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RW Pathology > Histopathology > Flashcards

Histopathology Flashcards

1
Q

Question

A

Answer

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2
Q

Neutrophil appearance + associated with

A

Polymorphonuclear granulocyte, multi-lobular

Marker of acute inflammation

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3
Q

Hyper-segmented neutrophil

A

> 5 lobes

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4
Q

Hallmark of acute inflammation

A

Neutrophils

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5
Q

Lymphocyte appearance

A

Large nucleus, little cytoplasm

Marker of chronic inflammation

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6
Q

Eosinophils appearance

A

Bilobed nucleus, granules

Associated with allergic reactions, parasitic infections, tumours

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7
Q

Mast cells appearance + associated with

A

Granules (histamine)

Associated with allergy and anaphylaxis

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8
Q

Macrophages appearance + associated with

A

Associatted with late acute inflammation (neutrophils arrive first, then macrophages clear debris) AND chronic inflammation (granulomas)

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9
Q

Activated macrophages are called

A

Epitheloid macropphages

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10
Q

Define carcinoma

A

Malignancy tumour of epithelial cells

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11
Q

Define sarcoma

A

Malignant tumour of connective tissue

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12
Q

Features of squamous cell carcinoma

A

Intercellular bridges, Keratin production

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13
Q

Features of adenocarcinoma

A

Mucin production, Glands

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14
Q

Ziehl-Neelsen stain

A

Acid fast bacilli

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15
Q

Prussian blue stain

A

Iron (e.g. haemachromatosis)

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16
Q

Congo Red stain

A

Amyloid (apple green birefringence)

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17
Q

Fontana stain

A

Melanin

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18
Q

+ve for Cytokeratin

A

Epithelium

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19
Q

Types of stains

A

Histochemical stains, Immunohistochemical stains (immunofluorescence, immunoperoxidase)

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20
Q

Immunofluorescence stain

A

Antibody binds to antigen, another antibody with fluorescent tag binds to that antibody

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21
Q

Immunoperoxidase stain

A

Antibody binds to antigen, antibody had a enzyme, if substrate added –> colour change

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22
Q

Composition of bone

A 
Inorganic component (65%) = calcium hydroxyapatite (99% of Ca store in body)
Organic components (35%) = bone cells, bone matrix
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23
Q

Cortical bone vs Cancellous bone

A 
Corticol bone (80%) - appendicular, mechanical and protective function
Cancellous bone (20%) - axial, metabolic function
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24
Q

Define osteon

A

= Haversian system = functional unit of compact Bone

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25
Q

Define Haversian canal

A

= central blood supply for each osteon

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26
Q

Bone cells + function

A

Osteoblasts build bone (small cell, single nucleus)
Osteoclasts consume / resorb bone (large cell, multi-nucleated)
Osteocytes (very small cell)

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27
Q

Osteoclast differentiation

A

Monocytes –> osteocyte precursors –> + RANK ligand + M-CSF –> DDx into osteoclasts
Osteoblasts have osteoprotegrin (OPG) surface protein to block RANK-RANKL interaction –> ↓DDx to osteoclasts

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28
Q

Ix for metabolic bone disease

A

Bone biopsy + histology (thickness, porosity, bone volume)

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29
Q

Osteoporosis - pathogenesis, aetio, Sx, Ix

A

Osteoporosis = loss of bone mass, normal mineralisation
Primary osteoporosis (age, post-menopause) and Secondary osteoporosis (drugs, systemic disease)
↑risk of fractures (low-impact fractures)
DEXA scan (T score 1-2.5 SD below normal = osteopaenia, T score 2.5 below normal = osteoporosis)
Bloods NORMAL in osteoporosis

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30
Q

Osteomalacia - pathogenesis

A

= Vitamin D deficiency = ↓bone mineralisation

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31
Q

X-ray findings in Rickets

A

Bowing of femur/tibia (Rickets)

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32
Q

X-ray findings in Osteomalacia

A

Horizontal fractures in Looser’s zone (pseudofractures)

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33
Q

Types of renal stone seen in hypercalcaemia

A

Calcium oxalate renal stones

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34
Q

Histological finding in Primary hyperparathyroidism

A

Brown cell tumour = multinucleate giant cells, due to ↑osteoclast activity (primary hyperparathyroidism)
Osteitis fibrosa cystica (= marrow fibrosis + cysts = Brown tumour)

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35
Q

X-ray finding in Primary hyperparathyroidism

A

Brown’s tumours
Salt and Pepper skull
Subperiosteal bone resorption in phalanges

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36
Q

Paget’s disease - pathogenesis

A

Paget’s disease = disorder of bone turnover

(1) Osteoclasts consume bone
(2) Osteoclasts consume bone + Osteoblasts build bone
(3) Quiescent phase –> Mosaic pattern

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37
Q

Paget’s disease - Sx

A

Bone pain
Microfractures
Nerve compression –> deafness

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38
Q

Site predilection in Paget’s disease

A

Lumbar spine, Skull

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39
Q

Complication of Paget’s disaese

A

1% risk of osteosarcoma

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40
Q

Bloods in Paget’s disase

A

↑↑ALP

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41
Q

X-ray finding in Paget’s disease

A

Cotton wool appearance

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42
Q

Histological finding in Paget’s disease

A 
Mosaic pattern (jigsaw puzzple like pattern of lamellar bone)
Huge osteoclasts (>100 nuclei)
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43
Q

Types of fractures

A 
Simple = bone fracture only, no damage to surrounding tissue
Compound = broken bone pierces skin
Greenstick = bone bends and breaks (children)
Comminuted = break in bone into more than 2 fragments
Impacted = broken ends of bone forced together
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44
Q

Stages of fracture repair

A

Haematoma –> fibrocartilaginous callus (replaced with hyaline cartiage) –> mineraliastion –> re-modelling (along weight-bearing lines)

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45
Q

Osteomyelitis organisms

A

Adults: S aureus (90%), E coli, Klebsiella, Salmonella
Children: H influezena, Group B strep
Rarer causes - TB (immunocompromised), syphilis (congenital/acquired)
Route of infection: haematogenous, direct extention, traumatic

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46
Q

Sx of osteomyelitis

A

Fever, Pain, Swelling, Redness, Heat, Loss of function

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47
Q

X-ray findings in Osteomyelitis

A

(from 10 days post-onset)
Mottled rarefaction
Lifting of periosetum
Lytic destruction of bone

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48
Q

Histological finding in osteomyelitis

A

Fibrosis, Chronic inflammatory cells (lymphocytes, histiocytes)

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49
Q

Histology of Pott’s disease / TB ostemyelitis

A

Multi-nucleated Langhans giant cells (horseshoe nuclei, granulomas)

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50
Q

Organism causing Syphilis

A

Treponema pallidum

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51
Q

Organism causing Lyme disease

A

Borrelia burgdorferi (found in ticks)

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52
Q

Lyme disease - Sx, Tx

A

Erythema chronicum migrans
Arthritis
Tx with ABx

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53
Q

Osteoarthritis - pathogenesis

A

Degenerative joint disease

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54
Q

Sites of predilection for Osteoarthritis

A

Knee, Hip, Vertebrae

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55
Q

Characteristic deformities of Osteoarthritis

A

Heberden’s nodes (DIPJ)

Bouchards’s nodes (PIPJ)

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56
Q

X-ray findings in Osteoarthritis

A 
LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis
Subchondral cysts
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57
Q

Histology in Osteoarthritis

A

Irregular arterticular surface
Signs of inflammation
Cartilage degeneration
Abnormal matrix calcification

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58
Q

Characteristic deformities of RhA

A 
Symmetrical deformities
Radial deviation of wrist
Ulnar deviation of fingers
Swan neck
Boutonniere deformity
Z shaped thumb
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59
Q

Sites of predilection for RhA

A

Small joints of hands and feet, wrist, elbow, ankles, knees

Sparing DIPJ

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60
Q

Ix in RhA

A

RhF +ve (80%), ↓Hb, ↑ESR

Anti-CCP antibodies

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61
Q

What is rheumatoid factor

A

Anti-IgG IgM

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62
Q

Histology in RhA

A

Proliferative synovitis
Pannus
Grimley-Sokoloff cells (multi-nucleate giant cells, similar to Langhans, but no horseshoe nucleus)

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63
Q

Gout vs Pseudogout

A

GOUT: monosodium urate crystals, needle-shaped, negative birefringence, perpendicular to axis of red compensator
PSEUDOGOUT: calcium pyrophosphate crystals, rhomboid shaped, positive birefringence, parallel to axis of red compensator

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64
Q

Sx of bone tumour

A

Pain, swelling, deformity, pathological fractures

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65
Q

Ix for bone tumours

A

X-ray

Jamshidi needle core biospy under radiological guidance

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66
Q

Benign bone tumours

A 
Bone differentiation
------- Osteoid ostoma
------- Osteoma
------- Osteoblastoma
Cartilaginous differentiation
------- Osteochondroma
------- Enchondroma
------- Chondroblastoma
Other
------- Fibrous dysplasia
------- Simple bone cyst
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67
Q

