Histopathology Flashcards

1
Q

cancellous bone

A

medulla

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2
Q

cortical bone

A

compact

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3
Q

long bone growth

A

endochondrial ossification

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4
Q

failure of calcification at the zone of bone formation

A

results in failure of bone growth

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5
Q

features of achondroplasia

A

short limbs
trident hands
NORMAL trunk length
contracted base of skull

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6
Q

commonest of the short-limb patters of dwarfism

A

achondroplasia

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7
Q

achondroplasia affects how many

A

1/30,000

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8
Q

sporadic achondroplasia?

A

75%

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9
Q

inheritence of achondroplasia

A

Dominant

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10
Q

Intramembranous bone growth

A

(1) flat bones (skull)
fibrous connective tissue
(2) thickening (appostional growth) of the long bones

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11
Q

Endochondral bone growth

A

peiphyseal growth lates

lengthening of bone

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12
Q

growth plates fuse at:

A

around 16y

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13
Q

achondroplasia bone growth

A

restriction in growth of length

architectural disturbance of the growth plates

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14
Q

achondroplasia histology

A

disrupted chondrocyte columns

no tidy structure and irregular ossification

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15
Q

subsequent ossification

A

well-ordered columns of chondrocytes, enlarge, get to end of bone, undergo calcification

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16
Q

achondroplasia genetic abnormality

A

FGFR
1/2/3
inhibits proliferation of chondrocytes

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17
Q

osteogenesis imperfecta collagen type

A

type 1

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18
Q

type 1 collagen makes up… of matrix

A

90%

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19
Q

mild imperfecta

A

limited amount of point mutations

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20
Q

defective organic matrix in imperfecta leads to

A

defective mineralisation of bone

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21
Q

osteopetrosis defect

A

osteoclast arm of bone forming unit

more formation than resorption

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22
Q

whats happening in osteopetrosis

A

thick bone but v fragile due to inadequate collagen 1 mineralisation

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23
Q

children with osteopetrosis present

A

defective osteoclasts

bones become increasingly dense leading to disappearance of the marrow and compromised haemopoeisis.

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24
Q

how do osteopetrosis patients present?

A

pancytopaenia

treat with bone marrow transplant

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25
Q

osteomyelitis

A

disease of growing skeleton

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26
Q

who gets osteomyelitis

A

18m-18y

haematological spread

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27
Q

main cause of osteomyelitis

A

s.aureus

then entero and e.coli

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28
Q

osteoporosis >50 fractures

A

men 1 in 10

women 1 in 3

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29
Q

causes of osteoporosis

A
POST-MENOPAUSAL 
disuse
diet
drugs (heparin, ethanol, steroids)
endocrine (adrenal failure, testicular or ovarian failure)
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30
Q

3 osteoporosis fracures

A

vertebral crush fractures
NOF
Colles’

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31
Q

zone of maximum stress in femoral neck

A

950lb/sq inch

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32
Q

osteoporosis histology

A

trabecula loss and fewer connections to each other

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33
Q

trabeculae in osteoporotic vertebra

A

more loss of vertical

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34
Q

peak bone mass

A

18-20 years

then plateau then down from 30.

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35
Q

treatment for osteoporosis

A
calcium and vit.D
Exercise
Bisphosphonates
Calcitonin
HRT
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36
Q

osteomalacia

A

metabolic

inadequate mineralisation of existing bone matrix

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37
Q

most common cause of osteomalacia

A

lack of activated vit D.

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38
Q

aetiology of osteomalacia

A

Vit.D disturbance (sun, malabsorption)
Kidney disease (tubular and CRF)
IEM- hypophosphate

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39
Q

vit D absorption happens in…

A

jejunum and ileum

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40
Q

osteomalacia histology

A

inadequate mineralisation at site of high bone turnover

surface of bony trabeculae covered by thick layer of unmineralised matrix- osteoid

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41
Q

osteomalacia xray

A

structural weakness at that site and micro fractures

Looser’s Zones.

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42
Q

osteitis fibrosa cystica

A

hyperparathyroidism

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43
Q

recklinghausens’s diease

A

hyperparathyroidism

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44
Q

osteitis fibrosa cystica

A

adenoma and hyperparathyroid

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45
Q

raised calcium?

A

think hyperparathyroidism

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46
Q

Pagets is….

A

abnormal coupling of OB and OC

osteosclerotic and osteoporotic areas

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47
Q

pagets increases your risk of

A

osteosarcoma

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48
Q

pagets histology

A

woven and lemellar mismatch

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49
Q

osteosarcoma prevalence

A

15% of the 1% of bone tumours

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50
Q

who gets bone cancer?

A

<30years

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51
Q

types of osteosarcoma

A

high grade intramedullary

then parosteal, then periosteal

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52
Q

osteosarcoma happens more in children because…

A

period of maximum skeletal growth.

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53
Q

which bone tumour can happen whenever?

A

paraosteal

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54
Q

where are osteosarcomas

A

metaphyseal bart of bone.

knee common in high grade

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55
Q

osteosarcoma radiology

A

tumour from medulla towards metaphysis.
mixture of destruction and new formation.
MOTH EATEN
bone formation outside cortex/beneath periosteum=CODMANS TRIANGLE

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56
Q

treatment for osteosarcoma

A

chemo then resect.

