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Cross reference - year 5 > Histopathology > Flashcards

Histopathology Flashcards

1
Q

neutrophils vs lymphocytes and inflammation

A 
neutrophils = acute inflammation
lymphocytes = chronic inflammation
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2
Q

what does an eosinophil look like on microscope?

A

bilobed nucleus, red granules

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3
Q

what are macrophages like in their current state vs chronic inflammatory conditions?

A
  • natural state: phagocytic

- chronic inflammatory conditions: secretory

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4
Q

cause of a caseating granuloma

A

TB

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5
Q

characteristics of an SCC

A

keratin production

intracellular bridges

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6
Q

characteristics of adenocarcinoma

A

mucin production

glands

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7
Q

what is the stain for melanin?

A

fontana stain

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8
Q

stain for iron overload?

A

prussian blue

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9
Q

what antibody shows it is an epithelial origin?

A

cytokeratin Ab

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10
Q

out to in structures of bone?

A

periosteum
cortex
medulla

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11
Q

diaphysis and epiphysis

A

diaphysis: main part of bone
epiphysis: head

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12
Q

what are the bone tumour-like conditions?

A
  • fibrous dysplasia
  • metaphyseal fibrous corticol defect/ non-ossifying fibroma
  • reporative giant cell granuloma
  • ossifying fibroma
  • simple bone cyst
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13
Q

what happens in fibrous dysplasia?

A

marrow replaced by fibrous stroma with rounded trabecular bone

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14
Q

X-ray features of fibrous dysplasia

A

soap bubble appearance
femoral head = Shepherd’s Crook
chinese letters

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15
Q

features of McCune Albright Syndrome

A
  • polyostotic fibrous dysplasia
  • endocrine problems
  • cafe au lait spots
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16
Q

cartilaginous benign bone tumours

A
  • osteochondroma
  • enchondroma
  • chondroblastoma
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17
Q

bone forming benign bone tumours

A

osteoid osteoma
osteoblastoma
osteoma

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18
Q

features of osteochondroma

A
  • end of long bones
  • young males
  • cartilaginous surface overlying normal trabecular bone
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19
Q

features of endochondroma

A
  • cartilaginous proliferation within bone
  • most in hands
  • popcorn calcification
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20
Q

what is a borderline bone malignancy? where is it formed?

A

giant cell tumour

end of long bones, mostly around knee

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21
Q

X-ray and histology of giant cell tumour

A

X-ray: lytic appearance

Histology: osteoclasts on background of spindle/ovoid cells

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22
Q

what are the tumours that metastasize to bone?

A 
breast
prostate
lung
kidney
thyroid
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23
Q

what are the types of malignant bone tumours?

A
  • osteosarcoma: forms bone
  • chondrosarcoma: forms cartilage
  • Ewing’s: undifferentiated mesenchymal tumour
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24
Q

X-ray chondrosarcoma findings

A

lytic with fluffy calcification

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25
Q

what is Ewings? X-ray finding

A

small round cell tumour

X-ray: onion skinning of periosteum, lytic +/- sclerosis

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26
Q

what are soft tissues tumours?

A

mesenchymal proliferation

occur in extra-skeletal non-epithelial tissues of body (exc meninges + LR system)

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27
Q

types of soft tissue tumours

A
  • liposarcoma: myxoid appearance
  • spindle cell sarcoma
  • pleomorphic sarcoma
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28
Q

bad prognostic sign in bone tumours

A

aneuploid/ hyperdiploid

>5cm

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29
Q

down side of cytopathology

A

does not show tissue architecture

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30
Q

different cytopathology grades

A 
C1: inadequate
C2: benign
C3: atypia, probably benign
C4: suspicious of malignancy
C5: malignancy
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31
Q

what stain do you use for breast pathology?

A

H+E

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32
Q

features of breast histology under H+E stain

A
  • purple = glandular tissue
  • pink = stroma around gland
  • duct with acini around
  • myoepithelial cells (help pump milk)
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33
Q

histology of duct ectasia

A

duct distended, proteinaceous material

foamy macrophages

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34
Q

what is fibrocystic disease? histology?

A

exaggerated response to hormonal influence

ducts dilated, may get calcified

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35
Q

what is a fibroadenoma

A

benign fibroepithelial neoplasm of breast

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36
Q

what is an intraductal papilloma?

A

benign papillary tumour, arising duct system

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37
Q

peripheral vs central papilloma

A
  • peripheral papilloma: small terminal ductules (clinically silent)
  • central papilloma: large lactiferous ductules (nipple discharge)
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38
Q

histology of intraductal papilloma

A
  • large dilated duct, polypoid mass in middle

- fibrovascular core

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39
Q

what is radial scar?