Fibrous dysplasia - pathogenesis

A

Bone replaced by fibrosis tissue

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68
Q

Fibrous dysplasia is associated with

A

McCune-Alright syndrome (polyostotic dysplias, café au lait spots, precocious puberty) is associated with Fibrous dysplasia

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69
Q

X-ray finding in Fibrous dysplasia

A

Soap-bubble osteolysis

Shepherd’s crook deformity

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70
Q

Histological finding in Fibrous dysplasia

A

Chinese letters (mis-shappen bone trabeculae)

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71
Q

Most common benign bone tumour

A

Osteochondroma

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72
Q

Osteochondroma - Pathogenesis, Sx

A

Cartilaginous surface overlying normal cortical/trabecular bone (cartilage capped bony outgrowth)
Swelling at end of long bone (near tendon attachment sites)

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73
Q

Histology of Osteochondroma

A

Cartilage capped bony outgowth

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74
Q

X-ray findings for Osteochondroma

A 
Bony protuberance from bone
Mushroom appearance (cartilage capped bony spur on surface of bone mushroom on X-ray)
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75
Q

Enchondroma - pathogenesis

A

Benign tumour of cartilage –> cartilaginous proliferation within bone
Often affects hands and feet (ENDS)

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76
Q

Enchondroma is associated with

A

Ollier’s syndrome and Maffuci’s syndrome

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77
Q

X-ray findings of Enchondroma

A

Cotton wool calcification / Popcorn calcification
Lytic lesions
O ring sign

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78
Q

Histology of Enchondroma

A

Proliferation of normal cartilage

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79
Q

Osteoma - pathogenesis

A

Bony outgrowths attached to normal bone

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80
Q

Osteoma is associated with

A

Associated with Gardner syndrome (GI polyps, osteomas, epidermoid cysts)

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81
Q

Histology of Osteoma

A

Normal bone

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82
Q

Osteoid osteoma - Sx

A 
Small benign bone-forming lesion
Night pain (relieved by aspirin)
Common in Adolescents
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83
Q

Histology of Osteoid osteoma

A

Normal bone (arises from osteoblasts)

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84
Q

X-ray of Osteoid osteoma

A

Bull’s eye sign (radiolucent nidus with sclerotic rim) found in osteoid osteoma
(Tip: bull’s eye is surrounded by rings, ∴osteoid osteoma)

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85
Q

Osteoblastoma - Sx

A

Same as Osteoid osteoma

  • Small benign bone-forming lesion
  • Night pain (relieved by aspirin)
  • Common in Adolescents
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86
Q

X-ray findings in Osteoblastoma

A

Speckled mineralisation (multiple bone cells diffusely ↑mineralisation?)

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87
Q

Simple bone cyst - Sx + X-ray

A

Fluid-filled unilocular cyst

Well defined lytic lesion

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88
Q

Primary bone tumours (malignant)

A

Osteosarcoma
Chondrosarcoma
Ewing’s sarcoma
Gaint cell (borderline malignancy)

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89
Q

Histology of Giant cell tumour

A

Well-dermacated, expansile lesions close to surface (can easily burst throug cortex into surroudings)
Osteoclast giant cells (non-neoplastic)
Background of spindle or ovoid cells - stromal cells (neoplastic)

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90
Q

X-ray of Giant cells

A

Lytic lesions right up to articular surface

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91
Q

Most common malignant bone tumour

A

Metastases (breast, prostate, lung, kidney, thyroid, neuroblastoma)

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92
Q

Most common primary bone sarcoma

A

Osteosarcoma

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93
Q

Site of predilection for Osteosarcoma

A

Knee

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94
Q

X-ray of Osteosarcoma

A

Codman’s triangle = elevated periosteum (periosteum usually runs along outer surface of bone, sclerotic/lytic lesions pushes periostem up)
Sunburst appearance

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95
Q

Histology of Osteosarcoma

A

Malignant mesenchymal cells +/- bone or cartilage formation

ALP +ve (Touch preparation)

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96
Q

Staining for ALP

A

Touch preparation

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97
Q

Chondrosarcoma - pathogenesis

A

Chondrosarcoma = malignant cartiagle producing tumour

> 40 years old

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98
Q

Site of predilection for Chondrosarcoma

A

Pelvis

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99
Q

X-ray of chondrosarcoma + epidemiology

A

Lytic lesion with Fluffy calcification

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100
Q

Histology in Chondrosarcoma

A

Malignant chondrocytes

Atypical cartilage formation

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101
Q

Ewing’s sarcoma is also known as

A

Peripheral primitive neuroectodermal tumour (PPNET) = Ewing’s sarcoma

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102
Q

Sites of predilection for Ewing’s sarcoma

A

Diaphysis of long bones

Pelvis

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103
Q

X-ray appearance of Ewing’s sarcoma

A

Onion skinning of periosteum

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104
Q

Histology of Ewing’s sarcoma

A

Sheets of small round cells

Lifting of periosteum

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105
Q

Molecular diagnosis in Ewing’s sarcoma

A

t(11;22) –> EWS/Fli1 fusion protein

Anti-CD99 antibody (against MIC2)

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106
Q

Elevated periosteum if found in (3)

A

Found in osteomyelitis, osteosarcoma (if in Codman’s triange) and Ewing’s sarcoma

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107
Q

Triple assessment

A

Examination
+ Imaging (mammography / USS / MRI)
+ Biopsy (FNA, Cytology)

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108
Q

Cytopathology codes for breast lump biopsy

A 
C1 = inadequate
C2 = benign clusters of cells
C3 = atypia
C4 = suspicious of malignancy
C5 = malignant
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109
Q

Inflammatory breast conditions

A

Duct ectasia
Acute mastitis
Fat necrosis

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110
Q

Duct ectasia - Sx, Ix

A

Inflammation of breast ducts
Thick, white nipple secretions
Breast pain, Breast mass, Nipple retraction
Cytology: Pink proteinaceous material, ductal distention, inflammatory cells

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111
Q

Acute mastitis

A

Milk stasis –> acute inflammation in lactating women
+/- Bacterial infection (Staph - most common, Strep)
Large, lumpy breast
Painful, red breast
Cytology: Neutrophils, Necrotic material

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112
Q

Fat necrosis

A

Trauma –> Damage to adipose tissue
Hard, firm lump
Painless breast mass
Cytology: large, empty spaces of fat + surrounded by gaint cells

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113
Q

Benign proliferative breast conditions (3)

A

Fibrocystic disease
Fibroadenoma
Gynaecomastia

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114
Q

Fibrocystic disease

A

Breast lump

Histology: Fibrosis + Cystic changes, Calcification, Thinner secretions (c.w. ductal ectasia)

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115
Q

Fibroadenoma

A

Well-circumscribed, mobile, bresat lump (breast mouse)
Histology: ↑number of acini per lobule (adenosis) –> glands compressed into “slit-like” spaces
- Overgrowth of stroma + glandular ducts
“Shelling out” is curative

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116
Q

Gynaecomastia

A

↑oestrogen in males –> enlargement of male breast
Histology: Epithelial hyperplasia, finger-like projections into ducts
No risk of malignancy

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117
Q

Benigh neoplastic conditions (5)

A 
Intraductal papilloma
Radial scar
Usual epithelial hyperplasia
Atypical ductal hyperplasia
In situ lobular neoplasia
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118
Q

Intraductal papilloma

A

Benign papillary tumour arising from the breast ducts (terminal ducts –> peripheral papilloma, larger ducts –> central papilloma)
Central papilloma –> Bloody discharge, no lump
Peripheral papilloma –> asymptoamtic
Associated with malignancy

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119
Q

Radial scar

A

Benign sclerosing lesion with central zone of scarring and radiating zone of proliferating glandular tissue
Mammogram: Stellate masses (resembles carcioma on mamorgram)
Histology: central stellate fibrous area with prolifeartion of ducts and anini

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120
Q

Usual epithelial hyperplasia (UEH)

A

Histology: Growth of glandular tissue –> form fronds, Irregular lumen, Bridges
NOT a precursor lesion for invasive breast carcinoma

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121
Q

Atypical ductal hyperplasia

A

Precursor to low-grade DCIS

Histology: multi-layered cells, punched out holes within proliferation)

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122
Q

Lobular in situ neoplasia (LCIS)

A

ALWAYS incidental finding on biopsy (since no calcifications, no stromal reactions)
Histology: solid proliferation WITHN acinar lobule
Loss of e-Cadherin and single chain file cells
Risk factor to subsequent invasive breast cancer

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123
Q

Malignanct breast disease (4)

A

Ductal carcinoma in situ
Invasive breast carcinoma
Basal-like carcinoma
Phyllodes tumour

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124
Q

Ductal carcinoma in situ (DCIS)

