NUR200 - EGCC - Med Surg 1 - Exam 2
Ch 11, 13,
Cell lysis occurs - ✔️✔️when the final components create holes in the cell membrane
and cause targeted cell death by membrane rupture.
In autoimmune disorders, healthy tissue can be damaged by compliment activation and
the resulting inflammatory response. Ex: RA and SLE.
The compliment system is an - ✔️✔️enzyme cascade (C1-C9) consisting of pathways
to mediate inflammation and destroy invading pathogens.
Major functions of the compliment system are - ✔️✔️enhanced phagocytosis,
increased vascular permeability, chemotaxis, and cellular lysis.
Inflammatory response - ✔️✔️is a sequential reaction to cell injury. It neutralizes and
dilutes the inflammatory agent removes necrotic materials and establishes and
environment suitable for healing and repair.
Inflammation - ✔️✔️is often but incorrectly used as a synonym for the term infection
Inflammation - ✔️✔️is always present with infection.
Infection - ✔️✔️is not always present with inflammation
A person who is neutropenic - ✔️✔️may not be able to mount an inflammatory
response.
The inflammatory response can be divided into - ✔️✔️a vascular response, cellular
response, formation of exudate, and healing.
Vascular response to injury - ✔️✔️Transient vasoconstriction,
Chemical mediators - Histamine, kinins, and prostaglandins are released locally.
Local vasodilation and hyperemia. Presence of albumin raises oncotic pressure that
further draws fluid from bv's
Increased capillary permeability and local edema.
,In the vascular response to injury, the plasma PRO fibrinogen leaves the blood - ✔️✔️It
is activated to fibrin by the products of the injured cells. Fibrin strengthens a blood clot
formed by platelets.
In tissues, the clot (formed by platelets) - ✔️✔️functions to trap bacteria, prevent their
spread, and serve as a framework for the healing process.
Platelets release - ✔️✔️Growth factors that start the healing process.
Chemotaxis - ✔️✔️The directional migration of WBC's to the site of injury, resulting in
an accumulation of neutrophils and monocytes at the site.
This occurs as part of the cellular response to injury. Neutrophils and monocytes move
from circulation to the site of injury.
Neutrophils - ✔️✔️First leukocytes to arrive at the injury site (6-12 hours).
Phagozytize bacteria, other foreign material, and damaged cells.
With their short life span (24-48 hours), dead neutrophils soon accumulate . These dead
neutrophils , along with digested bacteria, and other cell debris accumulates as a
creamy substance termed pus.
To keep up with the demand for neutrophils, the bone marrow releases more
neutrophils into circulation. This results in - ✔️✔️An elevated WBC count, especially
the neutrophil count.
Sometimes the demand for neutrophils increases to the extent that the bone marrow
releases immature forms of neutrophils (bands) into circulation.
The finding of increased numbers of band neutrophils in circulation is called a "shift to
the left," which is commonly seen in patients with acute bacterial infections.
Mature neutrophils aka - ✔️✔️Segmented neutrophils
Immature neutrophils aka - ✔️✔️bands
Monocytes are the - ✔️✔️second type of phagocytic cells that migrate from the
circulating blood.
Arrive at the site within 3-7 days after the onset of inflammation.
On entering the tissue spaces, monocytes transform into macrophages. Together with
the tissue macrophages, the monocytes assist in phagocytosis of the inflammatory
debris.
,This is an important role necessary to clean the area before healing can occur.
Macrophages have a long life span and can stay in the damaged tissue for weeks.
In cases in which particles are too large for a single macrophage, - ✔️✔️The
macrophages accumulate and fuse to form a multinucleated giant cell.
The giant cell is then encapsulated by collagen, leading to the formation of a granuloma.
Lymphocytes arrive later at the site of injury. Their primary role - ✔️✔️Is R/T humoral
and cell mediated immunity.
All of these processes are important mediators of the inflammatory response and
healing.
When cells are activated by injury, the arachidonic acid in the cell membrane is rapidly
converted - ✔️✔️To produce prostaglandins (PG's). (as part of the compliment
system),
Prostaglandins are generally considered - ✔️✔️pro-inflammatory and are potent
vasodilators contributing to increased blood flow and edema formation.
Prostaglandins also perform a significant role in sensitizing - ✔️✔️pain receptors to
arousal by stimuli that would normally be painless.
Prostaglandins have a pivitol role as pyrogens - ✔️✔️when stimulating the temperature
regulating area of the hypothalamus and producing a fibrile response.