A

benign sclerosing scar

central zone of scarring surrounded by radiating zone of proliferating glandular tissue

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40
Q

histology of radial scar

A

central stellate area

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41
Q

process of proliferative breast disease

A
  1. usual epithelial hyperplasia
  2. epithelial atypia/ atypical ductal carcinoma
  3. in situ lobular neoplasia (within acinar unit)
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42
Q

DCIS on mammography

A

areas of calcification

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43
Q

histology of DCIS

A
  • cribriform (punched out appearance)
  • cells large, not many lumens left
  • central lumen, full of necrotic material
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44
Q

2 distinct pathways to invasive breast cancer

A
  1. Low grade: from low grade DCIS, 16q loss

2. High grade: high grade DCIS, complex karotypes

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45
Q

cell type of invasive DUCTAL carcinoma

A

large pleomorphic nucleated cells

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46
Q

cell type of invasive LOBULAR carcinoma

A

linear, monomorphic

Indian file pattern

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47
Q

cell type of invasive TUBULAR carcinoma

A

elongated tubules

invade stroma

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48
Q

cell type of invasive MUCINOUS carcinoma

A

empty spaces, filled with mucin

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49
Q

what is breast cancer grading based on?

A

tubule formation
nuclear pleomorphism
mitotic activity

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50
Q

what receptor status are basal like carcinomas?

A

triple -ve

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51
Q

what is the most important prognostic factor in breast cancer?

A

axillary LNs

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52
Q

what does mammogram screening go on?

A

47-73

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53
Q

different mammogram gradings

A 
B1 = normal breast tissue
B2 = benign abnormality
B3 = lesion of uncertain malignant potential
B4 = suspicious of malignancy
B5 = malignant a/ DCIS b/ invasive
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54
Q

cells of anterior and posterior pituitary

A 
anterior = epithelial cells
posterior = nerve cells
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55
Q

what is a non-toxic goitre and when is it common?

A

enlargement without overproduction of thyroid hormones

common if impaired synthesis of thyroid hormones

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56
Q

how does a multinodular goitre form?

A

with time simple enlargement develops into multinodular pattern
hyperfunctioning nodule may develop

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57
Q

what is struma ovarii?

A

ovarian teratoma

ectopic thyroid

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58
Q

Hashimotos histology

A
  • lots of lymphoid cells within germinal centres
  • epithelial cells become large, lots of eosinophillic cytoplasm
    = Hurthle cell
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59
Q

histology of papillary carcinoma

A

optically clear nuclei
intranuclear inclusion
psommoma bodies

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60
Q

what can medullary carcinoma produce?

A

parafollicular C cells
calcitonin produced
deposited as amyloid

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61
Q

what is the problem in Cushing’s disease?

A

PITUITARY

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62
Q

hormone levels in CAH

A

dec cortisol production
inc ACTH
adrenal stimulation and inc androgen synthesis

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63
Q

acute causes of primary adrenal insufficiency

A
  • sudden withdrawal of corticosteroid therapy
  • haemorrhage (neonates)
  • sepsis with DIC (waterhouse-fridenston syndrome)
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64
Q

chronic causes of primary adrenal insufficiency

A

AI
TB
HIV
Metastastic

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65
Q

SLE SOAPBRAINMD

A 
Serositis 
Oral ulcers
Arthritis
Photosensitivity
Blood (all counts low)
Renal (proteinuria)
ANA
Immunologic (anti-dsDNA)
Neurologic (psych, seizures)
Malar Rash
Discoid Rash
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66
Q

auto-Abs in SLE

A
  • anti-dsDNA
  • anti-smith
  • anti-histone
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67
Q

what drug can cause SLE?

A

hydralazine

anti-histone

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68
Q

skin histology in SLE

A
  • lymphocytic infiltration of dermis
  • vascuolisation
  • extravasation of RBCs = rash
  • immune complexes at epidermal-dermal junciton
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69
Q

renal histology in SLE

A

wire loop capillaries (thickened = immune complex deposition)

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70
Q

what is Libman Sacks Endocarditis

A
  • non-infective
  • SLE associated
  • vegetation: lymphocytes/neutrophils/fibrin stranfs
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71
Q

diffuse vs limited scleroderma

A

diffuse: involves trunk, anti-topoisomerase (Scl 70)
limited: does not involve trunk, anti-centromere

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72
Q

pattern of immunofluoresence in scleroderma

A

nucleolar

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73
Q

vascular histology seen in scleroderma

A

intimal proliferation = onion skin appearance

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74
Q

pattern of ANA and what is signifies

A

ANA = speckled pattern

suggests mixed connective tissue disease

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75
Q

main feature of sarcoidosis

A

non-caseating granuloma

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76
Q

investigation results in sarcoidosis

A

hypergammaglobuloinaemia
raised ACE
hypercalacaemia

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77
Q

what are the 2 medium vessel vasculitis?