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57
Q

high grade osteosarcoma histology

A

disorganised sheets of malignant OB
pleiomorphism
nuclear phyperchromatism
irregular islands of non-structural tumour bone

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58
Q

most common cause of chronic kidney disease

A

glomerulonephritis

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59
Q

2 important causes of kidney disease

A

diabetes

hypertension

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60
Q

GFR stages

A
  1. > 90
  2. 60-90
    3A. 45-60
    3B. 30-45
  3. 15-30
    5.<15
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61
Q

symptomatic CKD stages

A

3A and up

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62
Q

AKI definition

A

within 48 hours

rapid reduction in renal EXCRETORY function

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63
Q

oliguric phase of AKI

A

metabolic acidosis

increase urea

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64
Q

recovery phase of AKI

A

polyuria

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65
Q

nephritic syndrome symptoms

A
haematuria
azotemeia (increase nitrogenous products)
mild oedma
variable proteinuria
mild-moderate hypertension
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66
Q

nephrotic syndrome symptoms

A

hypoproteinemia
oedema
hyperlipidaemia

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67
Q

commonest cause of nephrotic syndrome

A

minimal change disease/glomerulopathy

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68
Q

minimal change disease

A

no detectable immune deposit but immune response.

respiratory infections and immunization

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69
Q

diffuse effacement of foot processes

A

minimal change disease

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70
Q

majority of glomerulonephritis are the result of

A

immune complex deposition in the wall

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71
Q

granular immunoflourescence pattern of GN

A

local deposition of circulating immune complexes

depostition of antibodies against glomerular component

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72
Q

GN in adults vs. kids

A

kids- good prognosis

adults- usually permanent compromise

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73
Q

major cause of acute nephritis in kids

A

acute proliferative GN

after group A strep

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74
Q

acute proliferative GN shows:

A

enxocapillary hypercellularity
lots of neutrophils
closed glomerular capilaries
big glomerulus

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75
Q

anti-glomerular basal membrane antibodies

A

membranous GN

commonest cause of nephrotic in adults

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76
Q

membranous GN histology

A

marked thickening of GBM
capillaries still open (not in acute proliferative)
interstitial expansion and fibrosis.

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77
Q

membranoproliferative GN histology

A

increased mesangial
localised capillary wall thickness
increased cellularity
pronounced lobulation

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78
Q

membranous GN is…

A

nephritic and nephrotic

rapidly progressing.

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79
Q

tubulointersitial nephritis caused by

A

inflammatory reactions of tubules and interstitium

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80
Q

ATN caused by

A

ischaemia or toxic tubulary injury

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81
Q

ATN histology

A

focal necrosis and desquamation of cells into lumen.

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82
Q

acquired renal cystic disease

A

mostly post-dialysis

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83
Q

nephronophthisis-medullary cystic kidney disease

A

hereditary

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84
Q

ADPKD

A

adult
1 in 500
bilateral

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85
Q

symptoms of ADPKD

A
haematuria
UTI
Abdo mass
hypertension
beri-beri
cysts in other organs.
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86
Q

ARPKD

A

1/20,000
large abdo mass at birth
liver abnormalities

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87
Q

ARPKD prognosis

A

death shortly after birth
renal filaure
hypertension
portal hypertension

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88
Q

nephronoPHTHisis

A

medullary cystic disease

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89
Q

simple renal cysts

A

common autopsy finding

no significance

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90
Q

neohroLITHiasis

A

20-30y
males
recur

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91
Q

most common kidney stone

A

calcium oxalate

due to hypercalcaemia

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92
Q

2nd/3rd/4th most common stones

A

phosphate- proteus breaks down urea
urate (gout)
Cysteine (IEM)

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93
Q

causes of renal stones

A
dehyration
sarcoid hypercalcaemia
cushings
oxalate foods (brocolli)
Bladder obstruction
PCKD
Medullary sponge kidney
Stents, catheters, crystallisation, foreign substances.
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94
Q

acute inflammatory infiltrate in the interstitium and tubular lumina

A

acute pyelonephritis

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95
Q

chronic pyelonephritis histology

A

surface of kidney irregular.
irregular scarred area with remaining parenchyma bulging.

MANY colloid filled tubules.
THYROIDISATION of the kidney.

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96
Q

hypertensive kidney histology

A

fibrous intimal thickening or sclerosed renal arterioles

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97
Q

benign renal tumours

A

papillary adenomas (<5mm) fibromas

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98
Q

malignant renal tumours

A

RCC most common

then 20% TCC

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99
Q

RF for kidney RCC

A

smoking, high blood pressure, heavy metals, obesity, von hippel lindau

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100
Q

presentation of kidney RCC

A

paraneoplastic conditions
mass
haematuria
back pain

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101
Q

renal cell histology

A

clear cytoplasm

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102
Q

transitional cell carcioma is at the…

A

renal pelvis

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103
Q

TCC of kidney histology

A

pelvis growing in a pushing fashion around the medullary renal tubules.

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104
Q

normal thyroid

A

colloid filled acinus
follicular lining
vascular
regulates BMR

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105
Q

commonest cause of hypothyroidism

A

hashimotos
(antibodies to thyroid)
lymphocytic destruction of thyroid

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106
Q

deep voice in hypothyroidism

A

deposition of matrix substances in viscera and skin

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107
Q

atrophic thyroid

A

hashimotos

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108
Q

85% of hyperthyroidism cases

A

Graves

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109
Q

causes of hyperthyroidism

A
graves
hyperfunctional multinodular goiter
hyperfunctional adenoma (benign follicular tumour)
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110
Q

staring gaze, lid lag, exophthalmos

A

graves

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111
Q

diffuse toxic goitre

A

graves

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112
Q

symmetrical enlargement of thyroid

A

graves.

