroe’s microabscesses on microscopy

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69
Q

Lichenoid skin disease

A

LICHEN PLANUS

  • purple plaques on wrists and arms + white striae inside mouth
  • T-cell mediated destruction of deepest later of keratinocytes
  • Band-like lymphocytic infiltrate under the epidermis
  • Sawtoothing of Rete ridges
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70
Q

Vasculitis skin disease

A

Pyoderma gangrenosum

- ULCER WITH CLEAR EDGE

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71
Q

Seborrheic keratosis

A
  • Cauliflower lesion on old people

- Microscopy - horn cysts

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72
Q

Epidermoid cyst

A
  • Non-mobile lump with central punctum

- Keratin forms inside a cyst

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73
Q

Bowen’s disease

A
  • Keratin horns
  • Confined to epidermis, not invading BM
  • Affects sun-exposed areas
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74
Q

Pigmented skin lesions

A

BENIGN JUNCTIONAL NAEVUS
- Expansion of melanocytes at the bottom of the epidermis

COMPOUND NAEVUS

  • Two-tone
  • Melanocytes in dermis and epidermis

MALIGNANT MELANOMA

  • Breslow system for grading
  • Buckshot appearance
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75
Q

How do steroids cause osteoporosis?

A

Reduces osteoclastogenesis
Reduced osteoblasotogenesis
Increased osteocyte apoptosis

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76
Q

Hyperparathyroidism - histological association

A
  • Brown cell tumour

- Multinucleate giant cells (pink cells) in fibrous stroma with haemorrhage

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77
Q

Paget’s disease - histology

A

Cement lines
- Seen in the osteolytic-osteosclerotic phase

Mosaic pattern
- Seen in the quiescent phase

Thickened cortex
Thickened trabeculae

78
Q

Paget’s disease - X-ray

A

Cotton wool appearance

Bowed bone

79
Q

Types of fractures

A

Transverse (simple) fracture - straight across

Compound fracture - bone pierces through skin

Greenstick fracture - one side of bone is broken and the other side is bent

Comminuted fracture - 3+ pieces with fragments

80
Q

What happens in fracture repair?

A

Pro-callus - organisation of haematoma at the site of the fracture

Fibrocartilagenous fracture forms, and then mineralises

Remodelling of bone along weight-bearing lines

81
Q

X-ray changes in osteomyelitis

A
  • X-ray usually normal for first 7-10 days

WEEK 1 - INVOLUCURM
- irregular sub-periosteal new bone formation

WEEK 2 - irregular lytic destruction

82
Q

TB histology

A

CASEATING GRANULOMAS

LANGERHANS GIANT CELLS

83
Q

Osteoarthritis X-ray changes

A
  • Loss of bone space
  • Osteophytes
  • Subchondral sclerosis
  • Subchondral cysts
84
Q

Rheumatoid arthritis - features

A
  • Swan neck
  • Z-thumb
  • Boutonniere’s deformity
  • Pannus formation (abnormal layer of fibrovascular tissue)
  • GRIMLEY-SOKOLOFF CELLS
85
Q

Osteosarcoma

A
  • Bone-producing tumour
  • Peaks in adolescence
  • Codman’s triangle
  • Histology - bone, cartilage and stroma
  • ALP +ve
86
Q

Chondrosarcoma

A
  • Cartilage-producing tumours in axial skeleton
  • Age >40
  • X-ray shows LYTIC LESIONS with FLUFFY CALCIFICATION
  • Ring and arc mineralisation
  • Malignant chondrocytes - purple/blue - found in matrix
87
Q

Ewing’s sarcoma

A
  • t(11;22)
  • Age <20y
  • Joints of long bones but not in knees
  • Lytic lesions
    -ONION SKINNING OF PERIOSTEUM
    SHEETS OF SMALL ROUND BLUE CELLS
  • CD99 +ve, MIC2 +ve, ALP -ve
88
Q

What needle is used for bone biopsy?

