Term Test 2 - Neoplasia Flashcards by Giselle Carter

What is cell hypertrophy

Larger cells

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What is cell atrophy

Smaller cells

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What is tissue hypertrophy

Organ enlargement due to larger cells

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What is tissue hyperplasia

Organ enlargement due to more cells

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What is tissue hypoplasia

Organ shrinkage due to fewer cells

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What is tissue atrophy

Organ shrinkage due to smaller cells

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What is the opposite of hypertrophy

Atrophy

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What is the opposite of hyperplasia

Hypoplasia

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pathy indicates

diseased organ

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megaly indicates

enlarged organ

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what term describes a missing organ or tissue

aplasia or agenesis

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what is atresia

absence or unusual narrowing of an opening or passage

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name examples of cells that constantly proliferate

skin, small intestine, large intestine, bone marrow

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name examples of cells that can increase proliferation if needed, but usually have a low proliferation

liver, kidney

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name examples of cells that have little or no capacity to proliferate

heart, CNS, skeletal muscle

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What regulates cell proliferation (3)

1) hormones
2) growth factors and nutrition
3) demands on the tissue

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Give examples of factors that influence demand on tissue

Nerve stimulation, workload, hypoxia, compensation for tissue loss

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Name the 5 steps for gene transcription in response to a growth factor

growth factor
membrane receptor
signal transducer
transcription factor
response element

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Describe how hepatocyte growth factor leads to cell proliferation

HGF binds to c-Met -> c-Met phosphorylates mTOR -> mTOR causes cell proliferation

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Describe how cytokine signalling (ex. IL-6) leads to cell proliferation

IL-6 binds to IL6R -> IL6R phosphorylates STAT3 -> STAT3 causes cell proliferation

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what 3 growth factors/cytokines have both endocrine and paracrine signalling

TNF, IL6, epidermal GF

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give an example of an only endocrine growth factor/cytokine

any of: EPO, GM-CSF, insulin, IGF, thyroid stimulating hormone

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give an example of an only paracrine growth factor/cytokine

any of: TGFβ, PDGF, FGF, VEGF, HGF, KGF

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describe how HIF works to regulate EPO and VEGF under normal conditions

active HIF-1α (proline) regulates gene expression of EPO and VEGF -> erythropoiesis and angiogenesis -> increased O2 -> O2 catalyzes proline - hydroxyproline -> labile HIF-1α -> ubiquitinylation and degradation

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what happens when there is dysregulation of proliferative cells

hyperplasia (not cancer, will go away if stimulus is removed)

what happens when there is damage to proliferative cells

atrophy

how does hyperthyroidism cause cardiac disease

hyperthyroidism -> increased T4/T3 -> increased basal metabolic rate -> cardiac hypertrophy (compensatory) -> cardiopathy

what is a consequence of nutritional hyperparathyroidism? how?

fibrous osteodystrophy; high dietary phosphorus -> parathyroid chief cell hyperplasia -> increased PTH secretion -> increased bone resorption and hyperplasia of periosteal and endosteal fibroblasts

what would be a consequence of a congenital portosystemic shunt on the liver and why

hepatocellular atrophy; hepatotrophic factors coming from the GI tract bypass the liver

what would be the effect of systemic hypertension on the heart? whats one cause of systemic hypertension

hypertrophic cardiomyopathy (secondary); renal disease

what would be a consequence of poor myelination on muscles (ex. distal sensorimotor polyneuropathy) and why?

atrophy and muscle wasting due to poor stimulation

what are three causes of muscle atrophy

neuropathic, disuse, starvation

which is more likely to return to normal? a) infarcted lobe of liver b) post-necrotic (toxin) hyperplasia of liver

b) more likely to have intact vascular supply and CT framework (as well as more remaining healthy hepatocytes capable of dividing)

what is a consequence of colonic impaction in the horse?

pressure-induced and ischemic atrophy of the liver in contact with the impacted loop of colon

what would be the sequence of events following chronic inhalation of irritants

1. hyperplasia and inflammation 2. metaplasia (to squamous cells)

What % of dogs will get clinically significant neoplasms

30%

what is important in clinical assessment of cancers

imaging and gross appearance

what is important in specific diagnosis of cancers

histopathology

what are some behaviours of cancer cells (6)