Thromboxane (part of the compliment system) - ✔️✔️is a powerful vasoconstictor and
platelet-aggregating agent. It causes brief vasoconstriction and skin pallor at the site of
injury and promotes clot formation.
Short half life, and the pallor soon gives way to vasodilation and redness, which is
caused be prostaglandins and histamine.
Leukotrienes (part of the compliment system) - ✔️✔️form the slow-reacting substance
of anaphylaxis (SRS-A), which constricts smooth muscles of the bronchi, causing
narrowing of the airway, and increases capillary permeability, leading to airway edema.
Local manifestations of inflammation include - ✔️✔️Redness,
Heat,
Pain,
Swelling,
, and loss of fx.
Systemic manifestations of inflammation include - ✔️✔️Increased WBC count,
Shift to the left,
malaise,
Nausea,
anorexia,
increased pulse,
increased RR,
fever.
Fever is triggered by the release of - ✔️✔️cytokines, which cause fever by initiating
metabolic changes in the temperature regulating center in the hypothalamus.
The synthesis of prostaglandins is the most critical metabolic change. Prostaglandins
act directly to increase the themostatic set point.
The hypothalamus then activates the autonomic nervous system to stimulate increased
muscle tone and shivering and decreased perspiration and blood flow to the periphery.
Epiniphrine released from the medulla increases the metabolic rate.
When the hypothalamus raises the temperature set point - ✔️✔️the hypothalamus
signals an increase in heat production and conservation to raise the body temperature
to the new level. At this point the individual feels chilled and shivers.
Benefits of Fever - ✔️✔️The released cytokines and the fever that they trigger activate
the body's defense mechanisms.
The benefits include: increased killing of microorganisms, increased phagocytosis by
neutrophils, increased proliferation of T cells.
Higher body temp may also enhance the activity of interferon, the body's natural virus
fighting substance.
Redness / Rubor - ✔️✔️Cause: hyperemia from vasodilation.
Heat / Calor - ✔️✔️Cause: Increased metabolism at inflammatory site.
Pain / Dolor - ✔️✔️Cause: Change in PH. Nerve stimulation by chemicals (eg:
histamine and prostaglandins). Pressure from fluid exudate.
Swelling / Tumor - ✔️✔️Cause: fluid shift to interstitial spaces. Fluid exudate
accumulation.
Ch 11, 13,
Cell lysis occurs - ✔️✔️when the final components create holes in the cell membrane
and cause targeted cell death by membrane rupture.
In autoimmune disorders, healthy tissue can be damaged by compliment activation and
the resulting inflammatory response. Ex: RA and SLE.
The compliment system is an - ✔️✔️enzyme cascade (C1-C9) consisting of pathways
to mediate inflammation and destroy invading pathogens.
Major functions of the compliment system are - ✔️✔️enhanced phagocytosis,
increased vascular permeability, chemotaxis, and cellular lysis.
Inflammatory response - ✔️✔️is a sequential reaction to cell injury. It neutralizes and
dilutes the inflammatory agent removes necrotic materials and establishes and
environment suitable for healing and repair.
Inflammation - ✔️✔️is often but incorrectly used as a synonym for the term infection
Inflammation - ✔️✔️is always present with infection.
Infection - ✔️✔️is not always present with inflammation
A person who is neutropenic - ✔️✔️may not be able to mount an inflammatory
response.
The inflammatory response can be divided into - ✔️✔️a vascular response, cellular
response, formation of exudate, and healing.
Vascular response to injury - ✔️✔️Transient vasoconstriction,
Chemical mediators - Histamine, kinins, and prostaglandins are released locally.
Local vasodilation and hyperemia. Presence of albumin raises oncotic pressure that
further draws fluid from bv's
Increased capillary permeability and local edema.
,In the vascular response to injury, the plasma PRO fibrinogen leaves the blood - ✔️✔️It
is activated to fibrin by the products of the injured cells. Fibrin strengthens a blood clot
formed by platelets.
In tissues, the clot (formed by platelets) - ✔️✔️functions to trap bacteria, prevent their
spread, and serve as a framework for the healing process.
Platelets release - ✔️✔️Growth factors that start the healing process.
Chemotaxis - ✔️✔️The directional migration of WBC's to the site of injury, resulting in
an accumulation of neutrophils and monocytes at the site.
This occurs as part of the cellular response to injury. Neutrophils and monocytes move
from circulation to the site of injury.
Neutrophils - ✔️✔️First leukocytes to arrive at the injury site (6-12 hours).