A

Jamshidi needle, under USS guidance

89
Q

Features of malignant bone tumours

A
  • No normal marrow tissue
  • Irregular trabecular bone
  • Cartilagenous tissue infiltrates the marrow
90
Q

Fibrous dysplasia

A
  • Young people
  • Femur involved
  • X-ray: SOAP-BUBBLE OSTEOLYSIS
  • Bone Bx: marrow replaced with FIBROUS STROMA
  • SHEPHERD CROOK DEFORMITY if NOF involved
91
Q

Benign bone tumours?

A

Osteochondroma

  • Age 10-20, M>F
  • Cartilagenous surface overlying the normal bone
  • Affects knees and elbows

Endochondroma

  • Cartilganeous proliferation within the bone
  • Hands and feet
  • X-ray - POPCORN CALCIFICATION

Giant cell tumour

  • Borderline malignancy
  • Malignant stromal cells
  • Occurs in the epiphyses and can burst through the bone into surrounding tissue
  • X-ray - lytic lesions
  • Histology - osteoclasts, on a background of spindle cells
92
Q

Name the malignant bone tumours

A
  • Osteocarcoma :(
  • Chondrosarcoma :)
  • Ewing’s sarcoma :/
93
Q

What are the major manifestations of glomerular disease?

A
  • Raised creatinine and urea, as kidneys aren’t filtering these out
  • Haematuria and proteinuria, due to failure of maintaining barrier function
94
Q

What are the 3 layers of the kidney filtration barrier?

A

ENDOTHELIUM - inner layer, fenestrated

GLOMERULAR BASEMENT MEMBRANE - Type IV collagen

PODOCYTES - outer layer, cells have processed with interdigitate to completely cover the BM

95
Q

Immune complex deposition in the kidneys - variation by site?

A

MESANGIUM - some proteinuria, seen on dipstick

SUBEPITHELIAL (between BM and podocytes) - heavy proteinuria ad nephrotic syndrome

SUBENDOTHELIAL (between BM and endothelium) - activates inflammatory cells in the blood – irreversible glomerular damage and scarring

96
Q

How can we detect immune complexes in the kidneys?

A
  • Immunohistochemistry - using fluorescently-labelled IgG

- Electron microscopy - always look at the glomerulus with EM!!!!

97
Q

Polycystic kidney disease

A
  • Autosomal dominant
  • Cysts arise from all portions of the nephron and press on the surrounding parenchyma
  • PKD1 and PKD2 mutations
  • Associated with liver cysts and berry aneurysms
98
Q

Acute tubular necrosis - pathophysiology

A
  • Commonest cause of AKI
  • Damage to tubular epithelial cells (myoglobin, toxins)
  • Cells lose the brush border and cannot reabsorb
  • Some cells are lost into the lumen
  • Surviving cells can compensate at first, but not with repeat attacks
99
Q

Why does GFR drop in ATN?

A
  • Tubule lumens become blocked by casts
  • Fluid leaks from tubules to interstitium
  • Injured tubules send signals to JGA to drop the GFR
100
Q

ATN - Histology

A

Oedema - fluid-filled spaces between the tubules

Flattened tubular morphology

Tubules contain granular material (sloughed-off cells)

101
Q

Characteristic features of acute glomerulonephritis

A

Urine contains casts of RBCs and WBCs

Glomerular crescents - accumulation of cells in bowman’s space, indicates severe and irreversible damage

102
Q

Causes of acute crescenteric glomerulonephritis

A

IMMUNE COMPLEX DEPOSITION

  • Especially subendothelial deposition
  • Seen on immunohistochemistry and EM
  • e.g. IgA nephropathy, SLE

ANTI-GBM DISEASE

  • Antibodies can be detected in circulation
  • Linear deposition of IgG on the Type IV collagen on basement membrane

PAUCI-IMMUNE

  • Scanty deposits of immunoglobulin and complement in the glomeruli
  • Associated with p-ANCA
  • There is glomerular necrosis
  • Associated with vasculitis in other organs e.g. rash
103
Q

Goodpasture’s syndrome

A

Antibodies bind to the Type IV Collagen of basement membrane in kidneys and alveoli