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113
Q

multinodular goitre

A

usually euthyroid
larger ones may cause dysphagia
lumpy neck.
(don’t really need to be removed though).

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114
Q

thyroid adenoma

A

benign
euthyroid (usually)
when toxic=hyperthyroidism
solitary follicular nodule in NORMAL surrounding gland.

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115
Q

disproportionate nodule

A

hyperplastic in a nodular background

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116
Q

thyroid cancers

A

80% pappillary
15% follicular
medullary
anaplastic

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117
Q

papillary thyroid cancer

A

cystic
can be multifocal
PSAMMOMA bodies- empty nuclei of epithelium covered papillae cells.

(good prognosis)

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118
Q

follicular thyroid cancer

A

widely invasive

irregular margins

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119
Q

medullary thyroid cancer

A
from C cells (Celly in the middle)
neuroendocrine tumour- secrete calcitonin
amyloid stroma (pink)
MEN 2A/2B
BROWN STAIN POSITIVE
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120
Q

anaplastic thyroid cancer

A

old people
aggressive
no response to treatment
die in months

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121
Q

primary hyperparathyroidism causes

A

primary hypercalcaemia

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122
Q

primary hyperparathyroid causes

A

adenoma (95%)- one gland
hyperplasia- both glands
carcinoma- RARE

associated with MEN1/2A/2B

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123
Q

symptoms of primary hypercalcaemia

A

bones
stones (porosis, osteitis fibrosa cystica- cysts eat up Ca2+)
groans
psychiatric overtones

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124
Q

causes of secondary hyperparathyroidism

A

CRF

also Vit.D/calcium problems, malabsorption, low serum Mg, tissue resistance, pseudohypoparathyroidism

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125
Q

Sestamibi scan

A

radioactive tech99 PARATHYROID GLANDS

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126
Q

primary hyperPTH treatment

A

remove 3.5 glands so they don’t have to take Ca and Vit D forever.

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127
Q

parathyroid cancer

A

calcium >3.5

bone disease, renal stones, mets, laryngeal nerve damage

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128
Q

adrenal glands steroids

A

glucocorticoids (steroid)
mineralocorticoids (aldosterone)
sex steroids (oes and andro)
medulla- adrenaline

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129
Q

Primary adrenocortical insufficiency

A

Addison’s disease

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130
Q

Addison’s disease

A
autoimmune destruction
TB
metastatic cancer
AIDS
congenital hypoplasia
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131
Q

secondary adreno insufficiency

A

less ACTH produced

treatment with steroids

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132
Q

in addisons what happens to adrenaline

A

nothing

the medulla is unaffected.

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133
Q

Addison’s symptoms

A

weakness/tiredness
GI disturbance
hyperpigmentation
hypotension: potassium retained

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134
Q

why do we get hyperpigmentation in addisons?

A

precursor of ACTH and melanocyte stimulating hormone

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135
Q

what triggers an adrenal crisis?

A

infection
trauma
surgery

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136
Q

signs of an adrenal crisis

A

vomiting
abdo pain
hypotension
coma

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137
Q

Cushings

A

pituitary adenoma causing diffuse hyperplasia

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138
Q

most common cause of Cushing’s

A

iatrogenic

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139
Q

endogenous causes of Cushing’s

A

Pituitary adenoma (CD)

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140
Q

adrenal cortical adenoma

A

most non-functional

if functional- cushing’s syndrome or high aldosterone

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141
Q

adrenal cancer

A

usually FUNCTIONAL
virilism
large and invasive
venous and lymph spread

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142
Q

phaeochromocytoma

A

tumour in adrenal medulla
adrenaline
surgically correctable hypertension
XS urine adrenaline

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143
Q

90% of phaeochromocytomas are

A

unilateral
adrenal
benign
hypertension inducing

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144
Q

MEN syndromes

A

inherited

proliferative

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145
Q

MEN 1:

11q, tumor suppressor

A

Parathyroid adenoma/hyperplasia
Endocrine glands adenoma/hyperplasia
Carcinoid tumours

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146
Q
MEN 2(a):
10q
A

Parathyroid adenoma/hyperplasia
Medullary thyroid cancer
Phaeochromocytoma

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147
Q
MEN 2(b)
10q ret
A

Medullary thyroid cancer

Phaeochromocytoma

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148
Q

subtypes of endometrial hyperplasia

A

simple-cystic hyperplasia
complex hyperplasia
atypical hyperplasia=EIN

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149
Q

causes of endometrial hyperplasia

A
obesity
anovulatory cycles
prolonged oestrogen
PCOS
functioning ovarian or adrenal tumours.
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150
Q

Atypical endometrial hyperplasia

A

EIN
may progress to adenocarcinoma
may regress with just progesterone

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151
Q

Most common malignant tumour of female genital tract

A

endometrium

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152
Q

how many HNPCC get endometrial cancer?

A

20-30%

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153
Q

type 1 endometrial cancner

A

oestrogen dependent (most common)

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154
Q

type 2 endometrial cancer

A

oestrogen independent.

postmenopausal

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155
Q

ectocervix

A

squamous epithelium

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156
Q

endocervix

A

mucin secreting columnal

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157
Q

risk factors for cervical cancer

A
early age of first intercourse
multiple partners
smoking
genital infections
lots of sex
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158
Q

HPV

A

dsDNA
no envelope
anogenital
mucocutaneous

E6+E7 oncogenes- bind to retinoblastoma and p53- expands life span.

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159
Q

where does HPV work?

