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)