Lung haemorrhage + glomerulonephritis

104
Q

Systemic causes of nephrotic syndrome

A

DIABETES MELLITUS
- Mesangial expansion followed by nodular sclerosis

AMYLOIDOSIS

  • AA (acute phase protein)
  • AL (immunoglobulin light chains, seen in myeloma patients)

SLE
- ANA and anti-dsDNA

105
Q

Primary glomerular disease

A

MINIMAL CHANGE DISEASE

  • LM looks normal
  • EM shows loss of foot processes
  • Generally steroid-responsive

FOCAL AND SEGMENTAL GLOMERULONEPHRITIS

  • More common in adults
  • Glomeruli develop segmental scars

MEMBRANOUS GLOMERULONEPHRITIS

  • Immuno complexes deposit outside of the glomerular basement membrane
  • Associated with autoimmune disease
  • Screen for malignancy in elderly patients
106
Q

Microscopic haematuria

A

THIN BASEMENT DISEASE
- Hereditary defect in Type IV collagen

IgA NEPHROPATHY

  • IgA deposition in glomeruli
  • 30% progress to end-stage renal failure
107
Q

Autoantibodies in SLE

A

ANA = SCREENING TEST

  • Anti-dsDNA
  • Anti-ribonucleoproteins (most specific but not sensitive)
  • Anti-histone antibodies - seen in drug-related SLE
108
Q

Skin pathology in SLE

A
  • Lymphocytic infiltration of the upper dermis
  • Damage to basal epidermic
  • Extravasation of RBCs
  • Immune complex (IgG) deposition at the dermal-epidermal junction
109
Q

Renal pathology in SLE

A
  • Thickened pink glomerular capillary loops, these are clled wire loops
  • Immunofluorescence shows deposition of immune complexes
  • EM shows dark areas of immune complex deposits in the glomerular BM
110
Q

Cardiac pathology in SLE

A
  • Non-infective endocarditis = LIBMAN SACKS

- Presents the same as bacterial endocarditis

111
Q

Diffuse scleroderma

A

ANTI-SCL70

- Truncal skin involved

112
Q

Limited scleroderma

A

ANTICENTROMERE ANTIBODY

  • no truncal involvement
  • this is ‘CREST’ syndrome
113
Q

Initial screening for Scleroderma?

A

ANA screen shows nucleolar pattern immunofluorescence

114
Q

Scleroderma histology

A
  • Increased collagen deposition in dermis
  • Excess collagen in stomach and oesophagus (trichome staining)
  • Onion-skin thickening of the arteries
115
Q

Features of dermatomyositis

A
  • Tender, inflamed muscles

- Gottron’s papules (red rash on knuckles)

116
Q

Features of myositis

A
  • Raised CK

- Proximal muscle weakness and tenderness

117
Q

Sarcoidosis

A
  • Non-necrotising granuloma
  • Langerhans cells (multinucleated giant cells)
  • Histiocytes
  • Lymphocytes

Investigations;

  • Immunoglobulins (hypergammaglobulinaemia)
  • Raised serum ACE
  • Hypercalcaemia
118
Q

Giant cell arteritis

A

“Temporal arteritis”

  • Headaches and jaw claudication in patients aged 50+
  • Temporal artery pulse not palpable
  • ESR and biopsy for diagnosis

Histology

  • Narrowed lumen
  • Granulomas
  • Lymphocytic infiltration of the tunica media

Tx
- High dose steroids

119
Q

Polyarteritis nodosa

A

ASSOCIATED WITH HEP B

  • Necrotising arteritis, most commonly affecting the renal and mesenteric vessels
  • Renal impairment + gut ischaemia

Ix
- Angiogram - beading of vessels

120
Q

Granulomatosis with Polyangiitis

A

3 hallmarks:

  • ENT (nosebleeds, sinusitis and ear problems)
  • LUNGS
  • KIDNEYS

c-ANCA

121
Q

Eosinophilic Granulomatosis with Polyangiitis

“Churg-Strauss disease”

A

Triad:

  • ASTHMA
  • EOSINOPHILIA
  • VASCULITIS

p-ANCA (binds to MPO)

122
Q

2 main mechanisms of cerebral oedema

A

VASOGENIC - disruption of blood-brain barrier

CYTOTOXIC - secondary to cellular injury e.g. hypoxia

123
Q

What water transporter is found in the brain?