A

DCIS is NOT invasive
Microcalcification within lumen
Lump, Nipple discharge, Paget’s disease of nipple (eczematous change)
If untreated, high risk of progression to invasive breast carcinoma

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125
Q

Invasive breast cancer

A

DCIS or LCIS invades through basememnt membranes
Associated with ↑ oestrogen exposure
Associated with BRCA mutation (85% lifetime risk)

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126
Q

Histological categories for invasive breast cancer

A 
Ductal carcinoma (island of cells) - most common
Lobular carcinoma (linear arragement = Indian File Pattern)
Tubular carcinoma (tubules)
Mucinous carcinoma (produce mucin)
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127
Q

Basal-like carcinoma

A

Sheets of pleimorphic cells

Prominent lymphocytic infiltrate

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128
Q

Breast cancer screening

A

Age 47 - 73 (every 3 years) –> Mammogram (detect DCIS or early invasive breast cancinomas) - calcifications, lumps
If abnormal –> biopsy

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129
Q

Histological grading (Bloom-Richardson Grading)

A

Score out of 3 for each of Tubules, Nuclear pleomorphism, Mitotic activity
3-5 points = Well differentiatied (grade 1)
6-7 points = Moderately differentiated (grade 2)
8-9 points = Poorly differentiated (grade 3)

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130
Q

Breast cancer - assess for receptor status

A 
Oestrogen receptor (ER) - good prognosis (respond to Tamoxifen)
Progesterone receptor (PR) - good prognosis (respond to Tamoxifen)
HER2 status - bad prognosis
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131
Q

Phyllodes tumour

A

Left-like, fibroepithelial neoplasm
Enlarging mass
Cytology: overlapping cells, all smudged
Histology: Leaf like fronds / Artichoke-like appearance
Majority behave like fibroadenomas (borderline phyllodes)
Small proportion are aggressive (malignant phyllodes)

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132
Q

Plical fusion

A

Complication of salpingitis, resulting in fallopian tubes adhering to ovary

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133
Q

2nd most common cancer affecting women worldwide

A

Cervical cancer

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134
Q

Transformation zone

A

Area where columnar epithelium transforms into squamous cells (area is susceptible to malignant change)

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135
Q

CIN1

A

Lower 1/3 of epithelium (next to BM)

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136
Q

CIN2

A

Middle 1/3 of epithelium (i.e. 2/3)

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137
Q

CIN3

A

Full thickness

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138
Q

Cervical cancer

A

Through BM

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139
Q

FIGO Cervical cancer

A 
1 = Cervix
2 = Upper 2/3 of vagina
3 = Lower 1/3 of vagina + pelvic side wall
4 = Distant mets (bladder, rectum, distant mets)
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140
Q

Types of cervical cancer

A

Squamous cell carcinoma (from CIN)

Adenocarcinoma (from CGIN)

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141
Q

HPV proteins + action

A

E7 –> inactivates Retinoblastoma gene (TS)

E6 –> inactivates p53 (TS)

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142
Q

Characteristic cytological features in HPV infection

A

Koilocyte = large, irrecular, well-defined peri-nuclear halos = HPV vacuole

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143
Q

Name of HPV vaccine

A

Gardasil (quadrivalent - HPV 6, 11, 16, 18)

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144
Q

Most common type of uterine tumour

A

Fibroid (leiomyoma), no risk of malignancy

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145
Q

Leiomyosarcoma

A

Malignant counterpart to fibroid (leiomyoma), but arises de novo, post-menopausal women

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146
Q

Causes of endometrial hyperplasia

A 
Peri-menopausal
Persiant anovulation
PCOS
Granulosa cell tumour
Unpposed oestrogen therapy
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147
Q

Type 1 Endometrial cancer

A

(85%) Younger patients, Associated with atypical endometrial hyperplasia

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148
Q

Type 2 Endometrial cancer

A

(15%) Older, post-menopausal women, arise from atrophic endometrium

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149
Q

FIGO staging endometrial cancer

A 
1 = Endometrium
2 = Cervix
3 = Adnexae
4 = Distant mets
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150
Q

Complete vs Partial mole

A

Complete mole = diploid DNA, empty egg + 2 sperm

Partial mole = triploid DNA, normal egg + 2 sperm

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151
Q

Which types of mole has a risk of malignancy

A

Complete moles –> invasive mole

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152
Q

Types 1 Ovarian tumour

A

Low grade, indolent tumour
Precusor lesion = BOT and endometriosis
Includes serous, endometrioid, mucinous, clear cell carcinoma

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153
Q

Type 2 Ovarian tumour

A

High grade + aggressive

No precursor lesions

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154
Q

FIGO staging ovarian cancer

A 
1 = limited to Ovary
2 = limited to Pelvis (uterus, tubes, other pelvic organs)
3 = limited to Abdomen
4 = Distant mets
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155
Q

Most common type of ovarian tumour

A

Serous tumour

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156
Q

Ovarian tumours associated with endometriosis

A

Endometrioid tumour, Clear cell carcinoma

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157
Q

Which ovarian tumours secrete hormones

A

Sex cord stromal tumours
Granulosa –> oestrogen
Thecoma –> oestrogen
Sertoli-Leydig cell –> androgens

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158
Q

Signet ring cells in ovary

A

Krukenberg tumours = metastases to ovary, composed of mucin-producing signet rings cells

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159
Q

Paget’s diisease of vulva

A

Adenocarcinoma in situ, low risk of progression to invasive adenocarcinoma

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160
Q

BRCA-associated tumours

A

Breast and Ovarian (serous)

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161
Q

HNPCC-associated tumours

A

Colorectal, Endometrial cancer, Ovarian cancer (mucinous, endometrioid)

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162
Q

Posterior pituary hormones

A

Supraoptic + Paraventricular nuclei release ADH/Vasopressin and Oxytocin

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163
Q

Most common type of pitutiary adenoma

A

Prolactinoma (20%), Non-functioning (20%)

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164
Q

Prolactinoma Sx

A

Amenorrhoea, Galactorrhoea, Loss of libido, Infertility

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165
Q

GH pituitary adenoma

A

Gigantism in pre-pubertal children
Acromegaly in Adults
DM, HTN, Muscle weakness

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166
Q

Corticotroph cell adenoma

A

Cushing’s disease

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167
Q

Causes of Hypo-pit

A

Non-secretory pituitary adenoma
Ischaemic necrosis (sheehan’s)
Surgery
Irradiation

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168
Q

What do parafollicular C cells produce

A

Calcitonin

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169
Q

Most common cause of goitre worldwide

A

Iodine deficiency

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170
Q

Causes of hyperthyroidism

A

Primary - Graves’, multi-nodular goitre, adenoma, thyroiditis
Secondary - TSH-secreting pitutiary adenoma

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171
Q

Auto-antibody in Graves’

A

Anti-TSH receptor antibody

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172
Q

Auto-antibody in Hashimoto’s thyroiditis

A

Anti-thyroglobulin Ab and Anti-TPO antibody

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173
Q

Histology in Hashimoto’s thyroiditis

A

Infiltration with lymphoid cells
Presence of germinal centre within the thyroid
Hurtle cells = characteristic eosinophils

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174
Q

4 types of thyroid cancer

A

Papillary (most common), Follicular, Medullary, Anaplastic

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175
Q

Histology of Papillary carcinoma

A 
Non-functional thyroid carcinoma
Papillary architecture
Psammoma bodies (foci of calcification within cells)
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176
Q

Histology of Follicular carcinoma

A

Follicular morphology, similar to normal thyroid

Minimal invasion

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177
Q

Histology of Medullary carcinoma + what hormone

A

Derived from parafollicular C-cells

Secretes Calcitonin

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178
Q

Stain for medullary carcinoma

A 
Congo Red (stains for amyloid)
Excess calcitonin broken down into amyloid
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179
Q

Histology + prognosis Anaplastic carcinoma

A

Aggressive, metastasises early, death within 1 year

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180
Q

Causes of adrenal insufficiency

A

(Primary) Acute - stopping long-term corticosteroid therapy, haemorrhage into adrenals, Sepsis with DIC (waterhouse-friderichson syndrome)
(Primary) Chronic = Addion’s disease (TB, autoimmune, mets, amyloid)
Secondary - ↓ ACTH (non-functional pitutiary adenoma, pituitary infarction)

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181
Q

Features of SLE

A

SOAP BRAIN MD (4 out of 11 required)
Serositis (recurrent pleutric chest pain, recurrent abdo pain)
Oral ulcers
Arthritis
Photosensitivity
Blood disorders (AIHA, ITP, leucopenia) - ∑classical complement deficiency
Renal involvement (proteinuria, haematuria) / Raynaud’s
ANA +ve
Immune antibodies (anti-dsDNA, anti-Smith antibodies, anti-histone antibody - in drug-induced SLE) - Type III hypersensitivity
Neuro symptoms
Malar rash
Discoid rash