A

reserve cells of TZ

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160
Q

phases of HPV infection

A
latent infection (just one)
productive infection
integration
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161
Q

high frade CIN and CGIN evolve to

A

invasive carcinoma

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162
Q

how long does it take for CIN to progress to cancer?

A

10y

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163
Q

most common cervical cancer

A

squamous cell cancer

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164
Q

types of ovarian cancer

A

surface epithelial stromal- MOST COMMON
sex cord stromal
germ cell
metastatic

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165
Q

genetic factors and ovarian cancer

A

BRACA 1 and 2

HNPCC

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166
Q

Borderline epithelial ovary tumours

A

epithelial proliferation

no invasion of stroma

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167
Q

Adenocarcinoma of ovary

A

commonest subtype of SEROUS

present late

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168
Q

Germcell tumour ovary

A

primordian germ cells
most teratoma/dermoid
young girls and children

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169
Q

sex cord stromal tumours ovary

A

granulosa cell
theca sertoli cells
Leydig cells
abnormal oestrogen, inhibin and testosterone

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170
Q

metastatic ovarian cancer

A

FROM stomach, colon, appendix, breast pancreas

krukenberg- SIGNET RING

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171
Q

B lymphoid cell

A

naive b cell leaves bone marry and enters blood to secondary lymphoid follicles
expresses Ig on surface

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172
Q

Secondary b lymphoid follicle

A

t cell dependent b cell proliferation
antigen dependent
b cells become centeroblasts
centeroblasts make plasma cells and marginal zone b cells.

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173
Q

MALT

A

largest secondary lymphoid organ
surface epithelium with underlying lymphoid follicle and T zone
b and t cells enter the surface epithelium

174
Q

life of a primary t cell

A
thymus
t cell
t cell receptor rearragement
CD4 or CD8 cells
antigen INDEPENDENT process
exit as mature t cells.
175
Q

antigen dependent process of T cell

A

T zone of lymph node or MALT

176
Q

EBV associated with (cancers)

A

Burkitt
Hodgkin
post transplant lymphoma
AIDS lymphoma

177
Q

Hep C and lymphoma

A

low grade B cell non-hodg

178
Q

Kaposi sarcoma

A

HHV8

179
Q

Non hodgkins histo

A

1-5% malignant in background of inflammatory

REED STERNBERG

180
Q

Burkitt

A

EBV

mature b cell neoplasm

181
Q

prematurity counts for …. of infant deaths

A

45%

182
Q

cancer counts for … of child deaths

A

22%

183
Q

thick bowel secretions makes you think

A

CF

184
Q

best way to diagnose biliary atresia

A

livery biopsy

185
Q

congenital cystic adenomatoid malformation

A

lung has holes

may present with infection

186
Q

multicystic dysplastic kidney

A

unilateral

187
Q

kid cancers

A

leukaemia
CNS
lymphoma

188
Q

stenosis

A

30% single vessel disease
30% double
40% triple

189
Q

site of stenosis is usually

A

within first 4cm of LCA

more distal in RCA

190
Q

non arthero-sclerotic lesions of coronary arteries

A

emboli

arteritis (inflammation of vessel wall)

191
Q

2 types of MI

A
  1. full thickness

2. subendocardial type (extensive infarct of inner 1/3 of myocardium)- in triple disease

192
Q

Left coronary artery supplies

A

anterior wall
apex
anterior part of interventricular septum

193
Q

Left circumflex supplies

A

lateral wall

194
Q

Right coronary artery supplies

A

posterior wall

posterior IV septum

195
Q

biggest complication of MI

A

arrthymia

196
Q

cor pulmonale

A

R ventricle enlargement
due to pulmonary hypertension due to disease of the lung

right V dilatation and hypertrophy >0.5cm

197
Q

pickwickian syndrome

A

obesity causing decreased chest movement and subsequent cor pulmonale

198
Q

mitral stenosis

A

ONLY Rheumatic fever but rare

199
Q

aortic stenosis

A

most commonly due to calcification of valve

or a bicuspid congenital valve

200
Q

cardiomyopathy 3 types

A

dilated
restricted
hypertrophic

201
Q

dilated cardiomyopathy

A

alcohol
pregnancy
genetic
post-viral

202
Q

restricted cardiomyopathy

A

amyloid infiltration of myocardium in OLD

203
Q

hypertrophic cardiomyopathy

A

AD

asymmetrical LVhypertrophy in YOUNG

204
Q

atherosclerosis more common in

A

coronary
carotid
distal
femoral arteries

205
Q

Marfans and aneurysms

A

media in vessels is collagen (Marfans have collagen disorder)

206
Q

Large aneurysms

A

atherosclerotic
dissecting
syphillis

207
Q

Medium aneurysms

A

Berry
Mycotic
Traumatic

208
Q

Microaneurysms

A

Charcot-Bouchard
Diabetic
Cerebral amyloid

209
Q

chrons confined to colon

A

20%

210
Q

crohns biposy

A
mesentery thickened
oedematous
superficial ulcers at first
ulcers then deepen and coalesce to form transverse and longitudinal ulcers
COBBLESTONE
211
Q

crohns histo

A

transmural inflammation
granulomas (non-nec)
crypt
fissures in muscularis propria–> abscess
fistula formation
fibrosis and stricture formationa (apple coring)