1. self-sufficiency in growth signals 2. insensitivity to antigrowth signals 3. evade apoptosis 4. limitless replicative potential 5. sustained angiogenesis 6. tissue invasion and metastasis

Cancer is fundamentally a _________ disease

genetic

what is metaplasia

REVERSIBLE replacement of a normal cell type with another normal cell type that is not usually found there

what is dysplasia

disorganized cells or tissues

T/F developmental dysplasia is a risk factor for cancer later on in life

false

describe how cells can go from normal to neoplastic

hyperplasia and/or metaplasia -> preneoplastic dysplasia -> neoplasia

a plaque can become what (2)

a polyp or a papilloma

where do cysts form

in epithelial lined structures that secrete a substance

T/F some focal hyperplasias become neoplasia

True

what are 3 major abnormalities in neoplasms

1. altered cell phenotype (metaplasia/dysplasia) 2. dysregulated proliferation 3. accumulative growth

define neopasia

a new pattern of excessive and poorly controlled growth of cells with atypical differentiation

define neoplasm

a mutant population of cells with atypical differentiation, dysregulated proliferation and accumulative growth

define carcinoma

malignant neoplasm of epithelial cells

define adenocarcinoma

malignant neoplasm of glandular epithelial cells

define sarcoma

malignant neoplasm of mesenchymal cells

T/F cancers always develop when cells go from preneoplastic -> benign -> malignant

false

what is neoplastic transformation

change from preneoplastic to neoplastic

what is malignant conversion

change from benign to malignant

what is malignancy

propensity to progressively get worse

what 4 criteria are used in diagnostic evaluation of cancers

1. cell type 2. grade (how abnormal/aggressive) 3. stage (how far has it spread) 4. resection margins

what is the term for benign tumors

oma (or adenoma if of glandular epithelium)

almost all melanomas are ________________

malignant (even though the nomenclature suggests otherwise)

almost all lymphomas are _________________

malignant (even though the nomenclature suggests otherwise)

what is a myeloma

malignant plasma cell neoplasm

what is leukemia

neoplastic hematopoietic cells in blood and bone marrow

Describe the sequence for cancer development in the bladder

metaplasia -> dysplasia -> adenoma -> carcinoma

what is the T in TNM staging

tumor (primary)

what is the N in TNM staging

local nodes

what is the M in TNM staging

metastases

describe a stage 0 tumor using TNM

T: no invasion N: no local nodes impacted M: no metastases

describe a stage 1 tumor using TNM

T: shallow invasion N: no M: no

describe a stage 2 tumor using TNM

T: deep invasion N: no M: no

describe a stage 3 tumor using TNM

T: yes N: yes M: no

describe a stage 4 tumor using TNM

T: yes N: yes M: yes

if a tumor has metastasized, what stage is it

T/F not every cancer will spread to lymph nodes before metastasizing

True (in which case it becomes stage 4 automatically)

how is TNM modified in mammary carcinoma

if greater than 3cm, upstage to stage 3 (even if no lymph nodes are affected yet)

what criteria is used to grade tumors (4)

1. rate of proliferation 2. atypia 3. aneuploidies 4. local behaviour (growth, necrosis, invasion)

what grading system is used for mast cell tumors

1, 2 (low, high)

grading systems are meaningless in ___________ and ____________

osteosarcomas and hemangiosarcomas

how do neoplastic cells differ from normal cells (6)

1. atypical differentiation 2. heterogeneity 3. replicative activity 4. nuclear abnormalities 5. anaplasia 6. reduced cell death

what is an indicator of high replicative activity in cancers

high mitotic index (number of mitoses you see in the tissue)

how is heterogeneity measured

anisocytosis; anisokaryosis; high N/C ratio

what are common nuclear abnormalities observed in cancers (6)

hyperchromasia; multinucleation; aneuploidy/polyploidy; deletions/translocations; atypical mitoses; karyomegaly

what is anaplasia

lack of differentiation; reversion to a more primitive form

what are hallmarks of reduced cell death

loss of p53; increased bcl2; increased survivins; viral inhibitors