BLD 204 FINAL EXAM QUESTIONS AND ANSWERS WITH
COMPLETE SOLUTIONS GUARANTEED PASS !!!
Apoptosis: cell size shrinks,
nucleus condenses,
control mechanisms: mitochondrial death receptors, capsases break up the cell,
and apoptotic bodies appear with phagocyte receptors to get rid of the cell
WITHOUT an immune response to them
Necrosis: the cell size swells,
the nucleus fragments and fades,
there is no control mechanism the cell spews and falls apart,
this results in inflammation, the tissue is gone after receiving an immune
response.
Compare and Contrast Apoptosis and Necrosis. Use at least three cell characteristics to
show the differences between the two.
Four major steps to recruitment,
1. margination and rolling
2. adhesion to endothelium
3. transmigration through endothelium extravasation
4. migration into interstitial tissues
,Leukocyte rolls and attaches onto a selectin
proteoglycan attaches on to the leukocyte where integrin activation by
chemokines takes place
stable adhesion leads to migration through endothelium
fibrin and fibronectin are present
chemokines released microbes scatter
macrophage with microbes is present and cytokines are releases usually TNF and
IL-1
ANOTHER DESCRIPTION
leukocyte roll then become activated and adhere to endothelium, then
transmigrate across the endothelium, pierce through the basement membrane
and migrate toward chemoattractantts emanating from the source of injury.
selectins assist in rolling, chemokines assist in activating the neutrophils to
increase activity of integrins, integrins assist in firm adhesion
steps of WBC recruitment to inflamed tissue
1.clot
2.inflammatory successful
3.macrophages clean up the mess then bring in the fibroblasts
4.release growth factors, angiogenesis
5.granulation tissue
6.fibroblasts and blood vessels retract and fade away-apoptosis
,Explain the steps of wound healing from the macrophage influx until healing is
complete. You may use bullet points or paragraph form.
chronic versus acute
: duration of time is longer than acute
ACUTE: exudation of fluid and plasma proteins; emigration of leukocytes
ACUTE: redness, swelling, heat, pain, loss of function
ACUTE: rapid, onset, short duration, edema and neutrophils
CHRONIC: longer duration, lymphocytes and macrophages, proliferation of blood
vessels, fibrosis, tissue necrosis
CHRONIC: low grade persistent irritant, foreign bodies, viruses, bacteria, fungi,
autoimmune diseases, obesity
compare and contract chronic and acute inflammation
1. lipid peroxidation which leads to membrane damage
2. protein modification which leads to breakdown or misfolding
3. DNA damage whihc leads to mutations. free radicals are removed by
spontaneous decay and by specialized enzymatic systems.
excessive production leads to accumulation of free radicals in cells which may
damage lipids, proteins and DNA resulting in cell injury
List and describe three effects of increased reactive oxidative stress in the cell.
1. intrinsic/mitochondrial pathway: based on cell injury: GF withdrawal, DNA
damage and protein misfolding. sensors in BCL-2 family activate Bax and Bak
which make holes in the mitochondrial membrane. Mitochondiral proteins like
cytochrome c escape and activate the caspase cascade
, 2. the death receptor pathway/extrinsic: cell produce surface receptors that can
trigger apoptosis, receptor-ligand interaction with factors like TNF and Fas result
in activation of the caspase cascade. caspases then initiate, execute cleave,
activate nuclease and then all result in apoptic bodies that have controlls cell
fragmentation
two pathways of apoptosis, describe them
hypertrophy
Uterine enlargement during pregnancy is an example of
metaplasia
the reversible replacement of one adult cell type to another as an adaptation to stress is
called:
Lack of Vitamin D, calcium, or phosphate in rickets
Rickets is a disease caused by a lack of Vitamin D, calcium, or phosphate. The disease
causes the bones to be soft and weak, leading to an increased risk of fracture. what is
the etiology of the disease?
hypoxic
Carbon monoxide poisoning lowers the oxygen carrying capacity of the blood. The type
of cell injury that results from carbon monoxide poisoning is
coagulative
Charles had ischemic damage to his left kidney that resulted in necrosis. What type of
necrosis would be seen in a kidney?
caseous necrosis
COMPLETE SOLUTIONS GUARANTEED PASS !!!