212
Q

UC histology

A
crypt abscesses
neutrophils in lamina propria
architectural distorition
gland branching
loss of normal parallel arrangements. 
purple lymphocytes
213
Q

crohns and cancer

A

small bower

214
Q

UC and cancer

A

colon

215
Q

paralysis of the motor function of the transverse colon

A

toxic megacolon

216
Q

colon cancer generally starts with

A

polyps

217
Q

metaplasia

A

acquired form of altered differentiation

218
Q

dysplasia

A

abnormal growth and differentiation of tissue

may be premalignant

219
Q

types of colorectal polyp

A

Inflammatory
Hamartomatous
Neoplastic

220
Q

inflammatory pseudopolyps

A

seen in UC and Crohns
inflammatory tissue
hyperplastic mucosa

221
Q

hamartoma

A

benign tumout like lesion

222
Q

Peutz Jeger

A

GI polpys
AD- small bowel more
perioral pigmentation
lips, pals, genitalia

223
Q

juvenile polyps

A
cyst glands
normal or inflammed epithelium
SMAD4
80% rectum
bleeding, prolapse
224
Q

Peutx Jeger and cancer

A

73% get carcinoma

225
Q

adenoma=

A

non reversible dysplasia
disregulated proliferation
premalignant

226
Q

types of adenoma

A

tubular
tubulovillous
villous

227
Q

flat adenoma

A

high malignant potential

associated with NHPCC or FAP

228
Q

polpys more malignant if:

A

Villous
Big >5cm
Dyslastic

229
Q

polyps that aren’t dangerous

A

hyperplastic polyps

benign

230
Q

leiomyoma

A

not malignant
FIBROID
muscularis mucosa
can cause obstruction of ileocaeccal valve

231
Q

colon cancer

A

women- colon
men- rectum

RECTUM overall

232
Q

all carcinomas start from

A

adenomas

233
Q

DUKES staging for colon cancer

A

A- spread to tissue of bowel wall 99% survive
B- all the way through muscularis propria
C1- lymph nodes (even if not all the way though)
C2- apical node 35% survive
D- Distant mets. 5%

234
Q

HNPCC

A

dominant
younger
RIGHT SIDE
multiple

235
Q

Amsterdam criteria

A
  1. 2 first degree relatives with colorectal cancer
  2. 2 successive generations
  3. one of the cancers before 50 years
  4. FAP excluded
236
Q

FAP

A

will develop cancer unless we cut them out
entire colon affected
up to thousands

237
Q

liver adenoma

A

women
associated with OCP
some may become malignant

238
Q

focal nodular hyperplasia

A

mimics cirrhosis
central car
can become very large
women

239
Q

hepatocellular carcinoma

A

most common liver cancer

MEN

240
Q

causes of HCC

A
cirrhosis
Hep B/C (common in Africa)
ASH/NASH
autoimmune hepatitis
A1antitripsin
Wilsons
241
Q

HCC on histo

A

pseudoglandular formation

242
Q

Fibrolamerllar HCC

A

young people

no background cirrhosis

243
Q

Hepatoblastoma

A

children under 5
male
AFP raised
lobulated

light and dark pattern

244
Q

Angiosarcoma

A
rare
arsenic
anabolic steroids
vinyl
old men
245
Q

Cholangiocarcioma

A

aggressive and deadly
chronic inflammation of bile ducts

round glandular

246
Q

Hep A

A

faecal-oral
can be mild
can lead to liver failure

247
Q

Hep B

A

body fluids
acute and chronic
can lead to cirrhosis
HCC

248
Q

Hep C

A

blood
usually chronic
cirrhosis
HCC

249
Q

Hep D

A

friends with B

fulminant hepatitis

250
Q

Hep E

A

food/water
acute/fulminant hepatitis
severe if PREGGERS!

251
Q

fatty liver disease causese

A

alcohol
obesity
diabetes
drugs

252
Q

fatty liver disease can lead to

A

fibrosis
cirrhosis
v.common!

253
Q

autoimmune hepatitis

A

ALT raised.
IgG
ANA +
cirrhosis

254
Q

primary sclerosing cholangitis

A
males AMA/p-ANCA
ulcerative colitis
inflammation and fibrosis of larger intra and extra hepatic bile ducts
can lead to cirrhosis
colon cancer
255
Q

primary biliary sclerosis

A

women AMA
alk phos raised
small bile ducts
cirrhosis

256
Q

Wilson’s disease

A

chromosome 13
copper
childhood presentation
increased risk of HCC

257
Q

Haemochromatosis

A

chromosome 6
iron
cirrhosis
increased risk of HCC

258
Q

Alpha-1-antitrypsin

A
chromosome 14
protein accumulation in liver
fibrosis
cirrhosis
increased risk of HCC
259
Q

how many lung lobes

A

L-2
R-3
10 segments each have a branch of the artery and a bronchus

260
Q

hyaline membrane disease

A

preterms
surfactant
cyanosis after birth

261
Q

hyaline histology

A

alveolar damage and formation of hyaline membrane

262
Q

primary respiratory infection

A

no underlying cause

263
Q

secondary respiratory infection

A
weakened immune 
(loss of cough, ciliary defects, mucus, hypogammaglobulinaemia, pulmonary oedema)
264
Q

chronic bronchitis

A

cough+sputum for 3m in 2 years

265
Q

pneumonia histology

A

alveoli filled with suppurative exudate

266
Q

abscess vs pneumonia

A

abscess- fluid filled cavity with pus and lined with granulation tissue (new RBCs and FBs)

267
Q

causes of M.tuberculosis

A
m hominis
m bovis (milk/unpasteurised cheese)
268
Q

types of TB

A

primary
secondary
miliary (mets)

269
Q

TB on histology

A
granulomas
ZN stain (pink)
acid fast bacilli
caseating necrosis
Langerhans multinucleated giant cells are common
resists heat but killed by UV light.
270
Q

define congestion

A

increased volume of blood in affected tissue or part

not fluid like oedema

271
Q

2 types of oedema

A

hemodynamic

due to microvascular injury

272
Q

hemodynamic oedema

A

increased hydrostatic pressure
decreased osmotic pressure
lymphatic drainage

273
Q

increased hydrostatic pressure

A

left sided heart failure
mitral stenosis
volume overload
pulmonary vein obstruction

274
Q

decreased osmotic pressure

A

hypoalbuminaemia (nephrotic etc)

275
Q

oedema due to microvascular injury

A

infectious
toxins
liquid aspirate
etc.

