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NR-283 Pathophysiology Chamberlain University

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Chamberlain University

NR-283 Pathophysiology Chamberlain University

First line of defense: Mechanical Barriers- nonspecific: skin, saliva (mucous membranes)
 Blocks entry of bacteria or harmful substances into the tissues  Body secretions such as…  Saliva or  Tears… Contain enzymes or chemicals that inactivate or destroy potentially damaging material.
Second line of defense: Nonspecific : phagocytosis and inflammation.
 Phaghcythsis- process by which neutrophils (a leukocyte) and macrophages, randomly engulf and destroy bacteria, cell debris, or foreign matter.  Inflammatihn-involves a sequence of events intended to limit the effects of injury or a dangerous agent in the body.  Interserhns- nonspecific agents that protect uninfected cells against viruses.
Third line of defense: specific defense mechanism
 Specific antibodies, cell-mediated immunity.  Provides protection by stimulating the production of unique antibodies or sensitized lymphocytes following exposure to specific substances.
Normal Capillary Exchange:
 Generally not all capillaries in a particular capillary bed are open.
 Depends on the metabolic needs of the cells or need of removal of wastes (byproduct of metabolism)
Movement of fluid, electrolytes, oxygen, and nutrients on arterial end based on…
 Net hydrostatic pressure-net hydrostatic pressure is based on the difference between the hydrostatic pressure within the capillary (essentially arterial pressure) as compared with the hydrostatic pressure of the interstitial fluid in the tissues as well as the relative osmotic pressures in the blood and interstitial fluid  Differences in concentrations of dissolved substances in the blood and interstitial fluid promote diffusion of…  Electrolytes,
 Glucose,  Oxygen,  Other nutrients…across the capillary membrane.  Blood cells and plasma proteins (albumin, globulin, and fibrinogen) normally remain inside the capillary.
 Venous end- capillary hydrostatic pressure is decreased due to past movement of fluid into the interstitial fluid space
 Osmotic pressure -in vessels is high (because plasma proteins stay within capillaries)
 Facilitates movement of fluid, carbon dioxide, and other wastes.
 Excess fluid and proteins are recovered from the interstitial area by way of the lymphatic system and returned to the general circulation.
Physiology of Inflammation: The inflammatory response is a protective mechanism.
Disserence between inflammatihn and insectihn…
 Inflammation comes from infection (usually)-inflammation is a process  Inflammation is not the same as infection, although infection is one cause of inflammation.  The body’s nonspecific response to tissue injury, resulting in… -Redness, -Swelling, -Warmth, and -Pain, and -(Sometimes)-loss of function.
Disorders are named using the ending “ITIS”…
Inflammation-(ITIS)-is associated with many different types of tissue injury.
 Causes include direct physical damage such as… cuts or sprains,  Caustic chemicals such as…  Acids or  Drain cleaners,  Ischemia or infarction,  Allergic reactions,  Extremes of heat or cold,  Foreign bodies such as… splinters or glass, and infection. Anything ending with “ITIS”-is inflammatihn
EX: “ITIS”
 Cholecystitis- Inflammation of the gallbladder  Nephritis- Inflammation of the kidneys  Cystis- Inflammation of the bladder  Gastroenteritis- Inflammation of the gastrointestinal tract (also known as infectious diarrhea)
 Infection- microorganisms such as a bacteria, viruses, or fungi are always present at the site, causing the inflammation. This microbe can be identified and appropriate treatment instituted to reduce the infection, and the inflammation will subside.
When inflammation is caused by an allergy or a burn, no microbes are present.
Pathophysiology of inflammation
An injury to capillaries and tissue cells will result in the following reactions:
1.) Bradykinin is released from the insured cells. 2.) Bradykinin activates pain receptors. 3.) Sensation of pain stimulates mast cells and basophils to release histamine. 4.) Bradykinin and histamine cause capillary dilation-(Vasoldialation)…causes hyperemia-which is an increase in blood flow to an are a. This results in an increase of blood flow and increased capillary permeability and WBC count which leads to phagocytosis. (Second line of defense-nonspecific) 5.) Break in skin allows bacteria to enter the tissue. a. This results in the migration of neutrophils and monocytes to the site of injury. 6.) Neutrophils phagocytize bacteria. 7.) Macrophages leave the bloodstream and phagocytose microbes.
Chemical mediators in immune response:
Chemical mource Major Action
Histamine Mast cell mranules Immediate vasodilation and increased capillary per exudate
Chemotactic cactors Mast cell mranules For example, attract neutrophils to site
Platelet-activatinm cactor (PAF) Cell membranes oc platelets Activate neutrophils
Platelet ammremation
Cytokines (interleukins, lymphokines)
T lymphocytes, Macrophames Increase plasma proteins, ESR
Induce cever, chemotaxis, leukocytosis
Leukotrienes Synthesis crom arachidonic acid in mast cells
Later response: vasodilation and increased capillary perme chemotaxis
Prostamlandins (PGs) Synthesis crom arachidonic acid in mast cells
Vasodilation, increased capillary permeability, pain, cever, histamine eccect
Kinins (e.m., bradykinin) Activation oc plasma protein (kinomen)
Vasodilation and increased capillary permeability, pain, che
Complement system Activation oc plasma protein cascade
Vasodilation and increased capillary permeability, chemota increased histamine release
Function of cellular element in inflammatory response: Leukocytes Activity
Neutrophils Phamocytosis oc microormanisms
Basophils Release oc histamine leadinm to inclammation
Eosinophils Numbers are increased in allermic responses
Lymphocytes Activity
T lymphocytes Active in cell-mediated immune response
B lymphocytes Produce antibodies
Monocytes Phamocytosis
Macrophames Active in phamocytosis. These are mature monocytes that have mimrated into tissues crom the blood.
Signs and symptoms of inflammation can be lhcal and systemic:
Local:
 Swelling because of increase permeability,  Redness which causes hyporemia (increased amount of blood)  Loss of function (because of swelling),  Pain (because of pressure)
Systematic
 Fever (pyrexia)-(release of pyrogens-fever producing substances)-common if inflammation is extensive  Malaise(fatigue) and  Anorexia (meaning loss of appetite in this case)  Nausea and vomiting
Diagnose By:
 Physical assessment  Lab test-CBC-WBC count,  Blood smear or culture-determine bacterial or viral infection,  ESR-erythrocyte sedimentation rate-rate of the red blood cells-higher because body is fighting  Lactic acid test done for sepsis
Changes in blood with Inflammation:
Leukocytosis Increased numbers of white blood cells, especially neutrophils
Differential count Proportion of each type of white blood cell altered, depending on the caus

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NR-283 Pathophysiology Chamberlain University

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