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* Year 2 EMS > MOD - intro to mod + tumour characteristics/classification > Flashcards

MOD - intro to mod + tumour characteristics/classification Flashcards

1
Q

what is disease?

A

an abnormality of the body that causes loss of normal health

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2
Q

what is the natural history of a disease?

A

how far along the disease pathway the patient is

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3
Q

what does pathogenesis mean?

A

the mechanism by which the etiological factors lead to disease

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4
Q

what does the prefix dys- mean?

A

disordered

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5
Q

what does meta- mean?

A

change from one state to another

eg metastasis

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6
Q

what does the suffix -osis mean?

A

state or condition

eg osteoarthrosis

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7
Q

what does -oid mean?

A

bearing a resemblance to

eg rheumatoid disease

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8
Q

what does -penia mean?

A

lack of

eg thrombocytopenia

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9
Q

what does -cytosis mean?

A

increased number of cells

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10
Q

what does -plasia mean?

A

disorder of growth

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11
Q

what does -ectasis mean?

A

dilation

eg bronchiectasis

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12
Q

what are the 2 main types of autopsy?

A

coronial (forensic and non-forensic)

consented (aka hospital)

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13
Q

what is a labile cell population? name 3 examples

A

one that is constantly replenishing itself

eg skin, GI tract, blood cells in bone marrow

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14
Q

why don’t fibroblasts need to adapt to environmental change?

A

because they can survive severe metabolic stress without harm (eg absence of O2)

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15
Q

what is adaption?

A

(often) reversible change in cellular:
- size
- number
- phenotype
- metabolic activity
- function

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16
Q

what are the 2 types of stimuli that cellular adaption can be a response to?

A

Physiological stimulus –

responding to normal changes in physiology or demand.

Pathological stimulus –

responding to disease-related changes

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17
Q

what are the three different types of results that an adaptive response can lead to?

A
  1. Increased cellular activity -> incr cell size or no.
  2. Decreased cellular activity -> decr cell size or no.
  3. Change of cell function and morphology
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18
Q

what does hypertrophy mean?

A

increase in SIZE of cells

  • subsequent increase in functional capacity
  • -increased synthesis of structural components and metabolism

particularly seen in PERMANENT cell populations
- esp. cadiac and skeletal muscle

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19
Q

what does hyperplasia mean?

A

increase in NUMBER of cells

possible in labile and stable cell populations

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20
Q

what are the 3 most common causes of left ventricular hypertrophy?

A
  • hypertension
  • aortic stenosis
  • hypertrophic obstructive cardiomyopathy (HOCM)
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21
Q

what is hypertrophic obstructive cardiomyopathy (HOCM)?

A

an inherited condition causing abnormalities in certain proteins in the heart –> hypertrophy

highest cause of sudden cardiac death in young people (or athletes)

normally asympotomatic

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22
Q

what is a physiological example of hyperplasia?

A

females get hyperplasia of breast tissue during puberty, preganancy and lactation

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23
Q

what is it called when mean develop breasts and why can it occur?

A

gynaecomastia

  • happens in liver disease

as normal liver breaks down oestrogen –> increased oestrogen in blood –> signals to ‘breast’ tissue –> hyperplasia in ‘breasts’

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24
Q

what is a physiological and a pathological example of hyperplasia in thyroid tissue?

A

physiological;
- pregnancy and puberty, due to increased metabolic demands

pathological:
- graves disease, due to stimulating antibodies

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25
Q

what are 3 common symptoms of graves disease?

A
  • fine tremor (test by getting them to hold out hands and put bit of paper on them
  • proptosis (aka Exophthalmos), eyes bulging forwards, due to inflammation in muscles behind the eye??)
  • lid lag (eye lid is slower to close than pupil is to follow descending object)
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26
Q

What is adenomatous hyperplasia of the prostate (aka benign prostatic hyperplasia) and what does it lead to?

A

when the prostate gets enlarged in some old men (due to dihydrotestosterone). This compresses on the urethra, increasing the pressure in the bladder

this –> bladder cells growing and dividing more (bladder hypertrophy and hyperplasia) to increase pressure to try to overcome obstruction

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27
Q

what happens if one kidney is congenitally underformed?