276
Q

diffuse injury to microvascularture of lungs:

A

ARDS

277
Q

elderly more commonly have what type of pneumonia?

A

broncho

278
Q

tidal volume

A

amount in/ex in normal breath

279
Q

vital capacity

A

exhaled after max inhale

280
Q

residual volume

A

air left in lung after ex

281
Q

Total lung capacity

A

vital capacity and residual volume.

282
Q

FEV1 reduced with

A

restrictive/obstructive

283
Q

Forced expiratory ratio (FEV1:VC)

A

low in obstructive

284
Q

obstructive airway diseases

A

emphysema
chronic bronchitis
bronchiectasis
asthma

285
Q

restrictive airway disases

A

acute (ARDS)

chest wall deformity

286
Q

chronic bronchitis in adults caused by

A

cigarette

h.influenza and strep pneumoniae

287
Q

smoking and the lungs

A

decreased ciliary action
direct damage to epithelium
inhibits bacteria clearance

288
Q

pathogenesis chronic bronchitis

A
bronchiolitis
destruction of wall around
centri lobular emphysema
hypersecretion of mucus (hypertrophy of glands)
increased number of goblet cells.
289
Q

emphysema

A

permanent enlargement of airspaces distal to terminal bronchioles
destruction of walls
6 types

290
Q

6 types of emphysema

A
centrilobular
panlobular
paraseptal
irregular
bullous
interstitial
291
Q

what is an emphysema?

A

an air aneurysm

292
Q

smoking causes what type of emphysema?

A

centri-lobular
bronchioles of upper lobes in particular
dust laden macrophages

293
Q

panlobular emphysema

A

alpha-1-antitripsin people
all air spaces distal to terminal bronchioles
lower lobes

294
Q

what does alpha 1 antritipsin do?

A

inhibits collagenase elastase and other proteases

295
Q

paraseptal emphysema

A

upper lobes

periphery of lobules

296
Q

irregular emphysema

A

ACINUS
around old healed scars at apices
air trapping due to fibrosis

297
Q

bullous emphysema

A

10mm diameter

298
Q

interstitial emphysema

A

traumatic rupture of airway
can become sub-cutis
bubblewrap skin.

299
Q

bronchiectasis

A
necrotizing
dilation
irreversible
lower lobes
cough-fever-foul smelling purulent sputum
300
Q

causes of bronchiectasis

A

CF
Kartageners
foreign body
necrotizing pneumonia

301
Q

atopic asthma histology

A

mucus plugs
CRUSCHMANN spirals
CHARCOT LEYDEN crystals
mucus gland hypertrophy

302
Q

non-atopic asthma

A

aspirin induced

bronchoconstrictor leukotrines

303
Q

RF for bronchiogenic cancer

A
smoking
asbestos
radiation
oncogenes (C-myc and K-ras)
Scarring
304
Q

layers of GI tract

A

musculais propria
submucosa
muscularis mucosa
mucosa

305
Q

incisors to duodenum

A

40cm of oesophagus

306
Q

reflux oesophagitis risk factors

A
hiatus hernia
peptic ulcer
smoking
alcohol
excessive vomiting
pregnancy
diabetes
307
Q

complications of oesophagitis

A

stricture
barretts
neoplasia

308
Q

achalasia

A

distal oesophagus
inflammatory destruction of myenteric ganglion cells
can lead to SCC

309
Q

chagas disease

A

trypanosoma cruzi

blood sucking bug

310
Q

barretts metaplasia

A

replacement of squamous with glandular

reflux of acid and bile

311
Q

squamo columnar junction

A

length of barretts between SCJ and GEJ

312
Q

4 types of barretts metaplasia

A

gastric cardia
gastric body
pancreatic (Rare)
intestinal (most cancerous)

313
Q

oesophagus cancer

A
lower>upper>middle
men
mostly adenocarcinoma with 20% squamous
SCC- poor prognosis
adenocarcinoma- good prognosis
rare but lethal because patients present late
314
Q

progression of barretts

A

normal squamous
barretts
dysplasia
adenocarcinoma

315
Q

psueudo achalasia

A

stricture due to infection

316
Q

which stomach bit has special cells?

A

body- glandular

cardiac and antral have no special cells.