A

aqp4 :)

124
Q

Normal flow of CSF in the brain

A
  1. CSF produced in the CHOROID PLEXUS
  2. Flows to the LATERAL VENTRICLES –> 3RD VENTRICLE –> 4TH VENTRICLE
  3. From here, some CSF goes down into the spinal cord but most of it flows into the SUBARACHNOID SPACE
125
Q

Types of hydrocephalus

A

Communicating

  • No obstruction but there is problem with resorption of CSF
  • e.g. INFECTION

Non-communicating
- Obstruction to the flow of CSF

126
Q

What are the three sites of brain herniation?

A

SUBFALCINE

  • Cortex pushed under the FALX CEREBRI of the dura
  • Usually due to SOL

TRANSTENTORIAL
- Medial temporal lobe is pushed through the tentorial notch

TONSILLAR
- Cerebellar tonsil is pushed through the foramen magnum :(

127
Q

Non-traumatic intraparenchymal haemorrhage of the brain

A
  • Haemorrhage into the brain parenchyma, due to rupture of a small vessel
  • Most commonly in BASAL GANGLIA
  • Often due to HTN

Charcot-Bouchard aneurysm = associated with chronic HTN

128
Q

Cavernous angioma

A

Well-defined malformative lesions composed of closely packed vessels with no parenchyma in between

Bleeds can occur with low pressure
Recurrent small bleeds

T2 weighted MRI - TARGET SIGN

129
Q

Sub-arachnoid haemorrhage

A
  • Rupture of berry aneurysm
  • Highest risk of rupture at 6-10mm diameter

Associated conditions:

  • PKD
  • EDS
  • coarctation of the aorta
130
Q

Brain infarct versus brain haemorrhage

A

Infarct:

  • Tissue necrosis
  • Rarely haemorrhagic
  • Permanent damage - no recovery

Haemorrhage

  • Bleeding
  • Dissection of parenchyma
  • Limited tissue damage
  • Partial recovery
131
Q

Contusion

A

Collision of brain with suface of skull, causing bruising of the surface

Rebound of the brain after direct impact can cause CONTRECOUP damage to the opposite side

132
Q

Laceration

A

Rupture of the pia mater

133
Q

Genetic predisposition to brain tumours

A
  • Tuberous sclerosis
  • Li-Fraumeni syndrome
  • von Hippel Lindau syndrome
134
Q

What is the most common type of primary CNS tumour?

A

Glial tumour

135
Q

Glial tumours - classification

A

Circumscribed gliomas - Children

  • Rarely undergo malignant transformation :)
  • Most common type is PILOCYTIC ASTROCYTOMA
  • Others are pleiomorphic xanthoastrocytoma and subependymal giant cell astrocytoma

Diffuse infiltration - Adults

  • Can be astrocytomas or oligodendrocytomas
  • IDH1/2 mutation
  • Become more malignant over time
136
Q

Pilocytic astrocytoma

A
  • Most common primary CNS tumour in children
  • Infratentorial

Genetics:

  • Seen in NF1
  • BRAF mutation

Histological features:

  • Hallmark is piloid (hairy) cell
  • Rosenthal fibres
  • Granular bodies
137
Q

Astrocytomas - location and age?

A
  • Children - cerebellum

- Adults - cerebral hemispheres

138
Q

Natural history of astrocytomas

A

Astrocytomas eventually become glioblastomas

  • de novo gliocytomas are the most frequent and most aggressive form
  • IDH2 mutation
139
Q

What are the main neuroglial cells of the brain?

A

ASTROCYTES
- maintain BBB

EPENDYMAL CELLS

  • Cuboidal/columnar ciliated cells
  • Line the ventricles
  • Regular production and flow of CSF
140
Q

What are the main neuroglial cells of the brain?

A

ASTROCYTES
- maintain BBB

EPENDYMAL CELLS

  • Cuboidal/columnar ciliated cells
  • Line the ventricles
  • Regular production and flow of CSF
141
Q

Histological feature of ependymoma

A

Perivascular Pseudorosette

142
Q

What are the types of glial tumours?

