Test Bank For Pathophysiology: A Practical Approach 3rd
Edition By Lachel Story 9781284120196 Chapter 1-14
Complete Guide .
pathogenesis - ANSWER: development and evolution of a disease
-affected by time, quantity, location, and morphologic changes (structure)
cell proliferation - ANSWER: normal cell replication, cells divide and reproduce
cell differentiation - ANSWER: cells become different and specialized (muscle cells, skin cell), begins
after fertilization, generalized to specific cell
atrophy - ANSWER: cells shrink and less of them, reversible
ex) arm in a cast, remove and move arm to fix
hypertrophy - ANSWER: cells swell/get bigger, reversible
ex) physiologic: bodybuilding
pathologic: ventricle enlarges because hypertension causes more pressure
hyperplasia - ANSWER: increased number of cells, reversible, can be cancerous
ex) physiologic: callous, cells adapt to use of pencil
pathologic: endometrium
metaplasia - ANSWER: checks replaced with another type, reversible, can be cancerous
ex) smoking- cells in trachea replaced with cells that can stand smoke
dysplagia - ANSWER: change in cell size and type, precancerous, sometimes reversible
ex) cervix cells?
cell injury - ANSWER: begins most diseases, reversible or irreversible depending on severity and
intrinsic factors
causes of cell injury - ANSWER: hypoxia, chemicals (smoking, toxins), radiation, genetics, immune
system (autoimmune diseases), trauma, nutrition, infection
ischemia - ANSWER: low O2 to organs
anoxia - ANSWER: no oxygen
reperfusion - ANSWER: no O2 to tissue
apoptosis - ANSWER: physiologic cell death, cell condenses and shrinks, single cell, no inflammation,
internal or external factors, result: nothing
necrosis - ANSWER: pathologic cell death, cells swell and burst, many cells at once, always external
factors, Result: inflammation
coagulative necrosis - ANSWER: lack of blood supply and O2, most common in heart
liquefactive necrosis - ANSWER: liquid, abyss, mostly in brain
gangrenous necrosis - ANSWER: loss of blood supply, infection, often in limbs and diabetic feet (cause
amputation)
, caseous necrosis - ANSWER: means cheese, often in lungs
neoplasia - ANSWER: tumor, new growth
benign tumor - ANSWER: slow growing, regular border, more differentiated, resembles host, usually
no symptom
malignant tumor - ANSWER: rapid growing, irregular border, fatal, poorly differentiated
carcinogenesis steps - ANSWER: 1. initiation: exposed to stimulus (can be for years)
2. promotion: uncontrolled growth
3. progression: permanent malignant changes (metastasizes)
carcinogenesis - ANSWER: cancer development, caused by heredity, oncogenes, carcinogens
clinical manifestations of cancer - ANSWER: Change in bowels/bladder
A sore that hasn't healed
Unusual bleeding/discharge
Thickening or lump in breast or elsewhere
Indigestion/difficulty swallowing
Obvious change in wart or mole
Nagging cough/hoarseness
complications of cancer - ANSWER: anemia, cachexia (malnutrition, low appetite), fatigue, infection
b/c decreased immunity, leukopenia (low leukocyte levels), thrombocytopenia (low platelets), pain
tumor markers - ANSWER: drawing blood to see antigens
Staging-TNM - ANSWER: Tumor size, Nodal involvement, Metastasis
T1 - T4
N0-N3
M0-M1
Grading - ANSWER: according to histology
Stage I - more differentiated
Stage 4 - less differentiated
pathologist is the only one that can grade
treatments of cancer - ANSWER: chemotherapy (drug by mouth/IV)
radiation (kill cells by killing/damaging DNA, specific to one spot)
surgery (highest survival rate, only used in unmetastasized cancers)
autosomal dominant disorders - ANSWER: one bad gene, almost always one diseased parent, 50%
chance of passing to child
examples
polycystic kidney disease
Huntington's
Marfan's
autosomal recessive disorders - ANSWER: 2 bad genes (one from each parent), parents usually
asymptomatic carriers, 25% chance of passing to child
examples:
cystic fibrosis
sickle cell disease
X-linked disorders - ANSWER: usually in men (only 1 X), asymptomatic mom with diseased brother
examples:
Edition By Lachel Story 9781284120196 Chapter 1-14
Complete Guide .