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182
Q

Most common auto-antibody in SLE

A

ANA (95%), others include anti-dsDNA, anti-Smith

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183
Q

Skin immunofluorescence in SLE

A

Immune-complex deposition along the dermis-epidermis junction

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184
Q

Lupus erythematous cell (LE cells)

A

= denatured nuclei found in serum, engulfed by neutrophils

Old test, now superseded by ANA

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185
Q

Histology of lupus nephritis

A

Wire loop capillaries (thickening) - due deposition of immune complexes within GBM

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186
Q

Scleroderma = Systemic sclerosis - pathogenesis

A

Excess fibrosis + excess collagen –> tight skin

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187
Q

Auto-antibodies in Diffuse scleroderma

A

Anti-topoisomerase antibody (Anti-Scl70)

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188
Q

Auto-antibodies in Limited scleroderma

A

Anti-centromere antibody

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189
Q

Diffuse vs Limited SS

A

Diffuse scleroderma has truncal involvement, associated with pulmonary HTN
Limited scleroderma has NO truncal involvement (limited to distal to elbows and knees) + CREST features, associated with pulmonary fibrosis

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190
Q

CREST features

A

Calcinosis, Raynaud’s, Esophageal dysmotility, Sclerodactyly, Telangiectasia
Calcinosis = Calcium deposits
Sclerodactyly = tightening of skin on fingers

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191
Q

Histology of Limited SS

A

Collagen deposits in epidermis
Trichrome staining (2 acids + polyacid dye) –> red staining of muscle, blue staining of collage
Onion skin thickening of arterioles

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192
Q

Histology of Diffuse SS

A

Inflammation within or around muscle fibres

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193
Q

Speckled pattern (of ANA)

A

Seen in Sjogren’s syndrome and Mixed connective tissue disease

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194
Q

Dermatomyositis vs Polymyositis

A

Similar features - proximal muscle weakness, ↑CK, abnormal EMG
Dermatomyositis has skin features - Heliotrope rash, Gottron’s papules

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195
Q

Auto-antibody in Polymyositis

A

Anti-Jo-1

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196
Q

Auto-antibody in Dermatomyositis

A

Anti-Jo-1

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197
Q

Hallmark of Sarcoidosis

A 
Non-caseating granuloma
Schaumann bodies (inclusions of protein)
Asteroid bodies (inclusions of calcium)
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198
Q

Features of sarcoidosis

A

Bilateral hilar lymphadenopathy (DDx: sarcoidosis, TB, lymphoma, bronchial cancer)
Erythema nodosum
Lupus pernio
Arthritis
Lymphadenopathy
Uveitis
Hepatosplenomegaly
Hypergamaglobulinaemia
↑ ACE (due to abnormalities in lung where ACE is made)
Hypercalacemia (due to ectopic hydroxylation of Vitamin D)

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199
Q

Large vessel vasculitis (2)

A

Takayasu’s arteritis

Temporal arteritis

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200
Q

Medium vessel vasculitis (3)

A 
Polyarteritis nodosa (PAN)
Kawasaki
Thrombangitis obliterans (Buerger's disease)
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201
Q

Small vessel vasculitis (4)

A

Wegener’s granulomatosis
Churg-Strauss
Microscopic polyangiitis
Henoch-Schonlein purpura

202
Q

Takayasu’s arteritis

A

Absent pulses, Japanese women, Claudication

203
Q

Temporal arteritis

A

Elderly, scalp tenderness, temporal headache, jaw claudication, ↑ ESR, Skip lesions, granulomatous transmural inflammation

204
Q

Polyarteritis nodosa

A

Multiple beads of vessels (microaneurysms on angiography)
Focal arteritis
Renal involvement common

205
Q

Kawasaki’s disease

A

Fever, Conjunctivitis, Rash, Cervical adenopathy, Strawberry tongue, Hands and feet swollen, coronary artery aneurysm

206
Q

Buerger’s disease

A

Heavy smoker, Corkscrew appearance on angiogram (segmental occlusive lesions), arteritis of extremities (tibial, radial)

207
Q

Wegener’s granulomatosis =

A

Granulomatosis with polyangiitis

208
Q

Wegener’s granulomatosis auto-antibody

A

c-ANCA (against proteinase 3)

209
Q

Wegener’s granulomatosis TRIAD

A

Upper resp tract: saddle nose, sinusitis, nosebleeds
Lower resp tract: pulmonary haemorrhage
Renal: crescentic glomerulonephritis

210
Q

Churg-Strauss =

A

Eosinophilic granulomatosis with polyangiitis

211
Q

Churg-Strauss Sx

A

Asthma, Eosinophilia, Vasculitis

212
Q

Churg-Strauss auto-antibody

A

p-ANCA (against myeloperoxidase)

213
Q

Microscopic polyangiitis

A

Pulmonary-renal syndrome = pulmonary haemorrhage + glomerulonephritis
also p-ANCA +ve

214
Q

Henoch-Schonlein purpura

A 
IgA mediated vasculitis
Children < 10 years old
Preceding URTI
Palpable purpuric rash (lower limb extensors + buttocks)
Colicky abdo pain
Glomerulonephritis
215
Q

Steps of atherosclerosis

A

Endothelial injury
LDL enter sub-intimal space and oxidised
Macrophages take up oxidised LDL –> Foam cells
Apoptosis of foam cells –> cholesterol core
↑adhesion molecules for more macrophages and T cells to enter plaque
Vascular smooth muscle form fibrous cap

216
Q

Earliest lesion of atherosclerosis

A

Fatty steak

217
Q

Where do atherosclerotic plaques tend to occur

A

Points of disturbed flow, Branched points

Laminar flow is protective

218
Q

Types of acute plaque changes

A

Rupture, Erosion, Haemorrhage

219
Q

Point of critical stenosis

A

70% occlusion or <1mm diameter –> stable angina

220
Q

Types of angina

A

Stable angina = pain with exertion, relieved with rest
Unstable angina = pain at rest
Prinzmetal angina = coronary artery spasm –> narrowing

221
Q

Coronary arteries + % affected by occlusion

A

LAD (50%) - LV anterior wall, anterior septum, apex
RCA (40%) - LV posterior wall, posterior septum, posterior RV
LCx - LV lateral wall

222
Q

Order of cell entry to MI

A

Neutrophils, Macrophages, Angioblasts, Fibroblasts

223
Q

Histology of MI over time

A

< 6 hr: normal histology
6-24hr: loss of nuclei, necrotic cell death
1-4 days: neutrophils, then macrophages (clear up debris)
1-2 weeks: granulation tissue, myofibroblasts
Weeks-months: decellularising scar tissue

224
Q

Reperfusion injury

A

Area of necrosis suddenly starts receiving blood –> electrolyte imbalance –> arrhythmia

225
Q

Dressler syndrome

A

Post-MI pericarditis (days-months)

226
Q

Define sudden cardiac death

A

Unexpected death from cardiac cause in individual without cardiac symptoms or death within 1 hour of cardiac symptoms
90% have atherosclerosis
Commonly due to arrhythmias (VF)

227
Q

Common cause of cardiac death after MI

A

Arrhythmia (90% post-MI)

228
Q

Congestive heart failure

A

R heart failure + L heart failure

229
Q

Signs of L heart failure

A

SOB + pulmonary oedema

230
Q

Signs of R heart failure

A

Peripheral oedema
Ascites
Nutmeg liver

231
Q

Dilated cardiomyopathy

A

Loss of myocytes –> dilated heart (idiopathic)

232
Q

HOCM

A

LV hypertrophy due to thickening of septum –> narrows LV outflow (50% familial)

233
Q

Restrictive cardiomyopathy

A

Normal sized heart, too stiff, idiopathic or secondary to amyloidosis or sarcoidosis

234
Q

Acute rheumatic fever - pathogenesis + Tx

A

2-4 weeks after Group A strep infection (molecular mimicry)

Tx: Benzylpenicillin

235
Q

Acute rheumatic fever - Sx

A 
CASES (Jones' major criteria) - 2 major criteria
Carditis
Arthritis
Sydenham's chorea (St Vitus Dance)
Erythema marginatum
Subcutaneous nodules
236
Q

Histology of Acute rheumatic fever

A 
Beady fibrous vegetations (verrucae)
Aschoff bodies (small giant cell granuloma)
Anitschkov myocytes (regenerating myocytes)
237
Q

Rheumatic heart disease - valve

A

Mitral stenosis (70%)

238
Q

Cause of aortic stenosis

A

Calcification

239
Q

Causes of aortic regurgitation

A

Rheumatic heart disease, Endocarditis (destorys it), Marfans

240
Q

True aneurysm

A

All layers of wall involved

241
Q

False aneurysm

A

Extravascular haematoma (due to hole in artery which enables exsanguination)

242
Q

Types of endocarditis + characteristic vegetations

A

Rheumatic heart disease: warty vegetations (verrucae)
Infective endocarditis: irregular masses on valve cusps
Non-bacterial thrombotic endocarditis (DIC): small vetations attachment to lines of closure (thrombi)
Libman-Sacks endocarditis (SLE, anti-phospholipid syndrome): small warty vegetations, sterile, platelet rich