A

the other kidney undergoes compensatory hyperplasia tocompensate

by increasing no. of cells around tubules

(nb no. of tubules doesn’t actually increase!)

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28
Q

what is hyperplasia of the stratum corneum?

A

chronic pressure/friction on the skin causes thickening of skin (eg due to ill-fitting shoes

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29
Q

What is subcellular hypertrophy and hyperplasia?

give an example of it

A

subcellular hypertrophy and hyperplasia is an increase in size and number of SUBCELLULAR ORGANELLES

eg if patient takes a lot of barbituates
–> smooth ER hypertrophy –> increased p450 enzyme system activity –> increased metabolism of other drugs

also leads to drug resistance, keep having to take more drugs to have the same effect

barbituates are CNS depressants

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30
Q

what is atrophy?

A

decrease in cell size and/or number
–> decrease in size of tissue or organ

can be physiological (eg involution) or pathological

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31
Q

what are 3 examples of physiological involution?

A
  • when the ductus arteriosus closes after birth
  • thymus atrophys as you get older
  • uterus atrophys after pregnancy and then even more after menopause
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32
Q

what are the 6 types of pathological atrophy?

A

disuse atrophy

  • decreased workload –> strophy
  • eg in limbs w. cast on

atrophy due to diminished blood supply

  • eg cerebrovascular disease –> cerebral atrophy (nb atrophied brain = wider + deeper sulci
  • eg renal artery stenosis –> renal atrophy

atrophy due to increased pressure

  • eg hydronephrosis
  • – urine is blocked from leaving kidney, so builds up under pressure –> damaged kidney cells + atrophy
denervation atrophy (loss of innervation)
- eg polio

loss of endocrine stimulation
- eg negative feedback to adrenal gland from exogenous steroids –> adrenal atrophy as gland stops producing steroids

inadequate nutrition
- eg cachexia, starvation, chronic inflammatory process (in hyper-metabolic state), low nutrient absorption

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33
Q

what is agenesis?

A

organ or part of organ just doesn’t develop

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34
Q

what is aplasia?

A

organ fails to differentiate into organ-specific tissues

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35
Q

what is dysgenesis?

A

failure of structural organisation of tissues into organ

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36
Q

what is hypoplasia?

A

failure of organ to grow to full size

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37
Q

what is metaplasia?

A

transformation of one differentiated cell type into another

ie change in cell function

physiological of pathological

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38
Q

what is a physiological example of metaplasia in women?

A

changes to cervix over woman’s lifestyle (cell type changes at ‘transformation zone’ of uterus and cervix

  • important clinically as abnormal changes to the transformation zone may indicate early cervical cancer (basis of smeer testing)
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39
Q

describe 3 examples of pathological metaplasia

A

pseudostratified ciliated bronchial epithelium –> squamous epithelium
- due to cigarette smoke

transitional epithelium of bladder –> squamous epithelium (can predispose to squamous bladder cancer)

  • due to:
  • —bladder calculus (bladder stones)
  • —schistomosiasis
  • —longstanding catheter

oesophageal squamous epithelium –> columnar (glandular) epithelium (can predispose to cancer)
- due to acid reflux

nb squamous epithelium tends to replace cells where there is chronic inflammation!

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40
Q

what is a side effect of tamoxifen? and explain why this happens

A

can lead to endometrial cancer in uterus

tamoxifen blocks oestrogen receptors in breast tumours, but also acts on uterine oestrogen receptors, causing metaplasia here which can lead to cancer (so should be monitored for changes

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41
Q

what cancer can develop due to squamous metaplasia in the cervix?

A

cervical intraepithelial neoplasia (CIN)

squamous cell carcinoma

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42
Q

what cancer can develop due to squamous metaplasia in bronchus?

A

squamous cell carcinoma

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43
Q

what cancer can develop due to squamous metaplasia in bladder?

A

squamous cell carcinoma

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44
Q

what cancer can develop due to glandular metaplasia in oesophagus (barrets oesophagus)?

A

adenocarcinoma

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45
Q

what cancer can develop due to parathyroid hyperplasia due to chronic kidney failure?

A

adenoma

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46
Q

what does CIN stand for in terms of cancer?

A

carcinoma in situ

ie hasn’t metastasised

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47
Q

what is a neoplasm?