A

polyarteritis nodosa

Kawasaki

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78
Q

features of polyarteritis nodosa

A

rosary bead appearance on angio

associated with Hep B

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79
Q

temporal arteritis biopsy findings

A

lymphocytic infiltration of tunica media of temporal artery

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80
Q

triad seen in granulomatosis with polyangiitis (Wegner’s)

A
  1. ENT (nosebleeds, sinusitis, saddle nose)
  2. Lungs (haemoptysis, SOB)
  3. Kidneys (haematuria)
    cANCA
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81
Q

cANCA directed against

A

proteinase 3

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82
Q

triad in Churg Strauss (eosinophillic granulo w/ polyangiitis)

A
  1. asthma
  2. eosinophillia
  3. vasculitis
    pANCA
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83
Q

pANCA directed against

A

myeloperoxidase

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84
Q

what is hydrosalpinx?

A

enlarged fallopian tube filled with fluid

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85
Q

what proteins are encoded by HPV and what do they bind to?

A

E6 and E7 = transforming genes

bind to and inactivate 2 tumour suppressors (retinoblastoma, p53)

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86
Q

what does productive HPV look like on histology?

A

halo around nucleus (koilocyte)

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87
Q

CIN 1/2/3

A

1; lower 1/3

  1. lower 2/3
  2. entire epithelium
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88
Q

cervical smear programme

A

at 25y
25-49: 3 years
50-62: 5 years

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89
Q

histology of endometrial hyperplasia

A

increase in stroma and glands

driven by oestrogen

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90
Q

type 1 endometrial carcinoma

A

85%
endometrioid
mucinous
secretory

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91
Q

type 2 endometrial carcinoma

A

serous
clear cell
arise in atrophic endometrium

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92
Q

what carriers a better prognosis in Endometrial Carcinoma?

A

diploidy

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93
Q

FIGO staging in EC

A
  1. confined to uterus
  2. spread to cervix
  3. spread to adnexae, vagina, local lymph nodes
  4. distant spread
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94
Q

complete mole and possible complications

A

fertilisation of empty egg

can convert to invasive mole or malignancy

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95
Q

partial mole

A

normal ovum fertilised by 2 sperms

none progress to malignancy

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96
Q

issue with choriocarcinoma

A

rapidly invasive

wide mets

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97
Q

theory of endometriosis

A

metaplasia of pelvic peritoneum

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98
Q

what do ovaries consist of

A

surface epithelium
ovarian stroma
germ cells

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99
Q

types of ovarian epithelial tumours

A

type 1: low grade (low grade serous, endometrioid, mucinous, clear cell)
type 2: high grade (mostly serous, p53 mutation)

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100
Q

what are the benign ovarian tumours

A
  • serous cystadenoma
  • cystadenofibroma
  • mucinous cystadenoma
  • brenner tumour
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101
Q

tumours associated with endometriosis

A
  • endometrioid (better prognosis than mucinous and serous)

- clear cell (clear cytoplasm due to lots of glycogen)

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102
Q

types of germ cell tumours

A

dysgerminoma
teratoma
choriocarcinoma
endodermal sinus tumour (develop from extra embryonic tissue)

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103
Q

what are the steps of atherogenesis

A
  1. endothelial injury
  2. LDL enters intima, trapped in subintimal space
  3. LDL converted oxidized LDL = inflammation
  4. macrophages take up oxidized LDL via scavenger receptors
  5. form foam cells
  6. apoptosis of foam cells =inflammatio and cholesterol core of plaque
  7. increase adhesion molecules on endothelium
  8. more macrophages and T cells entering plaque
  9. VSMC form fibrous cap
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104
Q

what is the earliest change in atherosclerosis?

A

fatty streak

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105
Q

what are the different acute plaque changes?

A
  • rupture: exposes prothrombogenic plaque contents
  • erosion: exposes prothrombogenic subendothelial BM
  • haemorrhage into plaque: increase size
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106
Q

what is dilated cardiomyopathy?

A

progressive loss of myocytes

= dilated hearts

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107
Q

causes of dilated cardiomyopathy

A

infective
toxic (alcohol)
hormonal (peripartum, thyroid)
genetic (haemochromatosis)

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108
Q

histology following an MI: under 6 hours

A

normal histology

CK-MB normal

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109
Q

histology following an MI: 6-24 hours

A

loss of nuclei
homogenous cytoplasm
necrotic cell death

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110
Q

histology following an MI: 1-4 days

A

infiltration of polymorphs

then macrophages to clear up debris

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111
Q

histology following an MI: 5-10 days

A

removal of debris

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112
Q

histology following an MI: 1-2 weeks

A

granulation tissue
new blood vessels
collagen synthesis

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113
Q

histology following an MI: weeks to months

A

strengthening

decellularising scar

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114
Q

MI complications

A

contractile dysfunction (cardiogenic shock)
arrhythmia
myocardial rupture (free wall most common)
pericarditis
RV infarction
infarct extension (new necrosis adjacent to old)
infarct expansion (necrotic muscle stretches)

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115
Q

what is the cause of chronic ischaemic heart disease?

A

progressive HF due to ischaemic myocardial damage

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116
Q

what is the cause of sudden cardiac death?