243
Q

Acute infective endocarditis

A

Staph aureus / Strep pyogenes, high virulence, large vegetation

244
Q

Subacute infective endocarditis

A

Strep viridans, Staph epidermis, low virulence, small vegetation

245
Q

Which valves affected in IVDU

A

R sided valves

246
Q

Signs of IE

A

Fever, new heart murmur (MR/AR usually), Roth spots, Osler’s nodes, haematuria, Janeway lesions, Splinter haemorrhages

247
Q

Duke criteria for IE (major - 2 required)

A

+ve blood culture with typical IE organisms OR 2 +ve cultures > 12 hours apart
Evidence of vegations on echo or new regurg murmur

248
Q

ABx for subacute IE

A

Benzylpenicillin and Gentamicin

249
Q

ABx of acute IE

A

Flucloxacillin for MSSA

250
Q

Typical valves affected in IE

A

Aortic regurgitation, Mitral regurgitation

251
Q

Function of Stellate cell

A

Stores Vitamin A

252
Q

Limiting plate

A

Found between portal tract and hepatocytes

253
Q

Portal triad

A

Hepatic artery, Hepatic vein, Biliary duct

254
Q

Define cirrhosis

A

Whole liver affected
Fibrosis
Nodules of regenerating hepatocytes
Intrahepatic shunting (within liver) or extraheptic shunting (portal HTN, oesaphgeal varices, splenomegaly)

255
Q

Prognostic scoring system for cirrhosis

A

Child’s Pugh Score

256
Q

Types of porto-systemic shunts

A

Lower oesophagus, umbilicus, rectum

257
Q

Causes of micronodular vs macrodular cirrhosis

A

Micronodular < 2mm (alcohol) and Macronodular > 2mm (viral hepatitis)

258
Q

Causes of acute hepatitis

A

Hepatitis A, Hepatitis E, Drugs

259
Q

Histology of acute hepatitis

A

Spotty necrosis

260
Q

Histology of chronic hepatitis

A

Scarring
Piecemeal necrosis (inflammation across limiting place –> difficult to discern boundary between portal tract and hepatocytes)
Fibrosis

261
Q

Stages of alcoholic hepatitis

A

Fatty liver
Alcoholic hepatitis
Cirrhosis

262
Q

Histology of fatty liver

A

Fatty change (reversible) = Steatosis

263
Q

Histology of alcoholic hepatitis

A

Mallory Denk bodies - mainly in Zone 3

Ballooning (cell swelling)

264
Q

Cirrhosis

A

Micronodular cirrhosis

Fibrosis

265
Q

Histology of NASH

A

Same as Alcoholic liver disease

Difference arises clinical Hx

266
Q

Histology of Primary biliary cholangitis

A

Granulomatous destruction of bile ducts - pathognomonic lesion of PBC

267
Q

Auto-antibody in Primary biliary cholangitis

A

Anti-mitochondrial antibody

268
Q

Histology of Primary sclerosing cholangitis

A

Onion-skinning fibrosis of bile duct

269
Q

PSC is associated

A

Ulcerative colitis

270
Q

Diagnosis of PSC

A

ERCP/MRCP –> beading of bile ducts (due to multifocal strictures)

271
Q

PSC –> ↑risk of

A

Cholangiocarcinoma

272
Q

Haemochromatosis - Sx

A 
Mutation --> ↑iron absorption --> Iron deposition in parenchymal cells
Cardiomyopathy
Infertility
Bronzed diabetes
Chronic pancreatitis
273
Q

Histology of Haemachromatosis

A

Chocolate brown organs

274
Q

Tx for Haemachromatosis

A

Venesection, Desferrioxamine

275
Q

Histology of haemsiderosis

A

Accumulation of iron in macrophages (differs from haemachromatosis in where the iron lies)

276
Q

Stain for Iron (2)

A

Perl stain, Prussian blue stain

277
Q

Wilson’s disease - Sx, Ix

A 
↓ copper EXCRETION
Kayser-Fleischer rings
Deposition in basal gnalgia
↑serum copper
↓caeruloplasmin
↑24hr urinary copper
278
Q

Wilson’s disease - Tx

A

Lifelong penicillamine

279
Q

Stain for copper

A

Rhodanine stain

280
Q

Auto-antibody in autoimmune hepatitis

A

Anti-smooth muscle antibody (Anti-SMA Ab)

281
Q

Histology of α1 antitrypsin deficiency

A 
Intracytoplasmic inclusions (misfolded a1-antitrypsin)
Emphysema
282
Q

Histology of drug-induced liver damage

A

Worst damage in Zone 2 and Zone 3

283
Q

Most common liver cancer

A

metastases

284
Q

Primary liver tumours

A

Hepatocytes –> Liver cell adenoma –> Hepatocellular carcinoma (RF: Aflatoxin)
Cholangiocytes –> Bile duct adenoma –> Cholangiocarcinoma
Endothelial cells –> Haemangioma –> Haemangiosarcoma

285
Q

Most common causes of acute pancreatitis

A

Gallstones, Alcohol

286
Q

Most common causes of chronic pancreatitis

287
Q

Acute pancreatitis - pathogenesis

A

Activated enzymes –> Acinar necrosis –> further enzyme release (+ve cycle)
Fat necrosis –> Free fatty acids bind Ca2+ –> hypocalcaemia

288
Q

Acute pancreatitis - complications

A

Pseudocyst +/- abscess, Hypoglycaemia, Hypocalcaemia

289
Q

Cyst vs Pseudocyst

A 
Cyst = collection of fluid with epithelial lining
Pseudocyst = collection of fluid WITHOUT an epithelial lining (may be lined with fibrosis tissue)
290
Q

histology of acute pancreatitis

A 
Acinar necrosis (periductal or perilobular or panlobular)
Fat necrosis
Pseudocyst
291
Q

Histology of chronic pancreatitis

A

Fibrosis - defines chronic process
Loss of acinar cells
Duct strictures

292
Q

Chronic pancreatitis - Ix

A

Pancreatitis calcifications (diagnostic)

293
Q

Chronic pancreatitis - complications

A 
Malabsorption (loss of exocrine function)
Diabetes mellitus (loss of endocrine function)
294
Q

Anto-antibody in Autoimmune pancreatitis

A

IgG4 +ve plasma cells (specific monoclonal response)

295
Q

Types of pancreatic cancer

A

Ductal carcinoma - most common pancreatic cancer
Acinar carcinoma
Cystic neoplasis (serous, mucinous)
Pancreatic neuroendocrine tumour (e.g. insulinoma)

296
Q

Precursor lesions for pancreatic cancer

A

Pancreatic intraductal neoplasm (PanIN)

Intraductal mucinous papillary neoplasm (IMP)

297
Q

Most common mutation in pancreatic cancer

A

K-ras (95%)

298
Q

Histology of Pancreatic cancer

A

Adenocarcinoma (mucing-secreting glands)
Perineural invasion (wraps around nerves)
Ca19-9 +ve

299
Q

Types of pancreatic based on location

A

Head of pancreas associated with ductal carcinoma

Tail of pancreas associated with neuroendocrine tumour

300
Q

Complications of pancreatic cancer

A

Bile duct obstruction –> obstructive jaundice
Pancreatic duct obstruction –> chronic pancreatitis
Migratory thrombophlebitis = Trosseau’s sign of malignancy

301
Q

Histology of pancreatic neuroendocrine tumours

A

Most are non-secretory
Insulinoma is most common secretory type
Chromogranin +ve
Rosette formation of cells

302
Q

Role of podocytes

A

Podocyte’s foot processes (on oustide of BM) create a charge-dependent and size-dependent barrier
Podocyte slit barrer = thin area between end feet

303
Q

Define mesangium

A

Smooth muscle around arterioles (both afferent and efferent arterioles) - holds glomerular structure together

304
Q

Main functions of the kdiney

A 
Excretion of waste products
Fluid balance, eletrolyte balace, acid/base balance
Regulation of BP (RAAS)
Regulation of Ca2+
Regulation of haematocrit
305
Q

Glomerular disease results in

A

Failure of filter –> ↑Cr, ↑Ur

Failure to maintain barrier function –> proteinuria, haematuria

306
Q

Pathogenesis of immune complex deposition in kidney

A

Immune complex deposition in glomerulus –> inflammation + complement activation
May deposit at different rates (post-strep glomerulonephritis takes 2-3 weeks, HepB infection takes years)
May deposit at different areas
- Mesangial area –> mild proteinuria
- Sub-epithelial area (below podocytes) –> disrupts podocyte/filtration barrier
- Sub-endothelial area (between endothelium and BM) –> inflammatory activation (most severe)

307
Q

Ix for immune complex deposition in kidney

A

Immunohistochemistry, Electron microscopy

308
Q

PKD - Aetiology, Sx, Cx

A

Autosomal dominant mutation in PKD1/2 –> cysts in renal parenchyma
Associated with berry aneurysms and liver cysts
Presents with HTN, flank pain, haemturia

