Term Test 2 - Neoplasia Flashcards
What is cell hypertrophy
Larger cells
What is cell atrophy
Smaller cells
What is tissue hypertrophy
Organ enlargement due to larger cells
What is tissue hyperplasia
Organ enlargement due to more cells
What is tissue hypoplasia
Organ shrinkage due to fewer cells
What is tissue atrophy
Organ shrinkage due to smaller cells
What is the opposite of hypertrophy
Atrophy
What is the opposite of hyperplasia
Hypoplasia
pathy indicates
diseased organ
megaly indicates
enlarged organ
what term describes a missing organ or tissue
aplasia or agenesis
what is atresia
absence or unusual narrowing of an opening or passage
name examples of cells that constantly proliferate
skin, small intestine, large intestine, bone marrow
name examples of cells that can increase proliferation if needed, but usually have a low proliferation
liver, kidney
name examples of cells that have little or no capacity to proliferate
heart, CNS, skeletal muscle
What regulates cell proliferation (3)
1) hormones
2) growth factors and nutrition
3) demands on the tissue
Give examples of factors that influence demand on tissue
Nerve stimulation, workload, hypoxia, compensation for tissue loss
Name the 5 steps for gene transcription in response to a growth factor
- growth factor
- membrane receptor
- signal transducer
- transcription factor
- response element
Describe how hepatocyte growth factor leads to cell proliferation
HGF binds to c-Met -> c-Met phosphorylates mTOR -> mTOR causes cell proliferation
Describe how cytokine signalling (ex. IL-6) leads to cell proliferation
IL-6 binds to IL6R -> IL6R phosphorylates STAT3 -> STAT3 causes cell proliferation
what 3 growth factors/cytokines have both endocrine and paracrine signalling
TNF, IL6, epidermal GF
give an example of an only endocrine growth factor/cytokine
any of: EPO, GM-CSF, insulin, IGF, thyroid stimulating hormone
give an example of an only paracrine growth factor/cytokine
any of: TGFβ, PDGF, FGF, VEGF, HGF, KGF
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
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
- hyperplasia and inflammation
- 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)
- self-sufficiency in growth signals
- insensitivity to antigrowth signals
- evade apoptosis
- limitless replicative potential
- sustained angiogenesis
- 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
- altered cell phenotype (metaplasia/dysplasia)
- dysregulated proliferation
- 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
- cell type
- grade (how abnormal/aggressive)
- stage (how far has it spread)
- 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
IV
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)
- rate of proliferation
- atypia
- aneuploidies
- 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)
- atypical differentiation
- heterogeneity
- replicative activity
- nuclear abnormalities
- anaplasia
- 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