A

due to ischaemia-induced electrical instability

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117
Q

cardiac failure histology

A
  • dilated heart
  • scarring/thinning of walls
  • fibrosis and replacement of ventricular myocardium
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118
Q

what is the abnormality in Hypertrophic Cardiomyopathy?

A

abnormality in beta-myosin heavy chain

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119
Q

what is the problem in restrictive cardiomyopathy?

A

impaired ventricular compliance

normal heart size = big atria

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120
Q

cause of chronic rheumatic valvular disease

A

immune cross reactivity with cardiac valves

mitral

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121
Q

histology of chronic rheumatic valvular disease

A
  • thickening of valve leaflet
  • commissures fuse
  • thickening/shortening/fusion of chordae tendinae
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122
Q

causes of aortic regurgitation

A
  • rigidity (rheumatic, degenerative)
  • destruction (microbial endocarditis)
  • disease of aortic valve ring (Marfan’s, AS, dissecting aneurysm)
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123
Q

true vs false aneurysm

A

true: all layers of wall dilate
false: extravascular haemotoma

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124
Q

describe the endothelium in liver

A

is discontinuous

no tight junctions

125
Q

what do stellate cells do normally? Vs when activated?

A 
normally = store Vit A
activated = become myofibroblasts and lay down collagen
126
Q

what is found in liver zone 3?

A

more metabolically active enzymes

127
Q

what is the limiting plate?

A

ring of collagen around portal tract

128
Q

what changes occur in liver injury?

A
  • kupffer cells activated
  • endothelial cells stick together = hard for blood to flow through
  • BM-type collagens secreted into Space of Disse by activated Stellate cells
  • hepatocytes lose microvilli
129
Q

what happens in extrahepatic shunting?

A

blood never reaches liver

backlogs into sites of porto-systemic anastomosis

130
Q

what happens in intrahepatic shunting?

A

blood goes through liver
does not come into contact with hepatocytes
blood = unfused and toxic

131
Q

what histology do you see in acute hepatitis?

A

spotty necrosis

132
Q

what determines the grade and stage in chronic hepatitis?

A
  • grade = severity of inflammation

- stage = severity of fibrosis

133
Q

what is interface hepatitis ?

A

AKA piecemeal hepatitis

inflammation crosses limiting plate

134
Q

how does fibrosis stain? what would be seen in intrahepatic shunting?

A

stains blue

extends between portal tract and central vein

135
Q

3 presentations of alcoholic liver disease

A

fatty liver
alcoholic hepatitis
cirrhosis

136
Q

histology of alcoholic hepatitis

A
  • ballooning of cells
  • mallory denk bodies (pink deposits in cells)
  • apoptosis
  • pericellular fibrosis
137
Q

why is zone 3 particularly vulnerable to damage?

A

hypoxic

most metabolically active

138
Q

PBC

A

bile duct loss
chronic inflammation
granulomas

139
Q

PSC

A

periductal bile fibrosis

leads to loss

140
Q

Haemochromatosis gene

A

HFe gene on Chr 6

141
Q

Wilsons Chromsome

A

Chr 13

142
Q

where is the deficiency in A1AT?

A

deficiency in blood not hepatocytes
excess in hepatocytes, folds wrong and cannot leave = damage
hepatitis and emphysema

143
Q

causes of hepatic granuloma

A

PBC
Drugs
TB
Sarcoidosis

144
Q

exocrine and endocrine aspects of pancrea

A

exocrine: acini and ducts
endocrine: e.g. islets of Langherans

145
Q

2 pathogenesis of acute pancreatitis

A
  1. Duct Obstruction (gallstone and alcohol)

2. Direct Acinar injury (all other causes)

146
Q

how gallstone causes acute pancreatitis?

A

reflux of bile up pancreatic duct
damage to acini
release of enzyme

147
Q

how alcohol causes acute pancreatitis?

A

spasm/oedema of Sphincter of Oddi

148
Q

how does acute pancreatitis cause hypocalcaemia?

A

lipases released from inflamed pancreas = fat necrosis

Ca binds to free fatty acids = soaponification

149
Q

what is a pseudocyst?

A

collection of fluid without epithelial lining
lined by fibrous tissue
rich in pancreatic enzymes/necrotic materal

150
Q

IgG4 related disease (AI pancreatitis)

A

duct surrounded by loads of IgG4 expressing plasma cells

n.b. normal polyclonal response = different IgGs

151
Q

different tumours of pancreas

A
  • carcinomas: ductal (85%), acinar
  • cystic neoplasms: serous cystadenoma, mucinous cystic neoplasm
  • pancreatic neuro endocrine tumours
152
Q

what 2 types of dysplastic ductal lesions can ductal carcinoma arise from?

