NUR 104 Exam 2: Inflammation, Immunity,
Infection Exam/52 Q’s and A’s
inflammation (inflammatory response)? - -sequential reaction to cell injury.
1) neutralizes and dilutes the inflammatory agent, 2) removes necrotic
materials, 3) establishes environment suitable for healing and repair
-inflammation vs. infection? - -inflammation is always present with infection,
but infection is not always present with inflammation
-chronic conditions? - -cause chronic inflammation, immune system is
always fighting, more susceptible to other things
-cellular response assessment? - -pull labs, need to know normal range to
assess
-cells involved in inflammation? - -white blood cells, red blood cells,
platelets (all manufactured in bone marrow). if patient takes aspirin,
excessive bleeding
-steroids (medication) affects immune response? - -steroids increase blood
sugar which reduces immunity
-intensity of the inflammatory response depends on? - -severity of injury,
reactive capacity of injured
-inflammatory response steps? (4) - -vascular (blood supply - constriction
then dilation - capillary permeability causes redness, swelling, heat, pain),
cellular response (neutrophils, monocytes, lymphocytes,
eosinophils/basophils), exudate formation (fluid must exit for wound healing),
healing process
-inflammation vasodilation in lungs? - -less area for air flow
-neutrophils? - -first leukocytes (6-12 hrs), phagocytize bacteria, damaged
cells, short life (24-48 hrs)
-pus? - -dead neutrophils, digested bacteria, cell debris
-released by bone marrow in response to infection? - -neutrophils =
elevated WBCs in blood
-shift to the left? - -high premature neutrophil counts that are ineffective
because produced so quickly
, -monocytes? - -second leukocytes (3-7 days), transform into macrophages,
clean injury for healing
-lymphocytes? - -humoral immunity (acute), cell-mediated immunity (slow
developing bacterial infections, autoimmune infections, allergic reactions,
foreign cell rejection)
-complement system? - -enzymes to mediate inflammation and destroy
pathogens
-histamine and serotonin (from GI tract)? - -causes vasodilation, increased
capillary permeability
-kinin (e.g. bradykinin)? - -causes vasodilation and smooth muscle
contraction resulting in pain (results in area being instinctively protected)
-prostaglandins? - -pro-inflammatory vasodilators
-leukotrienes? - -substance released by anaphylaxis leading to airway
edema
-exudate characteristics? - -serous, serosanguinous, sanguineous, fibrinous
(fibers), hemorrhagic (bleeding), purulent (sticky)
-local response to inflammation? - -specific site: erythema (redness), heat,
pain, swelling (extra blood), loss of function (less space due to swelling)
-systemic response to inflammation? - -whole body: increased WBC (shift to
the left), malaise (unwell), nausea, anorexia, increased pulse/respiration,
fever (only if infection - cytokines trigger by initiating changes in
hypothalamus temperature-regulating center, epiniephrine increases
metabolic rate)
-high fever? - ->104 damage to body cells, >105 hypothalamus cannot
function to regulate temperature
-fever? - -increased phagocytosis (shivering is body's attempt to increase
temperature to fever level)
-types of inflammatory responses? - -acute (2-3 weeks healing, no residual
damage, mainly neutrophils), subacute (lasts longer than 2-3 weeks), chronic
(can last years, mainly macrophages/lymphocytes, can impact immune
system (autoimmune diseases))
Infection Exam/52 Q’s and A’s
inflammation (inflammatory response)? - -sequential reaction to cell injury.
1) neutralizes and dilutes the inflammatory agent, 2) removes necrotic
materials, 3) establishes environment suitable for healing and repair
-inflammation vs. infection? - -inflammation is always present with infection,
but infection is not always present with inflammation
-chronic conditions? - -cause chronic inflammation, immune system is
always fighting, more susceptible to other things
-cellular response assessment? - -pull labs, need to know normal range to
assess
-cells involved in inflammation? - -white blood cells, red blood cells,
platelets (all manufactured in bone marrow). if patient takes aspirin,
excessive bleeding
-steroids (medication) affects immune response? - -steroids increase blood
sugar which reduces immunity
-intensity of the inflammatory response depends on? - -severity of injury,
reactive capacity of injured
-inflammatory response steps? (4) - -vascular (blood supply - constriction
then dilation - capillary permeability causes redness, swelling, heat, pain),
cellular response (neutrophils, monocytes, lymphocytes,
eosinophils/basophils), exudate formation (fluid must exit for wound healing),
healing process
-inflammation vasodilation in lungs? - -less area for air flow
-neutrophils? - -first leukocytes (6-12 hrs), phagocytize bacteria, damaged
cells, short life (24-48 hrs)
-pus? - -dead neutrophils, digested bacteria, cell debris
-released by bone marrow in response to infection? - -neutrophils =
elevated WBCs in blood
-shift to the left? - -high premature neutrophil counts that are ineffective
because produced so quickly
, -monocytes? - -second leukocytes (3-7 days), transform into macrophages,
clean injury for healing
-lymphocytes? - -humoral immunity (acute), cell-mediated immunity (slow
developing bacterial infections, autoimmune infections, allergic reactions,
foreign cell rejection)
-complement system? - -enzymes to mediate inflammation and destroy
pathogens
-histamine and serotonin (from GI tract)? - -causes vasodilation, increased
capillary permeability
-kinin (e.g. bradykinin)? - -causes vasodilation and smooth muscle
contraction resulting in pain (results in area being instinctively protected)
-prostaglandins? - -pro-inflammatory vasodilators
-leukotrienes? - -substance released by anaphylaxis leading to airway
edema
-exudate characteristics? - -serous, serosanguinous, sanguineous, fibrinous
(fibers), hemorrhagic (bleeding), purulent (sticky)
-local response to inflammation? - -specific site: erythema (redness), heat,
pain, swelling (extra blood), loss of function (less space due to swelling)
-systemic response to inflammation? - -whole body: increased WBC (shift to
the left), malaise (unwell), nausea, anorexia, increased pulse/respiration,
fever (only if infection - cytokines trigger by initiating changes in
hypothalamus temperature-regulating center, epiniephrine increases
metabolic rate)
-high fever? - ->104 damage to body cells, >105 hypothalamus cannot
function to regulate temperature
-fever? - -increased phagocytosis (shivering is body's attempt to increase
temperature to fever level)
-types of inflammatory responses? - -acute (2-3 weeks healing, no residual
damage, mainly neutrophils), subacute (lasts longer than 2-3 weeks), chronic
(can last years, mainly macrophages/lymphocytes, can impact immune
system (autoimmune diseases))