Phagozytize bacteria, other foreign material, and damaged cells.
With their short life span (24-48 hours), dead neutrophils soon accumulate . These dead
neutrophils , along with digested bacteria, and other cell debris accumulates as a
creamy substance termed pus.
To keep up with the demand for neutrophils, the bone marrow releases more
neutrophils into circulation. This results in - ✔️✔️An elevated WBC count, especially
the neutrophil count.
Sometimes the demand for neutrophils increases to the extent that the bone marrow
releases immature forms of neutrophils (bands) into circulation.
The finding of increased numbers of band neutrophils in circulation is called a "shift to
the left," which is commonly seen in patients with acute bacterial infections.
Mature neutrophils aka - ✔️✔️Segmented neutrophils
Immature neutrophils aka - ✔️✔️bands
Monocytes are the - ✔️✔️second type of phagocytic cells that migrate from the
circulating blood.
Arrive at the site within 3-7 days after the onset of inflammation.
On entering the tissue spaces, monocytes transform into macrophages. Together with
the tissue macrophages, the monocytes assist in phagocytosis of the inflammatory
debris.
,This is an important role necessary to clean the area before healing can occur.
Macrophages have a long life span and can stay in the damaged tissue for weeks.
In cases in which particles are too large for a single macrophage, - ✔️✔️The
macrophages accumulate and fuse to form a multinucleated giant cell.
The giant cell is then encapsulated by collagen, leading to the formation of a granuloma.
Lymphocytes arrive later at the site of injury. Their primary role - ✔️✔️Is R/T humoral
and cell mediated immunity.
All of these processes are important mediators of the inflammatory response and
healing.
When cells are activated by injury, the arachidonic acid in the cell membrane is rapidly
converted - ✔️✔️To produce prostaglandins (PG's). (as part of the compliment
system),
Prostaglandins are generally considered - ✔️✔️pro-inflammatory and are potent
vasodilators contributing to increased blood flow and edema formation.
Prostaglandins also perform a significant role in sensitizing - ✔️✔️pain receptors to
arousal by stimuli that would normally be painless.
Prostaglandins have a pivitol role as pyrogens - ✔️✔️when stimulating the temperature
regulating area of the hypothalamus and producing a fibrile response.
Thromboxane (part of the compliment system) - ✔️✔️is a powerful vasoconstictor and
platelet-aggregating agent. It causes brief vasoconstriction and skin pallor at the site of
injury and promotes clot formation.
Short half life, and the pallor soon gives way to vasodilation and redness, which is
caused be prostaglandins and histamine.
Leukotrienes (part of the compliment system) - ✔️✔️form the slow-reacting substance
of anaphylaxis (SRS-A), which constricts smooth muscles of the bronchi, causing
narrowing of the airway, and increases capillary permeability, leading to airway edema.
Local manifestations of inflammation include - ✔️✔️Redness,
Heat,
Pain,
Swelling,
, and loss of fx.
Systemic manifestations of inflammation include - ✔️✔️Increased WBC count,
Shift to the left,
malaise,
Nausea,
anorexia,
increased pulse,
increased RR,
fever.
Fever is triggered by the release of - ✔️✔️cytokines, which cause fever by initiating
metabolic changes in the temperature regulating center in the hypothalamus.
The synthesis of prostaglandins is the most critical metabolic change. Prostaglandins
act directly to increase the themostatic set point.
The hypothalamus then activates the autonomic nervous system to stimulate increased
muscle tone and shivering and decreased perspiration and blood flow to the periphery.
Epiniphrine released from the medulla increases the metabolic rate.
When the hypothalamus raises the temperature set point - ✔️✔️the hypothalamus
signals an increase in heat production and conservation to raise the body temperature
to the new level. At this point the individual feels chilled and shivers.
Benefits of Fever - ✔️✔️The released cytokines and the fever that they trigger activate
the body's defense mechanisms.
The benefits include: increased killing of microorganisms, increased phagocytosis by
neutrophils, increased proliferation of T cells.
Higher body temp may also enhance the activity of interferon, the body's natural virus
fighting substance.
Redness / Rubor - ✔️✔️Cause: hyperemia from vasodilation.
Heat / Calor - ✔️✔️Cause: Increased metabolism at inflammatory site.
Pain / Dolor - ✔️✔️Cause: Change in PH. Nerve stimulation by chemicals (eg:
histamine and prostaglandins). Pressure from fluid exudate.
Swelling / Tumor - ✔️✔️Cause: fluid shift to interstitial spaces. Fluid exudate
accumulation.