A
  • pancreatic intraductal neoplasia (PanIN)

- intraductal mucinous papillary neoplasm

153
Q

ductal carcinoma mutation

A

K-Ras

154
Q

pathology of ductal carcinoma

A

mucin secreting glands set in desmoplastic stroma (adenocarcinoma)
most commonly in head

155
Q

cystic tumours features

A

serous/mucin secreting epithelium

156
Q

2 different types of gallstone

A
  • cholesterol (>50%): radiolucent (not seen on plain abdo X-ray)
  • pigment: Ca salts of unconjugated bilirubin, radio-opaque
157
Q

pathology of chronic cholecystitis

A
  • chronic inflammation
  • fibrosis
  • diverticula: Rokitansky-Aschoff sinuses (gall bladder contracting against obstruction)
158
Q

histology of body and fundus of stomach

A
  • lined by gastric mucosa, columnar epithelium
  • specialised glands in lamina propria (produce acids and enzymes)
  • muscularis mucosa
159
Q

which parts of the stomach are affected by H. pylori associated gastritis?

A

pyloric antrum/canal

160
Q

how is the histology of antrum/pyloric canal different?

A

same histology except no specialised glands

161
Q

are goblet cells normally seen in stomach?

A

goblet cells not normally seen in stomach

sign of intestinal metaplasia

162
Q

Barrett’s oesophagus changes

A

squamous to columnar metaplasia

if goblet cells visible = intestinal metaplasia = much higher risk of Cancer

163
Q

SCC of oesophagus

RFs and location

A

RFs: smoking, alcohol

mid/lower oesophagus, invades submucosa

164
Q

causes of acute gastritis

A
  • chemical (aspirin, alcohol, corrosives)

- infection (H. pylori)

165
Q

causes of chronic gastritis (ABC)

A
  • AI (anti-parietal cell)
  • bacteria (H. pylori)
  • chemical (NSAIDs, bile reflux)
166
Q

what are the histological sign of MALT?

A

lymphoid follicles in stomach (not normal)

H.pylori induces lymphoid tissue in stomach

167
Q

which form of H.pylori is associated with more chronic inflammation?

A

Cag-A +ve H. pylori

168
Q

what are the 2 pathways that lead to GI cancer?

A

metaplasia - dyplasia e.g. oesophageal

adenoma-carcinpoma e.g. colon cancer

169
Q

definition of ulcer

A

depth of tissue loss goes beyone=d muscularis mucosa into submucosa

170
Q

gastric adenocarcinoma subtypes

A
  1. intestinal: well differentiated, big glands, containing mucin
  2. diffuse: poorly differentiated, no gland formation
171
Q

types of diffuse adenocarcinoma

A

linitis plastica

signal ring cell carcinoma

172
Q

what is lymphocytic duodenitis?

A

inflammatory changes (inc IELs) without architectural changes

173
Q

what is the effect of ageing on skin?

A

fragile skin
little epidermis
collagen/elastic fibres poor quality

174
Q

different inflammatory reaction patterns

A
  • vesiculobullous (forms bullous)
  • spongiotic (becomes oedematous)
  • psoriasiform (thickened)
  • lichenoid (sheeny plaque)
  • vasculitis (ass/ w. vasculitides)
  • granulomatous
175
Q

features of bullous pemphigoid

A
  • flexor surfaces
  • tense bullae
  • IgG and C3 attack BM (dermo-epidermal junction)
176
Q

features of pemphigus vulgaris

A
  • flaccid blisters
  • IgG
  • damage occuring within keratinocyte layers
  • acantholysis
177
Q

what is definition of acantholysis?

A

loss of intraceullular connections

= loss of cohesion between keratinocytes

178
Q

features of pemphigus foliaceus

A
  • thin bullae, not intact
  • IgG mediated
  • damage to outer layer of keratinocytes/stratum corneum
179
Q

what is hyperparakeratosis?

A

thickening of skin on surface when you have been scratching

epidermis gets thicker

180
Q

histology of eczema

A

spongiotic

oedema in between keratinocytes

181
Q

plaque psoriasis histology

A

extensor silvery plaques
rapid turnover of cells = parakeratosis
no stratum granulosum = not enough time to form
Munro’s microabscesses (neutrophils) in epidermis

182
Q

lichen planus presentation in mouth

A

Wickham striae

183
Q

what histological finding can be seen in lichen planus and mycosis fungoides

A

band like lymphocytic infiltrate under epidermis

184
Q

seborrhoeic keratosis

A

stuck on

horn cysts

185
Q

what does BCCs arise from?

A

keratinocytes along bottom of epidermis

186
Q

what is an SCC in situ called?

A

Bowen’s disease

187
Q

what is Pagetoid spread?

A

melanocytes migrating up through epidermis

188
Q

3 forms of urinary calculi

A

75%: calcium oxalate (due to hypercalciuria)
15%: struvite
5%: uric acid

189
Q

features of struvite calculi

A 
proteus infection (urease production)
staghorn calculus
190
Q

3 types of benign renal neoplasm

A
  • papillary adenoma
  • renal oncocytoma
  • angiomyolipoma
191
Q

types of renal cell carcinoma

A
  • clear cell (70%)
  • papillary (15%)
  • chromophone (5%)
192
Q

features of clear cell carcinoma

A
  • lots of clear cells
  • golden yellow tumour, haemorrhagic areas
  • loss of Chr 3p
193
Q

what are the cells that make up nephroblastoma?

