NU 608 Study Guide Questions and Accurate Answers Graded A+
Atrophy:
decrease or shrinkage in cell size. Causes- decrease in workload (cast), result of disease,
decreased hormonal stimulation (breasts in old age), nutritional deficiency. Most common-
skeletal muscles, heart, and brain.
Hypertrophy:
Hypertrophy- increase in the size of cells and consequently in the size of the affected organ. A
result of increased accumulation of protein in the cellular components and not an increase in
cellular water. Response to increase in workload of the cell in cells that cannot self-reproduce.
Most common- heart and kidney. Three types- physiologic (healthy increase in workload of the
cell- muscles with exercise), pathologic (heart cells hypertrophy due to stressors that increase
the workload- HTN, valve problems), compensatory (adapting to an increased demand for work-
kidney removal).
Hyperplasia:
increase in the number of cells resulting from an increased rate of cellular division. Usually
secondary to a response to an injury that has been severe and prolonged enough to cause cell
death. Three types- physiologic (hormonal simulation- breast, uterus), pathophysiologic
(secondary to disease- enlarged thyroid), compensatory (enables certain organs to regenerate-
liver after partial removal).
Metaplasia:
reversible replacement of one mature cell by another somewhat less differentiated cell type
due to irritation. A new cell that is better fit for the inflammatory environment. Reversed if the
stressor is stopped. Example- tracheal replacement of normal epithelial cells by squamous
epithelial cells that don't secret mucous or have cilia.
,Dysplasia:
abnormal changes in size, shape, and organization of mature cells. Often found adjacent to
cancer cells. If the stimulus is removed, dysplastic changes are often reversible. Common- cervix
and respiratory tract.
Infection and inflammation are:
NOT SYNONYMOUS!
Inflammation:
a response to injury. Inflammation can occur in sterile areas, so it isn't always linked to infection.
Terminated when the offending agent is eliminated and the secreted mediators are broken
down or dissipated. Anti-inflammatory mechanisms prevent the inflammation from causing
excessive damage to the host.
Inflammation triggers:
gene imperfections, toxin release (bacterial, viral, fungal), mechanical injury, hypoperfusion,
ischemic injury, reperfusion injuries.
Inflammatory response and goals of (3):
consists of a vascular reaction in which the net result is the delivery of fluid, dissolved
substances and cell from the vascular bed into the interstitial tissues in an area of injury or
necrosis. Three goals of inflammatory response:1. Increase blood flow to the site of injury
(vascular response)2. Alert the products of healing to response to the site of injury (cellular
response- WBC, plt)3. Remove injured tissue and prepare site for healing
,Mast cell:
important inflammatory mediator Cellular bags of granules located in connective tissue close to
blood vessels and found in skin and lining of respiratory and GI tract (FIRST LINE OF DEFENSE
AREAS). Activated by the inflammatory response.
Major actions of mast cells (2):
1. Degranulation in which the bags release their granules, releasing histamine (causing
constriction of vessels, dilation of capillaries and increased capillary permeability).2. Mast cells
have the ability to synthesize other mediators: hint 1. Leukotrines- chemical mediators that
cause airway constriction and increase intestinal permeability leading to increased bacterial
translocation in the gut. 2. Prostaglandins (PGE)- chemical mediators causing increased vascular
permeability, which causes pain with inflammation (NSAIDS are prostaglandin inhibitors). 3.
Platelet activating factor (PAF)- platelet activation, making it easier to clot.
Neutrophil phagpcytosis:
Neutrophil function: MOST IMPORTANT- perform phagocytosis, which is the ingestion of the
bacteria. Neutrophils arrive to the site of infection in 90 minutes, responding to bacterial
endotoxin, SIRS mediators, and activation of complement system.
Neutrophil phagocytosis process (4):
1. Chemotaxis- ability to respond to chemical signals that flag inflammation and damage.2.
Margination- sticking of neutrophils to capillary walls before passing through the wall to enter
tissues.3. Diapedis- neutrophil movement through the cell wall, followed by migration towards
the site of damage.4. Phagocytosis- once the neutrophil encounters the bacteria it will be
phagocytized- ingested and killed.
, For phagocytosis to be successful:
1. Foreign particle must have a surface that can become absorbed through the cell membrane
of the neutrophil. Natural structures have a smooth surface that resists phagocytosis, but
bacteria has a rough surface.2. Phagocytes possess electronegative charges and bacteria
possess electropositive charges (opposites attract).3. Immune system develops antibodies
against the infectious agents. The antibodies adhere to the bacterial membrane. -This antibody-
antigen complex is called an OPSONINS. -Opsonins combine with complement (a series of
proteins that play a big role in the immune response) -That combination allows for adhesion of
the neutrophil to the bacteria surface allowing for phagocytosis. The opsonization process
makes the bacteria more tasty to the neutrophils.Opsonization is preparing the bacteria for
phagocytosis.
Alternative complement pathway:
One of three complement cascade phases. A number of things can activate this pathway and it
is the first line of defense. Endotoxin release can initiate it. It initiates chemotaxis. It can also
function in the absence of antibody formation.
Complement cascade phases (3):
Complement comprises of 20 circulating plasma proteins that circulate in the blood in an
inactive form. Once it attaches to a foreign cell it becomes activated. Major factor in the fight
against infection. The cascade is activated when antibody is formed and combines with an
antigen. 1. Classic- requires binding of a specific antigen/antibody2. Lectin- activated by certain
bacterial carbohydrates3. Alternative- FIRST LINE OF DEFENSE, several activators
Atrophy:
decrease or shrinkage in cell size. Causes- decrease in workload (cast), result of disease,
decreased hormonal stimulation (breasts in old age), nutritional deficiency. Most common-
skeletal muscles, heart, and brain.