309
Q

Acquired renal cystic disease - Aetiology, Cx

A

Associated with end-stage renal failure –> cysts develop –> replace kidney
↑risk of papillary renal cell carcinoma

310
Q

Acute tubular necrosis - causes

A

Ischaemic, toxins (contrast, Hb, myoglobin), drugs (NSAIDs)

Damage to tubular epithelial cells

311
Q

Histology of acute tubular necrosis

A 
Loss of brush border
Loss of polarity
Loss of integrins on basal surface --> cells drop off into lumen --> cell casts (muddy casts)
Necrosis of tubules
Tubules no longer back-to-black
Tubules appear flattened
312
Q

Acute tubulo-interstial nephritis - causes

A

Immune damage to tubules and interstitum

  • Acute pyelonephritis (bacterial infection, white cell cases in urine)
  • Chronic pyelonephritis (chronic obstruction, urine reflux)
  • Acute interstitial nephritis (hypersensitivity to drugs - ABx, NSAIDs, Diuretics)
  • Chronic interstial nephritis (elderly with long-term analgesic consumption)
313
Q

Histology of acute-interstitial nephritis

A

Signs of tubular injury (as above)

+ Inflammatory infiltrate (eosinophils, granulomas)

314
Q

Define casts

A

Solid cellular elements seen on urine microscopy

315
Q

Define glomerular cresents

A

Proliferation of cells within Bowman’s space –> pushes glomerulus to one side
Inflammation creates permanent holes in basement membrane (do not re-form)

316
Q

Causes of acute crescentic GN

A

(1) Immune complex
(2) Anti-GBM
(3) Pauci-immune
All characterised by presence of glomerular cresents
All rapidly progressive (end-stage renal failure within weeks)

317
Q

Immune complex crescentic GN - causes, pathogenesis

A

Subendothelial deposition of immune complexes (most severe type) –> inflammation
Causes: SLE, IgA nephropathy, Post-strep glomerulonephritis (subendothelial humps on EM, ↑ASOT titre)

318
Q

Immunohistochemistry of immune complex mediated C GN

A

Granular (lumpy bump) deposition of IgG immune complex on GBM/mesangium

319
Q

Anti-GBM disease =

A

Goodpasture’s syndrome = anti-GBM IgG antibodies against Type 4 collagen (GN, pulmonary haemorrhage) –> haemturia + haemopytsis

320
Q

Immunohistochemistry of anti-GBM disease

A

LINEAR deposition of IgG highlights glomerular basement membrane

321
Q

Silver stain look sfor

A

Presence of glomerular cresents

322
Q

Pauci-immune cresentic GN - pathogenesis

A

ANCA-associated (anti-neutrophil cytoplasma antibodies)-associated
——- c-ANCA = Wegener’s granulomatosis
——- p-ANCA - microscopic polyangiitis
Antibodies bind to neutrophils –> activation within glomeruli –> glomerular necrosis
No glomerular Ig deposits
Associated with vasculitis

323
Q

Immunohistochemistry of Pauci-immune cresentic GN

A

Fluorescence of neutrophils

Lack of immune complex deposition

324
Q

Thrombotic microangiopathy

A

Damage to endothelium
MAHA = deposition of fibrin –> shears RBC –> schistocytes, release Hb (↓haptoglobuin), release BR (jaundice)
HUS = MAHA + Thrombocytopaenia + AKI
TTP = HUS + Fever + CNS signs

325
Q

Nephrotic syndrome triad

A

Proteinuria, Hypoalbuminaemia, Oedema
Frothy urine
Swelling (classically facial swelling in children and peripheral oedema in adults)

326
Q

Causes of nephrotic syndrome

A 
Glomerular disease
------ Minimal change disease
------ Focal segmental glomerulosclerosis
Immune-complex mediated
------ Membranous glomerulonephritis
Systemic disease
------ DM
------ SLE
------ Amyloidosis
327
Q

Minimal change glomerulonephritis - light microscopy

A

Normal appearance

328
Q

Minimal change glomerulonephritis - electron microscopy

A

Loss of podocyte foot processes

329
Q

Minimal change glomerulonephritis - immunofluorescence

A

No immune deposits

330
Q

Most common cause of nephrotic syndrome in children

A

Minimal change glomerulonephritis

331
Q

Treatment of minimal change glomerulonephritis

A

Steroids (immunosupression)

332
Q

Focal segment glomerulosclerosis - Light microscopy

A

Focal and segmental glomerular consolidation
Scarring
Hyalinopsis

333
Q

Focal segment glomerulosclerosis - EM

A

Loss of podocyte foot processes (same as minimal change disease)
+ Scars within glomeruli

334
Q

Focal segment glomerulosclerosis - immunofluorescence

A

Ig and complement deposition within scarred areas

335
Q

Membranous glomerulonephritis - cause, pathogenesis

A

Caused by Anti-PLA2 receptor antibody (found on Podocytes) or secondary to epithelial malignancy, drugs, infection SLE
Immune deposition on outside of glomerular BM (subepithelially)
Subepithelial deposition ∴no inflammation

336
Q

Membranous glomerulonephritis - light microscopy

A

Diffuse GBM thickening

337
Q

Membranous glomerulonephritis - electron microscopy

A

Loss of podocyte foot process

Subepitheliual ‘spikey’ deposits

338
Q

Membranous glomerulonephritis - immunofluorescence

A

Ig and complement in granular deposits along entire GBM

339
Q

Most common cause of glomerulonephritis in adults

A

Membranous glomerulonephritis

340
Q

Stages of diabetic nephropathy

A

Stage 1 - thickening of BM
Stage 2 - ↑mesangial matrix
Stage 3 - Kimmelstiel-Wilson nodules (mesangial matrix nodules) –> at this point, nephrotic syndrome
Stage 4 - obliterated glomerulus (requires dialysis)

341
Q

Define amyloidosis

A

Deposition of extracellular protein with a β-sheet structure which is insoluble

342
Q

AA amyloidosis

A

Derived from serum amyloid-associated protein (SAA)

- SAA is an acute phase protein - ↑in RhA, SLE

343
Q

AL amyloidosis

A

Derived from Ig light chains

- Associated with multiple myeloma

344
Q

Stain for amyloid

A

Congo red stain –> salmon pink

+ Polarised light –> apple-green birefringence

345
Q

Lupus nephritis

A

Class I - immune complexes but minimal change in structure
Class 2 - mesangial pattern of injury
Class 3 + 4 - endothelial pattern of injury
Class 5 - epithelial pattern of injury —–> looks similar to membranous nephropathy
Granular lumpy bumpy pattern on Immunohistochemistry

346
Q

Causes of microscopic haematuria

A

Thin BM disease (autosomal dominant mutation in T4 collagen synthesis, associated with Alport’s syndrome)
IgA nephropathy - often presents 1-2 after URTI with frank haematuria

347
Q

DDx asymptomatic haematuria

A

Thin basement membrane disease (benign familial haematuria)
IgA nephropathy –> frank haematuria, more common in Asians
Alport syndrome

348
Q

Most common cause of glomerulonephritis worldwide

A

IgA nephropathy

349
Q

Histopathology of hypertension nephropathy

A 
Shruken kidneys
Nephrosclerosis
- Arteriolar hyalinosis
- Arterial intimal thickening
- Ischaemic glomerular changes
- Segmental and global glomerulosclerosis
350
Q

Nephritic syndrome

A 
PHAROH
Proteinuria
Haematuria (coke-coloured urine)
Azzotemia - ↑Urea, ↑Cr
Red cell casts (in urine)
Oliguria
Hypertension
351
Q

Alport’s syndrome

A

X-linked mutation in Type IV collage (α5 chain)

Nephritic syndrome + Sensorineural deafness + Eye disorders (cataracts, lens dislocation)

352
Q

Oesophagus epithelium

A

Stratified squamous epithelium

353
Q

Z line

A

Squamo-columnar epithelium

354
Q

Stomach fundus/body characteristics

A

Columnar epithelium, specialised glands secrete acid

355
Q

Stomach pylorus characteristics

A

Columnar epithelium, non-specialised glands, neuroendocrine cells, affected by H. pylori infection

356
Q

Goblet cells

A

Secrete mucin, define intestinal-type epithelium
Goblet cells are NOT normally found in the stomach
Goblet cells in stomach indicates intestinal type metaplasia

357
Q

Cause + Histology of acute oesphagitis

A

Caused by oesophgeal reflux of acid
Red, swollen
Neutrophils (acute inflammation)

358
Q

Cause + Histology of GORD

A

Caused by reflux of gastric acid into oesophagus
Ulceration = loss of surface epithelium
Surface epithelium replaced by fibrosis
Fibrosis (defines chronic disease)

359
Q

Complications of GORD

A

Haemorrhage, perforation, strictures

Barrett’s oesophagus

360
Q

Barrett’s oesophagus = columnar lined oesophagus (CLO)