A

malignant TRIPHASIC kidney tumour

  • blastema = small round blue cells
  • epithelial
  • stromal
194
Q

most common type of bladder carcinoma and RFs

A

transitional cell carcinoma

RFs: smoking, aromatic amines

195
Q

Gleason score

A

most common pattern + worst pattern

196
Q

features of testicular germ cell tumours

A

arise from germ cell neoplasia in situ

painless testicular lump

197
Q

RFs for testicular germ cell tumours

A

undescended testes

LBW

198
Q

5 subtypes of testicular germ cell tumours

A
  1. seminoma
  2. embryonal carcinoma
  3. post-pubertal teratoma
  4. yolk sack tumour
  5. choriocarcinoma (cytotrophoblasts + synctiotrophoblasts)
199
Q

histology of seminoma

A

clear cells

prominate lymphocytic infiltrate

200
Q

Tx of testicular germ cell tumours

A

platinum based chemo

201
Q

composition of bone

A
  • inorganic (Ca hydroxyapatite)

- organic (bone cells and matrix)

202
Q

what is the location of the growth plates?

A

metaphysis

203
Q

cortical bone features

A

long bones

mechanical/protective

204
Q

cancellous bone features

A

vertebrae/pelvis

metabolic

205
Q

osteocytes

A

osetoblast like cells

sit in lacunae

206
Q

what cell are osteoclast percursors derived from?

A

monocytes

207
Q

what are the 3 categories of metabolic bone disease?

A
  • non-endocrine (e.g. age related osteoporosis)
  • related to endocrine abnormality (e.g. vit D/PTH)
  • disuse osteopaenia
208
Q

what are the 2 types of osteomalacia?

A

vitamin D def

phosphate def

209
Q

what is a brown cell tumour? associated with what?

A

hyperparathyroidism

multinucleated giant cells

210
Q

what is Paget’s disease?

A

disorder of bone turnover

211
Q

what re the stages of fracture repair?

A
  1. haemotoma at site (pro-callus)
  2. formation of fibrocartilaginous callus
  3. mineralisation of fibrocartiaginous callus
  4. remodelling of bone along weight bearing lines
212
Q

what is salmonella osteomyelitis associated with?

A

SCD

213
Q

x-ray changes in osteomyelitis

A

7 days: irregular subperiosteal new bone = involucrum
10-14 days: irregular lytic destruction
3-6 weeks: some areas of necrotic cortex detached = sequestra

214
Q

lyme disease cause

A

tick bite from Ixodus dammini

organism: Borrelia burgdorferi

215
Q

some symptoms of lyme disease

A

multisystem illness
inflammatory arthropathy
erythema chronicum migrans

216
Q

histology of osteoarthritis

A
  • cartilage degeneration
  • fissuring
  • abnormal matrix calcification
  • osteophytes
  • synovium inflamed, infiltration of inflammatory cells
217
Q

what is RA?

A

severe chronic relapsing synovitis

218
Q

characteristic deformities in RA

A
  • radial deviation of wrist
  • ulnar deviation of fingers
  • swan neck and Botonniere deformity
  • Z shaped thumbs
219
Q

histology findings of RA

A
  • proliferative synovitis
  • pannus formation
  • Grimley-Sokoloff cells
220
Q

X-ray and Histology in Osteosarcoma

A

X-ray: lytic, elevated periosteum (Codman’s triangle)

Histology: malignant mesenchymal cells

221
Q

X-ray and histology in Chrondrosarcoma

A
  • X-ray: lytic with fluffy calcifications

- Histology: malignant chondrocytes

222
Q

cause of Hirschsprung’s

A

absence of ganglion cells of myenteric plexus

223
Q

associated genetic abnormality of Hirschsprung’s

A

RET proto-oncogene

224
Q

secretory and exudative diarrhoea

A
  • secretory: caused by toxin

- exudative: invasion and mucosal damage

225
Q

associated skin lesions in Chrons

A

pyoderma gangrerosum
erythema multiforme
erythema nodosum

226
Q

when can other parts of the bowel by caused in UC?

A

backwash ileilitis

terminal ileum inflamed

227
Q

complications of UC

A

severe haemorrhage
toxic megacolon
adenocarcinoma

228
Q

what are the tumours of colon/rectum?