A

lesion resulting from the autonomous growth (or relatively autonomous abnormal growth) of cells that persists in the absence of the initiating stimulus

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48
Q

what is dysplasia and what can it often be an early indication of?

A

abnormaility in orientation, size, shape +/or number of cells

cancer

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49
Q

what is a carcinoma?

A

cancer of the epithelial cells

50
Q

what is a sarcoma?

A

cancer of connective tissue

51
Q

what is histogenesis?

A

the differentiation of cells into specialised tissues and organs during growth from undifferentiated cells

52
Q

why is chemotherapy more effective on fast growing tumours than slower growing ones?

A

because the chemotherapy drugs often target the mechanisms that allow cells to replicate and so will have a greater effect on fast growing tumours

53
Q

what is differentiation?

in relation to tumours

A

the extent that neoplastic cells resemble the corresponding normal parenchymal cells, morphologically and functionally.

so basically the more differentiated a tumour is, the more it looks like the normal tissue it originated from

54
Q

what does anaplastic mean?

A

very poorly differentiated tumour, hard to tell what tissue it came from just by looking at it (do DNA tests to work out where it came from)

55
Q

are all malignant tumours poorly differentiated?

A

no, they can be anywhere from anaplastic to well-differentiated,

but benign tumours are pretty much always well-differentiated

56
Q

what is pleomorphism?

A
  • no uniformity in cells or nuclei appearance

- variation in size, shape

57
Q

describe abnormal nuclear morphology

A

nuclei appear too large for the cell they are in
- (they grow as more dna replication and protein synthesis occurring)

variability in nuclear shape
- (irregular, making pictures - raisins, clock faces etc)

chromatin distribution
- (coarsely clumped, or along cell membrane)

hyperchromatism
- (dark colour)

abnormally large nuclei

58
Q

what abnormal mitotic activity can be seen in malignant tumours?

A
  • tripolar or quadripolar

causes more genetic changes as cells loose or gain genes

59
Q

what is meant by the grade of a tumour?

A

how well DIFFERENTIATED tumour is!

Well differentiated = low grade / grade 1

Moderately differentiated = intermediate / grade 2

Poorly differentiated = high grade / grade 3

60
Q

what is meant by the stage of a tumour?

A

measure of cancer EXTENT!

ie how big tumour is, whether it’s got to lymph nodes, whether it’s metastasised etc

61
Q

what is the difference in local invasion between a benign and a malignant tumour?

A

benign has no capacity to infiltrate, invade or metastasise and normally have a rim of compressed fibrous tissue so have well defined borders (easier to palpate and excise)

62
Q

what is it called when a cancer metastasises via the bloodstream?

A

haematogenous spread

63
Q

what is direct seeding?

A

a relatively rare form of metastasis

  • neoplasm penetrates a natural open field without physical barriers (called coelemic spaces)

normally peritoneum or lung pleura (can be via pericardium, subarachnoid or joint spaces as well)

Eg most ovarian cancers arise in fallopian tubes just go out of fallopian tubes into stomach cavity

64
Q

what is the most common route of metastases?

A

lymphatic spread

65
Q

what lymph node does breast cancer spread to first?

A

the sentinel node in the axilla

66
Q

which cancers are more likely to spread via the blood? and where do they metastasise to?

A

typical of sarcomas (also seen in carcinomas)

follow the venous flow draining site of the neoplasm and often come to rest in first encountered large capillary bed (ie lungs, liver or brain)

67
Q

what is stroma?

A

connective tissue framework that neoplastic cells are embedded in

contains:
- cancer associated fibroblasts
- myofibroblasts
- blood vessels
- lymphatic infiltrate

68
Q

what is a desmoplastic reaction?

A

fibrous stroma formation due to induction of connective tissue fibroblast proliferation by growth factors from the tumour cells

69
Q

why does horner’s syndrome occur and what is it?

A

when top of sympathetic trunk is compressed and/or damaged.

The signs and symptoms occur on the same side as the lesion

signs/symptoms:

  • miosis (a constricted pupil)
  • ptosis (a weak, droopy eyelid)
  • anhidrosis (decreased sweating) on ipsilateral forehead
70
Q

what are local clinical complications of tumours?