A

Metaplasia from squamous epithelium –> columnar epithelium + Goblet cells (intestinal type epithelium)

361
Q

Metaplasia

A

Reverse change in cell type

362
Q

Dysplasia

A

Cytological and histological features of malignancy BUT no invasion (e.g. high nuclear-cytoplasmic ratio, mitotic figures)

363
Q

Types of oesophageal cancer

A

Adenocarcinoma of Oesophagus
——- invades basement membrane
——- Lower oesophagus (acid reflux)
——- Most common oesophageal cancer in UK
Squamous cell carcinoma of Oesophagus
——- invades basement membrane + submucosa
——- Mid oesophagus
——- Associated with alcohol and smoking
——- Most common oesophageal cancer worldwide
——- Histology: produces keratin, intercellular bridges

364
Q

Porto-systemic anatomoses

A

Oesophageal, Para-umbilical, Rectal, Retroperitoneal

Due to portal vein HTN

365
Q

Causes + Histology of acute gastritis

A

Redness, Swelling, Neutrophils

Caused by H pylori, NSAIDs, Alcohol, Corrosives

366
Q

Cause + Histology of chronic gastritis

A

Lymphocytes (chronic) +/- Neutrophils (acute on chronic)

Caused by anti-parietal antibodies (pernicious anaemia), H. pylori (MALToma), NSAIDs, Bile reflux

367
Q

CAG +ve H pylori

A

CAG +ve is associated with more severe + chronic inflammation
H pylori produces urease –> alters pH (less acidic, ∴stomach –> ↑H+ to kill H pylori)
H pylori does NOT invade epithelium, it binds to epithelium cells

368
Q

Complications of H pylori

A

CLO-IM-Dysplasia (columnar lined oesophagus - intestinal metaplasia - dysplasia)
↑Gastric cancer
↑Adenocarcinoma
↑MALToma

369
Q

Define ulcer

A

Ulcer = loss of tissue extends beyond muscularis mucosa

370
Q

Define erosion

A

Erosion = loss of surface epithlium +/- lamina propria

Erosion may progress to Ulcer

371
Q

2 pathways to GI cancer

A

Upper GI tract –> metaplasia-dysplasia pathway

Lower GI tract –> adenoma-carcinoma pathway

372
Q

Precursor lesion for gastric cancer

A

Gastric epithelium dysplasia (no invasion)

373
Q

Types of gastric cancer

A

Gastric adenocarcinoma - most common
—— Intestinal type (Well differentiated, large glands with mucin)
—— Diffuse type (poorly differentiated, no glands, signet ring cell carcinoma, linitis plastica / leather bottle stomach - diffuse spread of abnormal cells)
Squamous cell carcinoma
Gastric MALToma (B cell lymphoma, chronic antigen stimulation with H pylori)
Gastrointestinal stromal tumour
Neuroendocrine tumour

374
Q

Duodenitis

A

↑acid in stomach –> spills into duodenum –> duodenal metaplasia (intestinal type –> gastric type)
Gastric epithelium can withstand acid

375
Q

Giardia lamblia

A

Pear-shaped trophozoite

376
Q

Histology of Coeliac disease

A

Villous atrophy
Crypt hyperplasia
↑intraepithelial lymphocytes (CD8 T cells)

377
Q

DDx for flattened villi

A

Tropical spure (E ccoli)

378
Q

Dx of coeliac disease

A 
Anti-TTG antibodies
Anti-endomysial antibodies
Duodenal biopsy (villous atrophy)
379
Q

Enteropathy associated T-cell lymphoma

A

EATL = T cell lymphoma

Associated with uncontrolled Coeliac disease

380
Q

Nutmeg liver

A

R heart failure –> nutmeg lever (congestive hepatopathy)

381
Q

Thickened pleura

A

Mesothelioma (associated with asbestos)

382
Q

Lung infection confined to single lobe

A

Lobular pneumonia

383
Q

Seed-like deposits in lung

A

Miliary TB

384
Q

Outpouching of normal bowel lumen

A

Diverticular disease

385
Q

Oesophageal varices

A

Liver cirrhosis

386
Q

Infarcted spleen

A

Sickle cell disease

387
Q

Bleeding, change in bowel habit

A

Colon cancer (adenocarcinoma)

388
Q

Torrential bleeding, perforated stomach

A

Peptic ulcer (eroded through wall of stomach)

389
Q

Multiple deposits in liver

A

Liver mets

390
Q

Dilated renal pelvis

A

Renal stone

391
Q

Renal parenchyma replaced with cysts

A

Polycystic kidnes

392
Q

High impact trauma, LOC –> wakes up –> dies

A

Extradural haemorrhage (arterial bleed)

393
Q

Thunderclap headache, PMHx of polycystic kidney disease

A

Berry aneurysm in circle of willis –> Subarachnoid haemorrhage

394
Q

Death certificate 1a

A

Actual cause of death (e.g. PE) (e.g. Stroke)

395
Q

Death certificate 1b

A

Causes 1b (e.g. DVT) (e.g. Embolism due to MI)

396
Q

Death certificate 1c

A

Causes 1b, which causes 1a (e.g. Hip fracture)

397
Q

Death certificate 2

A

Contributing factors (e.g. Diabetes)

398
Q

Layers of skin

A 
Epidermis
- St. corneum
- St Granulosum
- St. spinosum
- St. basale
Dermis
Subcutaneous fat
399
Q

Bullous pemphigoiD - pathogenesis, Sx

A

Autoimmune disorder against basement membrane
Damages achoring filaments linking basal keratinocytes to BM –> whole epidermis lifts up
Tense bullae - found Deep

400
Q

Histology of bullous pemphigoid

A

Epidermis lifts up

Bullae

401
Q

Immunofluorescence of bullous pemphigoid

A

IgG and C3 highlights dermoepidermal junction (linear deposition)

402
Q

PemphiguS valgaris - pathogenesis, Sx

A

Autoimmune IgG against desmosomes –> acantholysis
Flaccid blisters with red surface underneath
Bullae are Superficial

403
Q

Histology of pemphigus valgaris

A

Acantholysis/Separation between layers of epidermis

404
Q

Define acantholysis

A

Loss of intercellular connections (e.g. desmosomes) –> loss of cohesion between keratinocytes (between layers)

405
Q

Pemphigus foliaceus - pathogenesis, Sx

A

Autoimmune IgG against desmosomes in upper epidermis –> acantholysis
Very thin bullae, no intact bullae

406
Q

Histology of pemphigus foliaceus

A

Acantholysis/Separation between upper layers of epidermis

Net like pattern of intercellular IgG deposits

407
Q

Discoid eczema - Sx

A

Silvery plaques, Itchy, Flexure surfaces

408
Q

Contact dermatitis - pathogenesis, Sx

A

Type IV hypersensitvitiy reaction to allergn (Nickel, Starch) = T cell mediated response

409
Q

Histology of Contact dermatitis

A

Hyperkeratosis (epidermis thickens)

Spongiosis (oedema between keratinocytes)

410
Q

Plaque psoriasis - Sx

A

White, silvery plaques on extensor surfaces

411
Q

Histology of plaque psoriasis

A

Thickened epidermis (rapid turnover of keratinocytes)
Loss of Granular cell layer (stratum granulosum) - due to rapid turnover
Munro’s micro-abscesses within the epidermis
Test tubes in rack appearance (clubbing of rete ridges)
Parakeratosis (nuclei in S corneum layer)

412
Q

Psoriasis - signs

A

Auspitz sign = rubbing causes pin-point bleeding

Koebner phenomen - lesions form at sites of trauma

413
Q

Lichen planus - Sx

A 
Papules, Plaques
Wickham striae (white lines)
414
Q

Histology of lichen planus

A

Difficult to see epidermal-dermal boundary
Band-like inflammatory infilrate under epidermis
Saw toothing of rete ridges

415
Q

Pyoderma gangrenosum

A

Vascultitis ulcer (well-defined edge), pus-like

416
Q

Histology of pyoderma gangrenosum

417
Q

Seborrhoeic keratosis

A

Cauliflower appearance
Easily removed
Stuck on appearance

418
Q

Histology of seborrhoeic keratosis

A

horn cysts (trapped keratin)

419
Q

Sebaceous cyst

A

Smooth surface, central puctum +/- infection

420
Q

Histology of sebaceous cyst

A

Kertin within a cyst

421
Q

Most common skin cancer in UK

A

Basal cell carcinoma

422
Q

BCC - Sx

A

Rolled, pearly white border
Rodent ulcer –> highly invasive
Does NOT metastasise

423
Q

Histology of BCC

A

BCC invades local tissue

424
Q

Bowen’s disease

A

Pre-cancerous (confined to epidermis)

Keratin horn

425
Q

Histology of Bowen’s disease

A

Dysplasia (pre-cancerous)

BM intact

426
Q

Histology of SCC

A

Perineural invasion (wraps around nerves)