Hypertrophy:
Hypertrophy- increase in the size of cells and consequently in the size of the affected organ. A
result of increased accumulation of protein in the cellular components and not an increase in
cellular water. Response to increase in workload of the cell in cells that cannot self-reproduce.
Most common- heart and kidney. Three types- physiologic (healthy increase in workload of the
cell- muscles with exercise), pathologic (heart cells hypertrophy due to stressors that increase
the workload- HTN, valve problems), compensatory (adapting to an increased demand for work-
kidney removal).
Hyperplasia:
increase in the number of cells resulting from an increased rate of cellular division. Usually
secondary to a response to an injury that has been severe and prolonged enough to cause cell
death. Three types- physiologic (hormonal simulation- breast, uterus), pathophysiologic
(secondary to disease- enlarged thyroid), compensatory (enables certain organs to regenerate-
liver after partial removal).
Metaplasia:
reversible replacement of one mature cell by another somewhat less differentiated cell type
due to irritation. A new cell that is better fit for the inflammatory environment. Reversed if the
stressor is stopped. Example- tracheal replacement of normal epithelial cells by squamous
epithelial cells that don't secret mucous or have cilia.
,Dysplasia:
abnormal changes in size, shape, and organization of mature cells. Often found adjacent to
cancer cells. If the stimulus is removed, dysplastic changes are often reversible. Common- cervix
and respiratory tract.
Infection and inflammation are:
NOT SYNONYMOUS!
Inflammation:
a response to injury. Inflammation can occur in sterile areas, so it isn't always linked to infection.
Terminated when the offending agent is eliminated and the secreted mediators are broken
down or dissipated. Anti-inflammatory mechanisms prevent the inflammation from causing
excessive damage to the host.
Inflammation triggers:
gene imperfections, toxin release (bacterial, viral, fungal), mechanical injury, hypoperfusion,
ischemic injury, reperfusion injuries.
Inflammatory response and goals of (3):
consists of a vascular reaction in which the net result is the delivery of fluid, dissolved
substances and cell from the vascular bed into the interstitial tissues in an area of injury or
necrosis. Three goals of inflammatory response:1. Increase blood flow to the site of injury
(vascular response)2. Alert the products of healing to response to the site of injury (cellular
response- WBC, plt)3. Remove injured tissue and prepare site for healing
,Mast cell:
important inflammatory mediator Cellular bags of granules located in connective tissue close to
blood vessels and found in skin and lining of respiratory and GI tract (FIRST LINE OF DEFENSE
AREAS). Activated by the inflammatory response.
Major actions of mast cells (2):
1. Degranulation in which the bags release their granules, releasing histamine (causing
constriction of vessels, dilation of capillaries and increased capillary permeability).2. Mast cells
have the ability to synthesize other mediators: hint 1. Leukotrines- chemical mediators that
cause airway constriction and increase intestinal permeability leading to increased bacterial
translocation in the gut. 2. Prostaglandins (PGE)- chemical mediators causing increased vascular
permeability, which causes pain with inflammation (NSAIDS are prostaglandin inhibitors). 3.
Platelet activating factor (PAF)- platelet activation, making it easier to clot.
Neutrophil phagpcytosis:
Neutrophil function: MOST IMPORTANT- perform phagocytosis, which is the ingestion of the
bacteria. Neutrophils arrive to the site of infection in 90 minutes, responding to bacterial
endotoxin, SIRS mediators, and activation of complement system.
Neutrophil phagocytosis process (4):
1. Chemotaxis- ability to respond to chemical signals that flag inflammation and damage.2.
Margination- sticking of neutrophils to capillary walls before passing through the wall to enter
tissues.3. Diapedis- neutrophil movement through the cell wall, followed by migration towards
the site of damage.4. Phagocytosis- once the neutrophil encounters the bacteria it will be
phagocytized- ingested and killed.
, For phagocytosis to be successful:
1. Foreign particle must have a surface that can become absorbed through the cell membrane
of the neutrophil. Natural structures have a smooth surface that resists phagocytosis, but
bacteria has a rough surface.2. Phagocytes possess electronegative charges and bacteria
possess electropositive charges (opposites attract).3. Immune system develops antibodies
against the infectious agents. The antibodies adhere to the bacterial membrane. -This antibody-
antigen complex is called an OPSONINS. -Opsonins combine with complement (a series of
proteins that play a big role in the immune response) -That combination allows for adhesion of
the neutrophil to the bacteria surface allowing for phagocytosis. The opsonization process
makes the bacteria more tasty to the neutrophils.Opsonization is preparing the bacteria for
phagocytosis.
Alternative complement pathway:
One of three complement cascade phases. A number of things can activate this pathway and it
is the first line of defense. Endotoxin release can initiate it. It initiates chemotaxis. It can also
function in the absence of antibody formation.
Complement cascade phases (3):
Complement comprises of 20 circulating plasma proteins that circulate in the blood in an
inactive form. Once it attaches to a foreign cell it becomes activated. Major factor in the fight
against infection. The cascade is activated when antibody is formed and combines with an
antigen. 1. Classic- requires binding of a specific antigen/antibody2. Lectin- activated by certain
bacterial carbohydrates3. Alternative- FIRST LINE OF DEFENSE, several activators