A

compression:

  • malignant: pancoast tumour (apex of lung) in lung can cause horner syndrome
  • benign: pituitary adenomas can affect vision

destruction:
- malignant tumour: mucosal surfaces - ulceration (eg GI - anaemia)

71
Q

what are the general metabolic clinical complications of tumours?

A

general:

  • hormones, cytokines
  • cachexia (due to high metabolic demand from tumour), neuropathies, myopathies
72
Q

give 3 examples of specific types of metabolic complications of tumours.

A

neurological
- eg lambert-eaton myasthenic syndrome
(rare autoimmune disorder - get antibodies against pre-synaptic calcium channels at NMJ, get muscle weakness of the limbs)

endocrine
- eg Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
(if have a tumour in pituatory that secretes ADH then get retention of water and subsequently low sodium concentrations)

haematological
- eg polycythaemia
(if tumour produces erythropoietin then no. of RBCs in blood will increase, increasing the proportion of RBC in blood about norm ~40-45% - called haematocrit)

73
Q

in what types of tissue does:

1) hypertrophy occur?
2) hyperplasia occur?

A

1) hypertrophy, PERMANENT cell populations (eg heart, muscle)
2) hyperplasia, LABILE cell populations (eg skin and GI epithelium) - (also liver)

74
Q

what are the two different types of stimulus which stimulate hypertrophy or hyperplasia to occur?

A
  • increased functional demand (=compensatory)

- stimulation by hormones or growth factors (=hormonal)

75
Q

what is the mechanism of barret’s oesophagus?

A
  • basal cells (deep to squamous epithelial cells of oesophagus) get different signals and so differentiate into stomach cells (instead of squamous epithelial ones) and then gradualy go up until they become the lining
  • ie the differentiated squamous epithelial cells lining the oesophagus don’t just change!
76
Q

what is dysplasia? and what histological characteristics are visible?

A

Dysplasia: disordered growth without invasion or metastasis, aka carcinoma in situ “premalignant”

  • Pleomorphic cells (cells all look different)
  • Large hyperchromatic nuclei (so producing lots of proitein etc)
  • Increased mitosis
  • Loss of organisation

nb malignancy = features of dysplasia with invasions (+/- metastasis)

77
Q

if the tumour looks nothing like the tissue type it originated from, what is this called?

A

anaplastic

aka poorly differentiated

78
Q

what is an abnormal mitotic figure normally found in malignant cells?

A

tripolar mitosis
- where cells divide by going to 3 poles instead of 2

(causes each cell to have less and/or mutated genetic material)

79
Q

what are two histological features of a rapidly growing tumour?

A
  • necrosis (as it grows so fast it looses blood supply so dies)
  • mitosis
80
Q

what is more common: carcinomas or sarcomas?

A

carcinomas

81
Q

what are fibroids?

A

laeiomyomas

(benign tumour of smooth muscle)

fibroids can form in the uterus

  • can occasionally become laeiomyosarcomas
82
Q

what is it called when tumours metastasise via the blood?

and what organ does a secondary tumour normally form in?

A

haemotogenous spread

lungs, liver and brain (as lots of small capillaries)

83
Q

why don’t all malignant cells metastasise?

A
  • Need right nutrients, metabolic factors, blood vessels to survive and divide
  • ## Ie need right tumour microenvironment
84
Q

name of benign tumour of surface (non-glandular/non-secretory) epithelium?

A

papillOMA

“you get PAPER cuts on your skin, and your skin is mostly non-secretory surface epithelium”

85
Q

name of benign tumour of glandular/secretory epithelium?

A

adenOMA

“secretory cells ADD stuff to the surrounding tissues”

86
Q

how are benign tumours of surface epithelium further identified?

A

CELL TYPE of origin

eg squamous cell papilloma

87
Q

how are benign tumours of glandular/secretory epithelium further identified?

A

GLANDULAR TISSUE of origin

eg colonic adenoma

88
Q

what is the name given to malignant epithelial tumours?

A

carcinomas

89
Q

how are malignant surface epithelial tumours named?

A

by prefixing ‘carcinoma’ with epithelial CELL OF ORIGIN

eg basal cell carcinoma

90
Q

how are malignant secretory epithelial tumours named?

A

adenocarcinomas

91
Q

is histology of tumours, is lots of cytoplasm a good or bad sign? why?