Apoptosis: cell size shrinks,
nucleus condenses,
control mechanisms: mitochondrial death receptors, capsases break up the cell,
and apoptotic bodies appear with phagocyte receptors to get rid of the cell
WITHOUT an immune response to them
Necrosis: the cell size swells,
the nucleus fragments and fades,
there is no control mechanism the cell spews and falls apart,
this results in inflammation, the tissue is gone after receiving an immune
response.
Compare and Contrast Apoptosis and Necrosis. Use at least three cell characteristics to
show the differences between the two.
Four major steps to recruitment,
1. margination and rolling
2. adhesion to endothelium
3. transmigration through endothelium extravasation
4. migration into interstitial tissues
,Leukocyte rolls and attaches onto a selectin
proteoglycan attaches on to the leukocyte where integrin activation by
chemokines takes place
stable adhesion leads to migration through endothelium
fibrin and fibronectin are present
chemokines released microbes scatter
macrophage with microbes is present and cytokines are releases usually TNF and
IL-1
ANOTHER DESCRIPTION
leukocyte roll then become activated and adhere to endothelium, then
transmigrate across the endothelium, pierce through the basement membrane
and migrate toward chemoattractantts emanating from the source of injury.
selectins assist in rolling, chemokines assist in activating the neutrophils to
increase activity of integrins, integrins assist in firm adhesion
steps of WBC recruitment to inflamed tissue
1.clot
2.inflammatory successful
3.macrophages clean up the mess then bring in the fibroblasts
4.release growth factors, angiogenesis
5.granulation tissue
6.fibroblasts and blood vessels retract and fade away-apoptosis
,Explain the steps of wound healing from the macrophage influx until healing is
complete. You may use bullet points or paragraph form.
chronic versus acute
: duration of time is longer than acute
ACUTE: exudation of fluid and plasma proteins; emigration of leukocytes
ACUTE: redness, swelling, heat, pain, loss of function
ACUTE: rapid, onset, short duration, edema and neutrophils
CHRONIC: longer duration, lymphocytes and macrophages, proliferation of blood
vessels, fibrosis, tissue necrosis
CHRONIC: low grade persistent irritant, foreign bodies, viruses, bacteria, fungi,
autoimmune diseases, obesity
compare and contract chronic and acute inflammation
1. lipid peroxidation which leads to membrane damage
2. protein modification which leads to breakdown or misfolding
3. DNA damage whihc leads to mutations. free radicals are removed by
spontaneous decay and by specialized enzymatic systems.
excessive production leads to accumulation of free radicals in cells which may
damage lipids, proteins and DNA resulting in cell injury
List and describe three effects of increased reactive oxidative stress in the cell.
1. intrinsic/mitochondrial pathway: based on cell injury: GF withdrawal, DNA
damage and protein misfolding. sensors in BCL-2 family activate Bax and Bak
which make holes in the mitochondrial membrane. Mitochondiral proteins like
cytochrome c escape and activate the caspase cascade
, 2. the death receptor pathway/extrinsic: cell produce surface receptors that can
trigger apoptosis, receptor-ligand interaction with factors like TNF and Fas result
in activation of the caspase cascade. caspases then initiate, execute cleave,
activate nuclease and then all result in apoptic bodies that have controlls cell
fragmentation
two pathways of apoptosis, describe them
hypertrophy
Uterine enlargement during pregnancy is an example of
metaplasia
the reversible replacement of one adult cell type to another as an adaptation to stress is
called:
Lack of Vitamin D, calcium, or phosphate in rickets
Rickets is a disease caused by a lack of Vitamin D, calcium, or phosphate. The disease
causes the bones to be soft and weak, leading to an increased risk of fracture. what is
the etiology of the disease?
hypoxic
Carbon monoxide poisoning lowers the oxygen carrying capacity of the blood. The type
of cell injury that results from carbon monoxide poisoning is
coagulative
Charles had ischemic damage to his left kidney that resulted in necrosis. What type of
necrosis would be seen in a kidney?
caseous necrosis