427
Q

Benign junctional naevus - Sx

A

Benign
Well circumscribed
Uniform pigmentation

428
Q

Histology of Benign junctional naevus

A

Melanocytes form nests at bottom of epidermis

429
Q

Compound naevus - Sx

A

Two-toned

Symmetrical

430
Q

Histology of compound naevus

A

Melanocytes within epidermis and dermis

431
Q

Histology of malignant melanoma

A

In epidemis –> in situ melanoma (cannot metstasise, Pagetoid spread) –> buckshot appearance
In dermis –> malignant melanoma

432
Q

Pagetoid spread

A

Invasion of melanocytes into epidermis

433
Q

Staging of malignant meloma

A

Breslow thickness

434
Q

SJS and TENS

A

<10% body surface area affected in SJS
>30% in TENs
Nikolsky sign +ve

435
Q

Pityriasis rosea

A

Salmon pink rash appears first (herald patch)

Christmas tree distribution

436
Q

Types of renal stones

A

Calcium oxalate - hypercalciuria
Magnesium Ammonium Phosphate - infection with urease-producing organisms (Proteus) –> Staghorn calculi
Uric acid - gout, chemotherapy

437
Q

Common sites of blockage

A

Pelvi-ureteric junction
Pelvic brim
Vesico-ureteric junction

438
Q

Benign renal neoplasms

A

Papillary adenoma
Renal oncocytoma
Angiomyolipoma

439
Q

Histology of papillary adenoma

A

<15mm
Well circumscribed
Disorganised papillae and tubules

440
Q

Histology of renal oncocytoma

A

Mahogony-brown tumour

Nests of pink oncocytic cells

441
Q

Histology of angiomyolipoma

A

3 components: blood vessels, smooth muscle, fat

Associated with tuberous sclerosis

442
Q

Types of renal cell carcinoma

A

Clear cell RCC - most common
Papillary RCC
Chromophobe RCC

443
Q

Histology of clear cell RCC

A

Nests of clear cells

Golden-yellow tumour

444
Q

Histology of papillary RCC

A

Papillae/Tubules >15mm
Type 1 - islands of cells (end-on papillae)
Type 2 - multilayering

445
Q

Histology of chromophobe RCC

A

Well circumscribed brown tumour

Plant-like cells (thick walls)

446
Q

Nephroblastoma =

A

Wilm’s tumour, 2nd most common tumour in children

Abdominal mass in children

447
Q

Types of urothelial carcinoma (transitional cell carcinoma)

A

Non-invasive papillary UC
Infiltrating UC (highly invasive)
Flat UC in situ (flat lesion with high grade features)

448
Q

Histology of non-invasive papillary UC

A

Frond-like lumps on bladder wall

449
Q

Histology of BPH

A

Expanding nodule

Glandular and stromal components of prostate (hyperplasia)

450
Q

Most common malignant tumour in men

A

Prostate cancer

451
Q

Prognostic scoring for prostate cancer

A

Gleason score (x + y, based on how they resemble glands)

452
Q

Types of testicular germ cell tumours

A

Seminoma = clear cells, lymphoid infiltrate
Embryonal carcinoma: anaplastic tissue
Teratoma: multiple tissue types
Yolk sac tumour: lace-like growth pattern
Choriocarcinoma

453
Q

Types of testicular non-germ cell tumour

A

Lymphoma
Leydig Cell tumour –> precocious puberty (due to hormone secretions)
Sertoli cell

454
Q

Paratesticular disease

A 
Epididymal cyst (benign cyst)
Epididymitis
Varicocele (dilated venous plexus)
Hydrocele (fluid between layers of tunica vaginalis)
Adenomatoid tumour
455
Q

Lichen sclerosus in males =

A

Balanitis xerotica obliterans (BXO) –> causes phimosis

456
Q

Peyronie’s disease

A

Curved penis (due to scarring)

457
Q

Fournier’s gangrene

A

Necrotising fasciitis (pain not in keeping with size of lesion)

458
Q

Define fistula

A

connection between two hollow tissues

459
Q

Pseudomembranous colitis - Aetiology, Ix

A

C difficile, ABx use

Ix: C diff toxin stool assay

460
Q

Histology of pseudomembranous colitis

A

Signs of inflammation (colitis)
Pseudomembrane formation (appear at wet cornflakes)
Neutrophil-composed conflakes (volcano like)

461
Q

Tx of pseudomembraneous colitis

A

Metronidazole and Vancomycin

462
Q

Histology of ischaemic colitis

A

Watershed zones (most affected) - furthest from blood vessels

463
Q

Histology of CD

A 
ANY part of GI tract
Skip lesions
TRANSMURAL inflammation
Non-caseating granuloma
Cobblestoning
Extra-GI features - pyoderma gangrenosum, erythema nodosums
464
Q

Histology of UC

A

Spreads in contiguous fashion (only affects large bowel)
Inflammation confined to mucosa and submocosa
Backwash ilietis
Extra-GI features - erythema nodosum, pyoderma gangrenosum, PSC
Cx: toxic megacolon –> perforation

465
Q

Complications of UC

A

↑risk of adenocarcinoma (UC>CD)

466
Q

Types of non-neoplastic polyps

A 
Hyperplastic - due to scarring producing excess tissue
Inflammatory pseudo-polyps - due to inflammation
Hamartomatous polyps (Juvenile, Peutz-Jeghers)
467
Q

Types of neoplastic polyps

A

Adenoma

  • Tubular adenoma (tube-like)
  • Tubulovillous adenoma
  • Villous adenoma (finger-like)
468
Q

Familial polyp syndromes

A 
Peutz-Jegher's
Familial adenomatous polyposis
- Gardner's syndrome
- Turcot syndrome
Hereditary non-polyposis colon cancer (HNPCC) = Lynch syndrome
469
Q

FAP - aetiology

A

autosomal dominant mutation in APC (tumour suppressor gene)

470
Q

Gardner’s syndrome

A

FAP + extra-Gi manifestations (osteomas)

471
Q

HNPCC - aetiology

A

autosomal dominant mutation in DNA mismatch repair gene

472
Q

Staging for colorectal carcinoma

A 
Dukes' staging (no longer used)
----- A = confined to bowel wall
----- B = through bowel wall
----- C = lymph node mets
----- D = distant mets
TNM
473
Q

Cervical screening ages

A

25 - 65 years old

474
Q

Ectocervix vs Endocervix

A

Ectocervix (outer region) lined by squamous epithelilum

Endocervix (inner region) lined by glandular epithelium / columnar epithelium

475
Q

Define dyskaryosis

A

pre-cancerous changes in outermost squamous cells of the cervix

476
Q

CIN1 changes

A

Large nucleus
Areas of dense chromatin
Lower 1/3 affected

477
Q

CIN2 changes

A

Metaplastic squamous cells
Irregular nuclei
Lower 2/3 affected (including middle 1/3)

478
Q

CIN3 changes

A

Full thickness epithelium involved

479
Q

Histology of HPV infection

A

Koilocyte = large, irrecular, well-defined peri-nuclear halos = HPV vacuole

480
Q

High risk HPV subtypes

A

HPV 16 and 18 –> cervical cancer

481
Q

Low risk HPV subtypes

A

HPV 6 and 11 –> genital warts

482
Q

Common mutation in Lung cancer

483
Q

Common mutation in Melanoma

484
Q

Common mutation in Breast cancer

485
Q

Common mutation in Colon cancer

A

AFP, K-ras

486
Q

Common mutation in Pancreatic cancer

A

K-ras (95%)

487
Q

Most common brain cancer

A

Metastases

488
Q

Most common primary brain cancer

A

Glial tumours

489
Q

WHO grading determines

A

Survival
Grade I - low grade, long term survival
Grade II - low grade, death in 5+ years
Grade III - high grade, death within 5 years
Grave IV - high grade, death within 1 year

490
Q

Change in WHO classification 2016

A

Genetic prolifing –> integrated diagnosis

491
Q

IDH1/2 mutation

A 
Good prognostic factor 
IDH mutant (+ve) = "I don't hurt"
IDH wildtype (-ve) = bad prognosis
492
Q

Gliomas

A

Astrocytoma
Oligodendroglioma
Pilocytic astrocytoma

493
Q

Most common brain tumour in children

A

Pilocytic astrocytoma

494
Q

2nd most common brain tumour in children

A

Medulloblastoma

495
Q

Pilocytic astrocytoma is associated with

496
Q

Histology of pilocytic astrocytoma

A

Piloid “hairy” cell
Rosenthal fibres
Granular bodies

497
Q

MRI of pilocytic astrocytoma

A

Well circumscribed, cystic lesion

498
Q

Diffuse astrocytoma may progress to

A

Glioblastoma

499
Q

Glioblastoma location

A

Children –> Cerebellum

Adults –> Cerebral hemispheres

500
Q

MRI of glioblastoma

A

Non-enhancing lesions

Poorly defined margins

RW Pathology (9 decks)

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