A

good sign

as if not much cytoplasm then means there’s lots of nuclear material due to high levels of mitosis

92
Q

what is the suffix given to benign mesenchymal tumours?

A

oma

93
Q

benign smooth muscle tumour?

A

leiomyoma

94
Q

benign skeletal muscle tumour?

A

rhabdomyoma

95
Q

benign adipose tumour?

A

lipoma

96
Q

benign blood vessel tumour?

A

angioma (or haemangioma)

97
Q

benign bone tumour?

A

osteoma

98
Q

benign cartilage tumour?

A

chondroma

99
Q

benign fibrous tissue tumour?

A

fibroma

100
Q

what is the suffix used for malignant mesenchymal tumours?

A

sarcoma

eg osteosarcoma
chondrosarcoma

101
Q

what is the difference between lentigos and freckles

A

Freckles have a relatively normal number of melanocytes but an increased amount of melanin. A lentigo has an increased number of melanocytes.

Freckles will increase in number and darkness with sunlight exposure, whereas lentigines will stay stable in their color regardless of sunlight exposure.

both are totally benign

102
Q

what is a malignant melanoma a cancer of?

A

pigment-containing skin cells known as melanocytes

103
Q

why are tumours of the CNS still a problem, even if they are benign?

A

because they take up space in skull etc, which can’t expand, so compress on other structures

nb many cancers metastasise to the brain but CNS tumours often don’t metastasise

104
Q

what is a meningioma a tumour of?

A

meninges

105
Q

where are the 3 places germ cell tumours are found? and why?

A
  • ovary (obvs)
  • testes (obvs)
  • MIDLINE (due to migration of germ cells down from midline to gonads in foetus, some are left behind after birth)

Germ cells don’t start off in the gonad, they start in yolk sac and then migrate, along the midline, to the gonadal ridge
And so a few germ cells get stuck in the midline, which can then go on to be cancerous later in life

106
Q

what is a dysgerminoma a cancer of?

A

germ cells in the ovary

107
Q

what is a seminoma a cancer of?

A

germ cells in the testes

108
Q

what is myeloma a cancer of?

A

mature plasma cells (which often produce random antibodies)

109
Q

what is the main difference between leukaemias and lymphomas?

A

leukemias start in the bone marrow (and blood), whereas lymphomas start in lymph nodes (or lymphoid tissue). From there, each disease can spread to other parts of the body. Leukemias can eventually involve lymph nodes, and lymphomas can eventually involve bone marrow and blood. So the distinction gets a bit murky.

110
Q

what is a blastoma?

A

A blastoma is a type of cancer, more common in children, that is caused by malignancies in precursor cells, often called blasts. Examples are nephroblastoma, medulloblastoma and retinoblastoma.

111
Q

what are blastomas increasingly being called instead?

A

small round blue cell tumours

112
Q

what is a hamartoma?

A

benign, non -neoplastic tissue overgrowth

A hamartoma is a benign, focal malformation that resembles a neoplasm in the tissue of its origin. This is not a malignant tumor, and it grows at the same rate as the surrounding tissues. It is composed of tissue elements normally found at that site, but which are growing in a disorganized mass.

113
Q

what is a choristoma?

A

a mass of histologically normal tissue in an abnormal location

it is non-neoplastic

114
Q

what would you call a benign tumour of blood vessels and fat?

A

angiolipoma

115
Q

what would you call a malignant tumour with epithelial and stromal components?

A

carcinosarcoma

116
Q

what are tumours of secretory epithelium called if they have a cystic component?

A

cystadenoma = benign

cystadenocarcinoma = malignant

117
Q

what percentage of tumours have an unknown site of primary tumour?

A

3-5% of patients

118
Q

name 4 tumours which have seemingly benign names but are actually malignant?

A
  • melanoma
  • mesothelioma (of pleura, norm caused by asbestos)
  • myeloma
  • lymphoma
119
Q

what is a benign tumour of transitional epithelium of the bladder called?

and malignant?

A

transitional cell papilloma (or urothelial papilloma)

urothelial carcinoma

120
Q

what is a benign tumour of glandular epithelium of the thyroid called?

A

follicular adenoma

* Year 2 EMS (7 decks)

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