pathogenesis - ANSWER: development and evolution of a disease
-affected by time, quantity, location, and morphologic changes (structure)
cell proliferation - ANSWER: normal cell replication, cells divide and reproduce
cell differentiation - ANSWER: cells become different and specialized (muscle cells, skin cell), begins
after fertilization, generalized to specific cell
atrophy - ANSWER: cells shrink and less of them, reversible
ex) arm in a cast, remove and move arm to fix
hypertrophy - ANSWER: cells swell/get bigger, reversible
ex) physiologic: bodybuilding
pathologic: ventricle enlarges because hypertension causes more pressure
hyperplasia - ANSWER: increased number of cells, reversible, can be cancerous
ex) physiologic: callous, cells adapt to use of pencil
pathologic: endometrium
metaplasia - ANSWER: checks replaced with another type, reversible, can be cancerous
ex) smoking- cells in trachea replaced with cells that can stand smoke
dysplagia - ANSWER: change in cell size and type, precancerous, sometimes reversible
ex) cervix cells?
cell injury - ANSWER: begins most diseases, reversible or irreversible depending on severity and
intrinsic factors
causes of cell injury - ANSWER: hypoxia, chemicals (smoking, toxins), radiation, genetics, immune
system (autoimmune diseases), trauma, nutrition, infection
ischemia - ANSWER: low O2 to organs
anoxia - ANSWER: no oxygen
reperfusion - ANSWER: no O2 to tissue
apoptosis - ANSWER: physiologic cell death, cell condenses and shrinks, single cell, no inflammation,
internal or external factors, result: nothing
necrosis - ANSWER: pathologic cell death, cells swell and burst, many cells at once, always external
factors, Result: inflammation
coagulative necrosis - ANSWER: lack of blood supply and O2, most common in heart
liquefactive necrosis - ANSWER: liquid, abyss, mostly in brain
gangrenous necrosis - ANSWER: loss of blood supply, infection, often in limbs and diabetic feet (cause
amputation)
, caseous necrosis - ANSWER: means cheese, often in lungs
neoplasia - ANSWER: tumor, new growth
benign tumor - ANSWER: slow growing, regular border, more differentiated, resembles host, usually
no symptom
malignant tumor - ANSWER: rapid growing, irregular border, fatal, poorly differentiated
carcinogenesis steps - ANSWER: 1. initiation: exposed to stimulus (can be for years)
2. promotion: uncontrolled growth
3. progression: permanent malignant changes (metastasizes)
carcinogenesis - ANSWER: cancer development, caused by heredity, oncogenes, carcinogens
clinical manifestations of cancer - ANSWER: Change in bowels/bladder
A sore that hasn't healed
Unusual bleeding/discharge
Thickening or lump in breast or elsewhere
Indigestion/difficulty swallowing
Obvious change in wart or mole
Nagging cough/hoarseness
complications of cancer - ANSWER: anemia, cachexia (malnutrition, low appetite), fatigue, infection
b/c decreased immunity, leukopenia (low leukocyte levels), thrombocytopenia (low platelets), pain
tumor markers - ANSWER: drawing blood to see antigens
Staging-TNM - ANSWER: Tumor size, Nodal involvement, Metastasis
T1 - T4
N0-N3
M0-M1
Grading - ANSWER: according to histology
Stage I - more differentiated
Stage 4 - less differentiated
pathologist is the only one that can grade
treatments of cancer - ANSWER: chemotherapy (drug by mouth/IV)
radiation (kill cells by killing/damaging DNA, specific to one spot)
surgery (highest survival rate, only used in unmetastasized cancers)
autosomal dominant disorders - ANSWER: one bad gene, almost always one diseased parent, 50%
chance of passing to child
examples
polycystic kidney disease
Huntington's
Marfan's
autosomal recessive disorders - ANSWER: 2 bad genes (one from each parent), parents usually
asymptomatic carriers, 25% chance of passing to child
examples:
cystic fibrosis
sickle cell disease
X-linked disorders - ANSWER: usually in men (only 1 X), asymptomatic mom with diseased brother
examples:
