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First Exam CHSO 404 – Questions & Answers
First Exam CHSO 404 – Questions & Answers
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First Exam CHSO 404 – Questions & AnswersKarolysis ✔️Ans - DNA is degraded
Pyknosis ✔️Ans - Nucleus shrinks in size
Karyorrhexis ✔️Ans - fragmentation of nucleus
Differentiation ✔️Ans - process in which cells become specialized in
structure and function
Less differentiated ✔️Ans - seen in cancer cells, tumors
Proliferation ✔️Ans - an increase in number, multiplication
cancer cells ✔️Ans - increase in proliferation, decrease in differentiation
atrophy ✔️Ans - shrinkage of tissue or organ size due to reduction in cell
size
hypertrophy ✔️Ans - increase in cell size in response to stress
-cardiac myocytes cannot divide, so adapt by getting bigger i.e. left
ventricular hypertrophy
hyperplasia ✔️Ans - increase in the cell number and is distinct from
hypertrophy
-epithelial cells may undergo hyperplasia under streess
-uterine lining has hyperplasia before bleeding - thickened wall
metaplasia ✔️Ans - -Mature cell type is replaced by a different mature
cell type
-ex - chronic irritation or inflammation
dysplasia ✔️Ans - -disordered growth and maturation of the cellular
components of a tissue
-vary in size, shape and organization
-precursor to cancer if not removed
,accumulations during cell stress ✔️Ans - -lipids - heart and liver
-glycogen - particularly in liver and skeletal muscles
-melanin - formed by melanocytes in skin
-hemosiderin - formed from hemoglobin
-bilirubin - normally in liver
-lipofuscin- fine granular golden brown pigment formed from
phospholipids and proteins derived from degenerating membranes
-wear and tear pigment
-heart, liver, nerve
-minerals - calcium = calcification
-hyaline change - non specific indicator; formed from protein, light pink on
slide
ROS clean up system ✔️Ans - ROS --> hydrogen peroxide --> water and
oxygen
2 enzymes - superoxide dismutase. catalase
excess ROS causes ___ ✔️Ans - -cellular damage
-leaking membranes
-calcium influx
-cell death
ischemic cell injury and death ✔️Ans - - decrease in o2 leads to
anaerobic metabolism - which decreases pH bc causes increase in lactic
acid - low pF is denaturing
coagulative necrosis ✔️Ans - -basic cell outline is preserved
-acidosis denatures proteins
-protein denaturation causes coagulation
liquefactive necrosis ✔️Ans - -results from autolysis of heterolysis
-involves digestion of cell remains
-abscess or pus formed
caseous necrosis ✔️Ans - -combination of coagulative and liquefactive
necrosis
,-seen in TB
-necrotic debris is not digested completely by hydrolyses, so tissues appear
soft and granular
fat necrosis ✔️Ans - -refers to focal areas of fat destruction
-destruction of lipids is associated with abnormal release of pancreatic
enzymes (lipase)
-saponification - formation of soap from lipids mixing with minerals
(calcium, magnesium)
dry gangrene ✔️Ans - coagulative necrosis as a result of ischemia
wet gangrene ✔️Ans - occurs when tissue is infected with bacteria and
phagocytic cells are recruited
-enzymes released that lead to a liquefactive process
gas gangrene ✔️Ans - occurs when the infection is caused by Clostridium
app (perfringens) - anaerobic bacteria that produces toxins that damage
the connective tissue and cause gas
necrosis ✔️Ans - -initiated by pathologic stimuli from outside the cell
and results in the removal of that cell
-involves activation of enzymes that digest cellular components -
AUTODIGESTION
-this process may stimulate an inflammatory response
-there are nuclear changes - KARYOLYSIS, PYKNOSIS, KARYORRHEXIS
-most necrosis is either coagulative or liquefactive
apoptosis ✔️Ans - -involves activation of a coordinated internal cellular
program (sequence of events) that are mediated by defined cellular
proteins
-specific, energy dependent,
-programmed cell death that helps maintain homeostasis
-characterized by fragmentation of DNA, formation of distinct structures
called apoptotic bodies
-dead cells removed by phagocytosis - no inflammatory response
Virchow's triad ✔️Ans - 1. change in vessel wall
, 2. decreased blood flow, stasis
3. increased coag of blood
benign neoplasm ✔️Ans - -well differentiated
-localized
-demarcated
malignant neoplasm ✔️Ans - -less well-differentiated
-grow rapidly
-invade neighboring tissues and have the capacity
cell cycle/division ✔️Ans - series of events that cells go through as they
grow and divide
-cancer cells are autonomous or independent of normal growth controls
-
3 causes of cellular abnormalities ✔️Ans - -telomerase
-change in p53
-change in pRB
pRB ✔️Ans - -governs cell cycle rate
-loss of pRB = unregulated cell growth
p53 ✔️Ans - -slows cell cycle to allow for repair of DNA mutations before
cell division
-mutations with p53 = a lot of diff cancers
-activates DNA repair genes
-stops cell cycle to allow DNA repair genes to fix mutation
-initiates apoptosis if DNA damage cannot be reversed
telomerase ✔️Ans - -telomere are at the end of cells
-cancer cells replace telomeres by activating telomerase - cells can divide
indefinitely
-immortal - bc cancer cells never lose telomeres so they never die
tumor suppressor gene ✔️Ans - -p53, pRB
-mutation in BOTH copies of alleles
-typically these TSG.restrain tumor growth
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