A
  • Astrocytoma
  • Pilocytic astrocytomas
  • Glioblastoma multiforme
  • Oligodendrocytoma
143
Q

Meningioma

A
  • 2nd most common primary intracranial tumour after glioma
  • Patients >40y
  • Causes focal symptoms

Pathophysiology

  • Come from arachnoid mater cells
  • Multiple meningiomas seen in NF2
  • Causes focal symptoms

Histology
- Psammoma bodies

Grading

  • Depends on histology
  • Mitotic activity is an important factor in grading
  • Also brain invasion
144
Q

What do oligodendrocytes do?

A

Produce myelin

145
Q

Glioblastoma multiforme

A
  • Highly malignant
  • MRI - contrast enhancement
  • Histology -. microvascular proliferation + necrosis
  • Genetics - IDH mutation
146
Q

Oligodendroglioma

A
  • Young adults (aged 20-40)
  • Presents with a long history of neuro signs e.g. seizures
  • MRI shows no/little contract enhancement
  • Histology - round cells with clear cytoplasm (fried eggs)
  • Genetics - IDH 1/2 mutation or co-deletion 1p/19q
147
Q

Medulloblastoma

A
  • Common in children
  • Embryonal tumour
  • ALWAYS IN CEREBELLUM

Histology

  • Small round blue cells
  • Very little differentiation
  • HOMER-WRIGHT ROSETTES
148
Q

Neuropathology of Alzheimer’s Disease

A
  • Extracellular plaques (amyloid-beta)
  • Neurofibrilliary tangles
  • Central amyloid angiopathy - proteins deposit in vascular walls
  • Neuronal loss
  • Amyloid precursor protein - cleaved to form amyloid-beta, which is toxic
149
Q

Parkinson’s disease - neuropathology

A
  • Death of dopaminergic cells in substantia nigra
  • Abhorrent metabolism of alpha-synuclein
  • Lewy bodies = collections of alpha-synuclein and beta-amyloid
  • GOLD STANDARD = alpha-synuclein staining

Braak staging is also used for Parkinson’s disease

150
Q

Pick’s Disease

A
  • Fronto-temporal atrophy
  • Disorders of frontal lobe function e.g.executive function

Histology

  • Gliosis
  • Neuronal loss
  • Ballooned neurons
  • Tau-positive Pick’s bodies

Pick’s disease is a 3-R tauopathy

151
Q

Cardiomyopathy

A

DILATED CARDIOMYOPATHY
- Progressive loss of myocytes

HYPERTROPHIC CARDIOMYOPATHY

  • LVH
  • Familial in 50% cases
  • Thickening of the septum causes left ventricular outflow obstruction

RESTRICTIVE CARDIOMYOPATHY

  • Impaired ventricular compliance
  • Can be idiopathic, or secondary to myocardial disease (e.g. amyloid)
  • Normal size heart with big atria
152
Q

Rheumatic valvular disease

A
  • Previous rheumatic fever, with immune cross-reactivity with the cardiac valves
  • Almost always mitral stenosis
  • Button hole valves
153
Q

Causes of aortic regurgitation

A

RIGIDITY

  • Rheumatic disease
  • Degenerative

DESTRUCTION
- Bacterial endocarditis

DISEASE OF AORTIC VALVE RING

  • Dilatation
  • Marfan’s
  • Syphilis
154
Q

Aneurysms

A

TRUE ANEURYSM
- All layers of the wall dilate

FALSE ANEURYSM
- Extravascular haematoma

Causes of aneurysms:

  • Congenital e.g. Marfan’s syndrome
  • Atherosclerosis
  • Hypertension
155
Q

Cardiac failure

A

LEFT-SIDED CARDIAC FAILURE

  • Pulmonary oedema
  • SOB

RIGHT-SIDED CARDIAC FAILURE

  • Peripheral oedema
  • Nutmeg liver
  • Most common cause of right-sided heart failure is left-sided heart failure!