317
Q

types of gastritis

A

A for autoimmune
B for bacterial
C for chemical

318
Q

type A gastritis

A

chronic atrophic gastritis

IM

319
Q

type B gastritis

A

chronic superficial gastritis

320
Q

type C gastritis

A
reflux gastritis (bile)
reactive gastritis (aspirin, NSAIDS, alcohol)
oedema telangiectasia and lack of inflammatory cells.
321
Q

gastritis histology

A

changes in length of glands
increase size of blood vessels
fibrosis
minimal immune inflammation

322
Q

diseases caused by H. pylori

A

gastritis
ulcer
MALT lymphoma
carcinoma

323
Q

MALT lymphoma and h.pylori

A

eradiation of pylori with PPI and Abx can regree the lymphoma

324
Q

gastric cancer progression

A
normal mucosa
h pylori creates superficial gastritis
atrophic gastritis
intestinal metaplasia (pre cancerous)
dysplasia
carcinoma
325
Q

h pylori likes to hang out…

A

in the antrum

326
Q

types of stomach cancer

A

adenocarcinoma
lymphoma
neuro-endocrine tumour
GIST

327
Q

adenocarcinoma of the stomach

A
men
japan
diet (high salt)
h.pylori
poor prognosis if advanced
328
Q

gastrointestinal stromal tumour

A
GIST
rare
stomach>small intestine>oesophagus 
mutation of tyrosine kinase
give them TK inhibitors!
329
Q

coeliac

A

intraepithelial lymphocytosis

infiltration of lamina propria by plasma cells and lymphocytes

330
Q

refractory sprue

A

in coeliac (non-responsive to gluten-free) can indicate developing ulcerative jejunitis
a precursor for lymphoma
ENTEROPATHY ASSOCIATED T CELL LYMPHOMA

331
Q

commonest small bowel protozoa

A

giardiasis
contaminated water
more in AIDS

332
Q

giardia histology

A

small intestine mucosa can be normal to inflammed
can see the little buggers
if seen suspect immunosupression

333
Q

small bowel cancers

A
adenomas- benign, polyps
adenocarcinoma- coeliac, crohns, FAP
Lymphoma (b cell-Burkitt, EATL)
GIST
neuro endocrine tumours
334
Q

neuroendocrine tumours

A

carcinoids
if functional and liver mets–carcinoid syndrome

vomiting
abdo pain
nausea
lethargy

335
Q

coopers ligament

A

CT underlying pectoralis fascia to skin of breast

336
Q

glandular element of breast divided into

A

branching duct system and

terminal duct lobular units

337
Q

secretory part of breast

A

TDLU

338
Q

TDLU connects to

A

sub-segmental ducts then
segmental ducts to
collecting duct (lactiferous)
which empties to nipple

339
Q

how many collecting ducts in breast?

A

15-20 per boob

340
Q

ductal lobular normal histology breast

A

inner epithelium
outer myoepithelium
very different on histology

341
Q

epithelial breast cells

A

epithelial membrane antigen

342
Q

myoepithlial breast cells

A

best marker is actin

343
Q

reticulin stain

A

for basement membrane in breast

344
Q

inflammatory breast things

A

acute mastitis
chronic mastitis
mammary duct ectasia
fat necrosis

345
Q

proliferative breast things

A

fibrocytic change

radial scar

346
Q

benign breast tumours

A

adenoma
fibroadenoma
papilloma

347
Q

malignant breast tumours

A

carcinoma
sarcoma
Paget’s disease
Phylloides

348
Q

bloody nipple discharge

A

duct papilloma

carcinoma

349
Q

peau d’orange breast

A

carcinoma

oedema

350
Q

fibrocystic breast change

A

25-45

hormonal

351
Q

fibrocystic breast histology

A
TDLU
cysts
fibrosis
apocrine metaplasia
epithelial hyperplasia
calcification
352
Q

fibroadenoma

A

commonest benign breast tumour

20-35

353
Q

fibroadenoma histology

A

proliferating ducts

connective tissue stroma

354
Q

phylloides

A
leaf like
40-50
benign or malignant
mesenchymal bit is malignant
EXCISE OUT!
355
Q

phylloides histology

A

epithelial and mesenchymal elements.

356
Q

breast cancer RF

A
female
age
oestrogen
obesity
family history
BRCA 1 (17)
BRCA 2 (2)
357
Q

BRCA 1

A

ovary and breast

358
Q

insitu breast cancer

A

ductal

lobular

359
Q

invasive breast cancer

A

ductal

lobular

360
Q

paget’s disease nipple

A

underlying ductal cancer in 2%

361
Q

paget’s nipple histology

A

involvment of epidermis by malignant ductal cancer cells.

362
Q

breast screening

A

50-69

3 yearly mammogram

363
Q

what is the marker for breast cancer?

A

microcalcification!

364
Q

microcalcification

A

not always malignant
not all cancers
usually associated with ductal carcinoma in situ

365
Q

breast cancer histology

A

stellate lesions
circumscribed soft tissue
density/mass

366
Q

triple approach

A

breast clinicians
radiologists
pathologists

FNA
core biopsy

367
Q

breast cancer CYTOLOGY staging

A
C1 inadequate
C2 benign
C3 atypia
C4 suspicious of malignancy
C5 Malignant
368
Q

breast cancer HISTOLOGY staging

A
B1 normal
B2 benign
B3 benign but uncertain
B4 suspicious of malignancy
B5 malignant

a in situ
b invasive

369
Q

babies of diabetic mums

A

macrosomia
perinatal death
malformation
hypertrophy of langerhans/b cell hyperplasia

370
Q

b cells are stimulated by glucose….

A

after 24 weeks gestation

371
Q

macrosomia

A

big organs (liver, heart, adrenals)
lots of fat
30% transient cardiomegaly

372
Q

infants of insulin dependent mums are….