A
  • non neoplastic polyps
  • neoplastic epithelial lesions (adenoma, adenocarcinoma, carcinoid tumour)
  • mesenchymal lesions (stromal, lipoma, sarcoma)
  • lymphoma
229
Q

different non-neoplastic polyps

A

hyperplastic
inflammatory (pseudopolyp)
haemartomatous (jeuvenile, Peutz-Jeghers)

230
Q

types of neoplastic polyp

A

tubular adenoma
tubulovillous adenoma
villous adenoma

231
Q

RFs for cancer of a polyp

A
  • size of polyp (>4cm)
  • proportion of villous component
  • degree of dysplastic change
232
Q

familial syndromes characterised by polyps

A
  • Peutz-Jeghers
  • FAP (Gardner’s, Turcot)
  • HNPCC
233
Q

mutation in FAP

A

APC tumour suppressor on CHr 5q21

234
Q

gene mutation in HNPCC

A

DNA mismatch repair gene

+ extra colonic cancers (e.g. endometrium, prostate, breast, stomach)

235
Q

Duke’s staging

A

A: confined to bowel wall
B: through bowel wall
C: LN mets
D: distant mets

236
Q

molecular mutation in lung adenocarcinoma

A

EGFR

ALK-1

237
Q

molecular mutation in melanoma

A

BRAF

238
Q

molecular mutation in breast

A

BRCA1/2

CERB-B2

239
Q

molecular mutation in colon cancer

A

APC

KRAS

240
Q

extra-axial tumours

A

coverings

tumours of bone, cranial soft tissue, meninges, nerves, metastatic deposits

241
Q

intra-axial tumours

A

parenchyma

normal cell population of CNS/other cell types

242
Q

WHO grading of CNS tumours

A

I: benign, long term survival
II: death > 5 yrs
III: death < 5 yrs
IV: death < 1 year

243
Q

what are glial tumours and the 2 types?

A

most common primary tumour of CNS

  1. diffuse infiltration
  2. circumscribed glioma
244
Q

diffuse infiltration types and genetics

A

adults
astrocytoma or oligodendrogliomas
genetics: IDH 1/2 mutations

245
Q

circumscribed glioma type and genetic

A
  • children
  • MAPK mutation (BRAF)
  • pilocystic astrocytoma = most common
246
Q

pilocystic astrocytoma unique features and MRI

A

NF1
often cerebellar
piloid (hairy cell), Rosenthal fibres
MRI: well circumscribed, cystic and enhancing

247
Q

astrocytoma features and MRI

A
  • malignant progression –> eventually gliobastoma
  • de novo glioblastoma = most aggressive/frequent
    MRI: non-enhancing
248
Q

features of glioblastoma multiforme

A

type 4

high cellularity and mitotic activity

249
Q

features and histology of oligodenroglioma

A

long history of neuro signs
better prognosis than astrocytoma
histology: round cells with clear cytoplasm (fried eggs)

250
Q

Meningioma features

A

MRI: extra-axial, contrast enhancing

focal symptoms

251
Q

what is a medulloblastoma

A

originates from neuroepithelial precursors of cerebellum

small blue round cell tumour

252
Q

which cancers metastasise to CNS? where are mets seen?

A

lung, breast, melanoma

seen at grey-white junction

253
Q

what are the 2 main types of cerebral oedema?

A
  1. vasogenic: disruption of BBB

2. cytotoxic: secondary to cellular injury (hypoxia/ischaemia)

254
Q

what is the flow of the CSF?

A
  1. choroid plexus pumps out of CSF
  2. goes into 3rd ventricle through intraventricular foramen
  3. goes down cerebral aqueduct into 4th ventricle
  4. down into medulla and central canal of spinal cord
255
Q

how does CSF return back to systemic circulation?

A

CSF will circulate through subarachnoid space

and via arachnoid granules returns to systemic circulation

256
Q

what are the 2 forms of hydrocephalus?

A
  • non-communicating: obstruction to flow of CSF (usually involving cerebral aqueduct)
  • communicating: NO obstruction, problem with reabsorption of CSF into venous sinuses (e.g. infection)
257
Q

what is the normal ICP?

A

7-15mmHg

258
Q

what is subfalcine herniation?

A

cortex pushed under rigid falx cerebri

259
Q

what is transtentorial (uncal) herniation?

A

herniation of median temporal lobe through tentorial notch

260
Q

what is tonsillar herniation?

A

tonsils (cerebellum) pushed through foramen magnum

261
Q

what causes intra-parechymal haemorrhage?

A

due to rupture of small intraparenchymal vessel

usually due to HTN

262
Q

what is a cavernous angioma?

A

closely packed vessels

no parenchyma interposed between vascular space

263
Q

cavernous angioma vs AVM

A

similar to AVM but no brain substance wrapped up amongst vessels

264
Q

where are most SAH?

A

most at internal carotid bifurcation

265
Q

what is a contusion?

A

when brain collides with internal surface of skull

= bruising of surface

266
Q

what is it called if pia mater is ruptures?

A

laceration

267
Q

what is contrecoup damage?

A

rebound of brain after direct impact causes damage to opposite side of brain

268
Q

what is the issue in prion protein?