Histology

  • Dilated heart
  • Scarred, thin walls
  • Fibrosis
156
Q

Acute Coronary Syndrome

A
  • Occurs when a stable plaque becomes unstable

- There is often a superimposed thrombus

157
Q

Angina pectoris - definition

A

Transient ischaemia which does not produce myocyte necrosis!

158
Q

Angina pectoris - types

A

STABLE

  • Comes on with exertion
  • Relieved by rest
  • No plaque disruption

UNSTABLE

  • Pain comes on with less exertion or at rest
  • Due to disruption of plaque, with superimposed thrombus

PRINZMETAL

  • Uncommon
  • Due to coronary artery spasm
159
Q

Dressler’s syndrome

A

Pericarditis following MI

160
Q

Myocardial infarction - definition

A

Death of myocardial tissue following prolonged ischaemia

161
Q

Myocardial infarction - histology

A

1-3 days:

  • Coagulation necrosis
  • Loss of nuclei and striations
  • Neutrophil infiltration

10-14 days

  • Granulation tissue
  • Macrophages
162
Q

Reperfusion injury after MI

A
  • When blood flows back into an area of myocardial necrosis, there is oxidative damage, calcium overload and inflammation
  • Causes further injury
163
Q

Acute pancreatitis - causes

A

Most common causes = gallstones (50%) and alcohol (33%)
- These cause duct obstruction

All other causes - direct acinar injury

164
Q

Patterns of injury in acute pancreatitis

A
  • Periductal injury - most common, usually secondary to obstruction
  • Perlobular injury - necrosis at edges of lobules
  • Panlobular injury - develops from periductal or perilobular injury
165
Q

Why does hypocalacaemia occur in acute pancreatitis?

A
  • Release of lipases results in fat digestion and fat necrosis
  • Calcium ions bind to free fatty acids, forming soaps
166
Q

Causes of chronic pancreatitis

A

Metabolic/toxic causes

  • Alcohol (80%)
  • Haemochromatosis

Duct obstruction

  • Gallstones
  • Abnormal duct anatomy
  • Cystic fibrosis

NB drugs do not play a role in chronic pancreatitis!

167
Q

Pancreatic pseudocysts

A
  • Occur in acute and chronic pancreatitis
  • There is necrotic tissue, lined with fibrotic tissue
  • no epithelial lining !
  • Usually contain fluid that is rich with pancreatic enzymes
168
Q

Autoimmune pancreatitis

A

IgG4-POSITIVE PLASMA CELLS

Tx with steroids

169
Q

Pancreatic neoplasms

A

CARCINOMA

  • 85% of all pancreatic cancers are ductal carcinomas
  • Acinar carcinoma

CYSTIC NEOPLASMS - usually benign

  • Seroud cystadenoma
  • Mucinous cystadenoma
170
Q

Pancreatic ductal carcinoma

A
  • Usually at head of pancreas
  • K-RAS MUTATION!!

Ductal carcinoma arises from dysplastic ductal lesions in one of 2 pathways:

  1. Pancreatic Intraductal Neoplasm (PanIN)
  2. Intraductal Mucinous Papillary Neoplasm (IMP)
171
Q

Pancreatic islet cell tumours

A
  • Non-secretory
  • MEN1
  • commonest = insulinoma
  • arises from B-cells and causes hypoglycaemia
172
Q

Chronic cholecystitis

A
  1. Thickened GB wall
  2. Rokitansky Acschoff sinuses
    - Diverticula in the gallbladder
    - Seen in chronic cholecystitis
    - Occur with gallstones
173
Q

PID - Causative organisms

A

Sexually active women - Chlamydia, Gonorrhea

Post-abortion:

  • Staph
  • Strep
  • Coliform
  • Clostridium perfringens
174
Q

Characteristic histological feature of HPV infection

A

Halo around the nucleus (koilocyte)

175
Q

Most common location of fibroids?