A

8x more likely to have major malformation

373
Q

coloboma

A

keyhole in eye

374
Q

diabetses and the placenta

A

single umbilical artery
villous maturity
villous oedema
variable villous vascularity

375
Q

clinodactyly

A

curved 5th finger

376
Q

AVSD and downs

A

deficient AV septum

377
Q

complete AVSD

A

large ventricular component beneath either or both the superior or inferior bridging leaflets of the AV valve. The defect involves the whole area of the junction of the upper and lower chambers of the heart

378
Q

partial AVSD

A

In the partial AVSD, there is a defect in the primum or inferior part of the atrial septum but no direct intraventricular communication

379
Q

anencephaly

A

missing major bit of brain

380
Q

encephalocele

A

sac like protrusions from the brain

381
Q

hydranencephaly

A

brain’s cerebral hemispheres are absent to varying degrees and the remaining cranial cavity is filled with cerebrospinal fluid

382
Q

iniencephaly

A

a defect to the occipital bone, spina bifida of the cervical vertebrae and retroflexion (backward bending) of the head on the cervical spine

383
Q

hyrtl anastomosis

A

unique communicating vessel between 2 umbilical arteries that regulates even distribution

384
Q

wharton’s jelly

A

mucus
connective tissue in umbilical cord
gelly
insulates umbilical blood vessels.

385
Q

furcate cord insertion

A

umbilical vessels separate and fork
lose protection from Wharton’s Jelly
liable to thrombosis and damage

386
Q

velamentous cord insertion

A

the umbilical cord inserts into the fetal membranes (choriamniotic membranes) not the usual middle of placenta

387
Q

amnion

A

innermost membrane that encloses the embryo

388
Q

chorion

A

the outermost membrane surrounding an embryo

389
Q

decidua

A

the thick layer of modified mucous membrane which lines the uterus

390
Q

yolk sac

A

a membranous sac containing yolk attached to the embryos

391
Q

amnion nodules

A

nodules on the fetal surface of the amnion, and is frequently present in oligohydramnios

392
Q

circummarginate

A

insertion of the membranes away from the placenta without a distinct ridge at the point of insertion

393
Q

chorion frondosum

A

the embryonic portion of the placenta

394
Q

cotyledon

A

Each cotyledon consists of a main stem of a chorionic villus as well as its branches and subbranches

395
Q

hofbauer cells

A

oval eosinophilic histiocytes with granules and vacuoles found in the placenta, which are of mesenchymal origin, in mesoderm of the chorionic villus, particularly numerous in early pregnancy.

396
Q

testes lymph

A

para-aortic

397
Q

testicular lobules

A

250

each has 4 seminiferous tubules

398
Q

seminiferous tubules contain

A

sertoli cells and germ cells

399
Q

sperm

A

spermatagonium
spermatocyte
spermatid
spermatazoon

400
Q

interstitium cells testes

A

Leydig cells

401
Q

rete testis

A

hilus
receives luminal contents from tubules
emptes to efferent ducts

402
Q

efferent ducts

A

12-15 tubules in head of epididymus

403
Q

epididymus

A

connects efferent ducts to vas deferens

404
Q

vas deferens

A

empties into prostatic urethral at

velumontanum

405
Q

cryptorchidism

A

most unilateral
sterility
germ cell tumours
need to operate before 6 years

406
Q

mumps orchitis

A

painful due to stretched tunical albugenia

usually tests become atrophic and bilateral infertility

407
Q

idiopathic granulomatous orchiditis

A

uncommon
unilateral
middle aged men
reaction to extravasated sperm??

408
Q

syphilis orchitis

A

rare

granulamatou inflammation with central necrosis (gumma)

409
Q

ecto/endo/meso

A

ecto- skin, brain, spinal cord
meso- everything else except…
endo- gut

410
Q

most germ cell tumours are

A

malignant.

painless unilateral testes enlargement

411
Q

kleinfelters increases your risk of

A

germ cell tumours

412
Q

types of germ cell tumours

A
in situ (intratubular)
invasive
413
Q

invasive germ cell tumours

A

seminoma
non-seminiferoud (embyo, yolk sac, chorio, teratoma)
mixed

414
Q

seminoma vs. non seminoma treatment

A

seminoma- radiotherapy

non-seminoma- chemotherapy

415
Q

commonest type of testicular tumour

A

seminoma

416
Q

classical seminoma histology

A

sheets of rounded cells with clear cytoplasm and variable lymphocytic infiltrate

417
Q

spermatocytic seminoma

A

old
mixed population of small, intermediate and giant cells
good prognosis

418
Q

non-seminiferous EMBRYONAL

A

20-30 years
aggressive
cells are anaplastic and arranged in glands, alvoli, solid or papillary growth.
usually mixed.

419
Q

non-seminiferous YOLK SAC

A

<3years
Schiller-Duval bodies
serum AFP raised

420
Q

non-seminiferous CHORIOCARCINOMA

A

rarely pure form
cyto and syncitioblasts
MALIGNANT hightly
raised hCG

421
Q

non-seminiferous TERATOMA

A

can have mature or immature tissue
second most common in kids
good prognosis
adult form rare

422
Q

mixed testicular tumours

A

treated as non-seminoma

423
Q

spread of testicular tumours

A
rete testis
epididymus
para-aortic lymph
mediastinal lymph
lung, liver, bone
424
Q

staging germ cell tumours

A

1: testis
2. testis+para aortic
3. testis +mediastinal or sypraclavicular lymph
4. mets

425
Q

prostate anatomy

A

5 lobes
inner zone- nodular hyperplasia
outerzone- carinoma

426
Q

increased weight of prostate in BPH

A

60-100gms (from 20)

427
Q

prostate cancer aetiology

A

blacks>whites>asians

428
Q

gleason’s score

A

grading the growth pattern

429
Q

staging prostate cancer

A

A not palpable
B palpable confined
C extracapsular
D metastasis

430
Q

normal PSH

A

50-60 <5