A

prion protein change’s host protein into pathological form

269
Q

histology in prion disease

A

spongiform encephalopathy = lots of vacuoles

270
Q

features of vCJD and its cause

A
  • sporadiac neuropsych
  • cerebellar ataxia, dementia
  • link to BSE (mad cow disease)
271
Q

neuropathology of Alzheimer’s

A
  • extracellular plaques (amyloid-beta)
  • neurofibrillary tangles
  • cerebral amyloid angiopathy (deposition of proteins in blood vessels)
  • neuronal loss (cerebral atrophy)
272
Q

how does tau cause Alzheimer’s?

A

hyperphosphorylated tau
intracellular accumulation
cell death

273
Q

histology of Parkinson’s

A
  • Lewy Bodies (alpha-synuclein)
  • loss of dopaminergic cells from substantia nigra
  • substantia nigra connects to basal ganglia
274
Q

what staging system is used in Parkinson’s and Alzheimer’s?

A

Braak stages

275
Q

3 main differentials for Parkinson’s?

A
  • multiple system atrophy
  • corticobasal degeneration
  • progressive supranuclear palsy
276
Q

which of these are tauopathies?

A

corticobasal degeneration

progressive supranuclear palsy

277
Q

what is multiple system atrophy?

A

alpha-synucleinopathy
targets glial cell, tends to affect cerebellum
patient presents with fall

278
Q

histology of Pick’s disease

A
  • gliosis and neuronal loss
  • balloon neurones
  • Tau +ve Pick bodies
279
Q

what are the 2 species of Tau in our brain?

A

3R and 4R

280
Q

what is ARDS?

A

diffuse alveolar damage

281
Q

phases to ARDS

A
  1. exudative phase (congested and leaky lungs)
  2. hyaline membranes
  3. organisation of exudates to form granulation tissue
282
Q

acute histological changes in asthma

A
  • bronchospasm
  • oedema
  • hyperaemia
  • inflammation
283
Q

chronic histological changes in asthma

A
  • muscular hypertrophy
  • airway narrowing
  • mucus plugging
284
Q

pathology in chronic bronchitis

A
  • dilated airways
  • mucus gland hyperplasia
  • goblet cell hyperplasia
  • mild inflammation
285
Q

what is emphysema?

A

permanent loss of alveolar parenchyma distal to terminal bronchi
secondary to inflammation

286
Q

emphysema in smoking vs A1AT

A 
smoking = centrilobular damage
A1AT = panacinar (damage throughout lungs)
287
Q

what is bronchiectasis?

A

permanent abnormal dilation of bronchi with inflammation and fibrosis
infection = most common cause

288
Q

complications of bronchiectasis

A

recurrent infection
haemoptysis
pulmonary HTN
amyloidosis

289
Q

CF genetics

A

Chr 7
CFTR gene
Delta F508

290
Q

what are the affects of CF on the different organs?

A
  • GI: mec ileus, malabsorption
  • Pancreas: pancreatitis, malabsorption
  • liver: cirrhosis
  • male: infertility
291
Q

organisms affecting lungs in CF patients

A

S. pneumoniae
H. influenzae
P. aeruginosa
B. cepacia

292
Q

Gram -ve causes of HAP

A

Klebsiella

Pseudomonas

293
Q

Bronchopneumonia features

A

infection centred around airways

low virulence organisms

294
Q

histopathology of lobar pneumonia

A
  1. congestive
  2. red hepatisation
  3. grey hepatisation
  4. resolution
295
Q

what is a granuloma?

A

collection of macrophages and mutli-nucleate giant cells

296
Q

what is pneumonitis?

A

interstitial inflammation

297
Q

with lung cancers are near the airways?

A

SCC

298
Q

with lung cancers are near the peripheral alveolar spaces?

A

mainly adenocarcinoma

299
Q

what are the non-small cell carcinoma?

A

SCC
Adenocarcinoma
large cell carcinoma

300
Q

which lung cancers is smoking associated with?

A

SCC

small cell

301
Q

features of squamous cell carcinoma

A
  • central
  • arising from bronchial epithelium
  • spreads locally, mets late
302
Q

features of adenocarcinoma

A
  • periphery
  • glandular
  • mets common and early
303
Q

what is the pre-cursor lesion in lung adenocarcinoma?

A

atypical adenomatous hyperplasia

304
Q

mutations in smokers

A

K-ras
DNA methylation issues
p53

305
Q

mutations in non-smokers

A

EGFR

306
Q

what are the features of large cell carcinoma?

A

poorly differentiated large cells

poorer prognosis

307
Q

small cell carcinoma features

A

central, near bronchi
advanced disease, poor prognosis
paraneoplastic syndrome

308
Q

histology in small cell carcinoma

A

small poorly differentiated

P53, RB1 mutation

309
Q

adenocarcinoma main molecular changes

A

EGFR mutation
ALK translocation
Ros1 translocation

Cross reference - year 5 (22 decks)

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