A

Intramural

176
Q

Classification of endometrical carcinoma

A

Type 1 (85%)

  • Secretory, endometroid and mucinous
  • Oestrogen dependent
  • Occur with atypical endometrial hyperplasia
  • Low-grade tumours

Type 2 (15%)

  • Serous and clear cell carcinomas
  • Older patients
  • Less oestrogen-dependent - they arise in atrophic endometrium
  • Serous is associated with p53 mutation
177
Q

Types of ovarian cancer

A

Most common is epithelial tumour (95%)

Others:

  • germ cell tumours
  • sex cord tumours
178
Q

Types of teratoma

A

MATURE TERATOMA

  • Benign
  • Mature adult-type tissues e.g. bone, hair, teeth

IMMATURE TERATOMA

  • Malignant
  • Contains embryonic elements (usually neural tissue)
  • Spreads within peritoneal cavity and metastasises to distant organs

MATURE CYSTIC TERATOMA WITH MALIGNANY TRANSFORMATION

  • Rare
  • Most commonly a SCC
  • Any type of tissue in the teratoma can become malignant, so it can become BCC, melanoma, thyroid cancer etc
179
Q

Krukenberg tumour

A
  • Secondary ovarian tumour
  • Comes from gastric or breast cells
  • Mucin-producing signet cells
180
Q

Name the benign bone tumours

A
  • Osteochondroma
  • Endochondroma
  • Giant cell tumour
181
Q

Histological features of Crohn’s disease

A
  • Mouth to anus
  • Transmural

SKIP LESIONS
COBBLESTONE MUCOSA
NON-CASEATING GRANULOMA

The first lesion is an APTHOUS ULCER (rosethorn)
Ulcers join to form SERPENTINE ULCER

182
Q

Non-neoplastic polyps

A

HAMARTAMOUS POLYPS
- These can be JUVENILE POLYPS or PEUTZ-JEHGER SYNDROME

Juvenile polyps

  • Children <5, rectum
  • Malformation of mucosa and lamina propria

Peutz-Jehger syndrome

  • AD
  • mutated LBK1
  • Multiple polyps and macules

HYPERPLASTIC POLYPS

  • Cells build up due to shedding of endothelium
  • Affects middle-aged people
183
Q

Carcinoid Syndrome

A
  • Group of tumours of the ENTEROCHROMAFFIN CELLS
  • These produce 5-HT

Presentation
- Headache, flushing, diarrhoea, bronchoconstriction

Ix - 24h urinary 5HAA
Mx - Ocreotide

184
Q

What are the different types of lung cancer?

A
  • Squamous cell carcinoma
  • Adenocarcinoma
  • Small cell carcinoma
  • Large cell carcinoma
  • Mesothelioma
185
Q

Squamous cell carcinoma - lung

A
  • Associated with smoking
  • Affects central bronchi
  • c-myc/P53 mutations
  • Local spread, late mets
  • Cavitation
  • Hypercalcaemia

HISTOLOGY:

  • Keratinisation
  • Desmosome = intracellular prickles
186
Q

Small cell lung cancer

A
  • Associated with smoking
  • Arises from NEUROENDOCRINE CELLS
  • usually central
  • ECTOPIC ACTH SECRETION

EARLY METS :(

Histology - small poorly differentiated cells

187
Q

Lung adenocarcinoma

A

NON-SMOKER’S CANCER :(

Occurs peripherally with early mets
EGFR MUTATION

GLANDULAR PROLIFERATION
MUCIN PRODUCTION

Cytology - mucin vacuoles

188
Q

Large cell carcinoma

A
  • Large cells
  • Large nuclei
  • Prominent nucleoli
  • Poor prognosis
  • No evidence of squamous or glandular differentation
189
Q

Diffuse alveolar damage

A
  • RDS/ARDS
  • Rapid onset respiratory failure

Post-mortem histology:

  • Heavy, plum-coloured lungs
  • Airless
  • Expanded
  • Firm
190
Q

Histological features of asthma

A
  • Charcot-Leyden crystals

- Curschmann spirals (shed epithelium)

191
Q

Idiopathic pulmonary fibrosis

A
  • Honeycomb fibrosis

- CLUBBING

192
Q

Lung pneumocytes?

A
  • Type 1 = thing alveolar cells, for gas exchange

- Type 2 = produce surfactant

Year 5 (22 decks)

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