Chapter 13 - Inflammation and Wound Healing
1. Explain the inflammatory response
**cellular injury
**vascular response: release of histamines, kinins, and prostaglandins increases blood flow to tissue causing edema and swelling, WBCs adhere to thickened blood
**cellular response: movement of WBCs for phagocytosis
**healing: by primary, secondary, and tertiary healing
2. Explain the cellular response, types of WBC’s and their normal values
**cellular response
-chemotaxis (migration of WBCs) to injury site, margination (movement of neutrophils and monocytes to capillary wall), and diapedesis (movement of neutrophils and monocytes throught capillary wall) to injury site for phagocytosis
-migration of lymphocytes, eosinophils, and basophils for more specialized role in response
-phagocytosis results in cellular exudate at injury site
**types of WBCs and normal values
-eosinophils: 3% of WBC count, associated with parasitic infections
-basophils: normally lacking in circulation, associated with allergic reactions from mild to severe
-lymphocytes (T and B cells): 20-40% of WBC count, elevated count indicates “shift to right”, viral infection
-granulocytes (neutrophils): 55-70% of WBC count, elevated count plus elevated bands indicate “shift to left”, bacterial infection
-agranulocytes (monocytes): 2-8% of WBC count, macrophage
3. List and explain the chemical mediators and their effects on homeostasis (Table 13-1)
*complement system: increases inflammatory response by enhancing phagocytosis, vascular permeability, chemotaxis, and cellular lysis
-kills bacterial cells
*prostaglandins and leukotrienes: causes vasodilation and stimulates chemotaxis, respectively
-allows increased local blood flow for immune response
*histamine: causes vasodilation and increased vascular permeability
-allows increased local blood flow for immune response
*serotonin: causes vasodilation and increased vascular permeability
-allows increased local blood flow for immune response
*kinins: contraction of smooth muscle and dilation of blood vessels to stimulate pain
-sends body message of injury
*cytokines: increase pulse, respiration, and metabolism to increase body temperature
-increases immune response
4. Use the NP to explain the nursing management of a patient with an inflammatory response.
**assessment
-subjective: pain, loss of function, diet, past medical history, age, lifestyle, medications, surgery, altered elimination pattern
-objective: swelling, redness, drainage, color, heat, fever, high BP and P, malaise, nausea, and anorexia
-dx: CBC, WBC, wound culture
**diagnoses:
-acute pain r/t inflammation process
-hyperthermia r/t inflammation process
-risk of FVD r/t increased metabolic rate
-risk for imbalanced nutrition: less than body requirements r/t decreased intake of essential nutrients
**planning:
-drug therapy: fever, inflammation, nutrients
-nutritional therapy: promote healing and nutrients/fluids to meet energy demands
**implementation:
-RICE: rest, ice/heat, compression/immobilization, elevation
-anti-pyretics for fevers greater than 104 degrees F
-anti-enemics for nausea
-vitamins to promote healing process
-continue observations of swelling and wound, if present
-adequate nutritional/fluid intake and output
**evaluation
-is the patient running a harmful, high-grade fever?
-is the patient in pain?
-is the patient nutritional needs getting met?
Chapter 14 - Genetics, Altered Immune Responses and Transplantation
1. Differentiate the different types of Immunity
*natural: immunity exists prior to contact with antigen
*passive: receives antigen, rather than synthesizing it
-artificial: injections from immune animal or human
-natural: mother to child
*active: invasion of foreign substances resulting in development of antibodies and lymphocytes
-artificial: immunization with antigen
-natural: getting over a flu
2. Differentiate between cell-mediated immunity from humoral immunity (Table 14-7)
*cell-mediated: involves T lymphocytes and macrophages which produce sensitize T cells and cytokines against fungus, intracellular viruses, and chronic infectious agents
*humoral: involves B lymphocytes which produce antigens against bacteria, extracellular viruses, and respiratory and GI pathogens
3. Explain the effects of aging on the immune system (pg. 224)
*decline in cell-mediated immunity specifically from decreased size and activity of thymus gland
4. Explain and differentiate between the different types of hypersensitivity reactions. Give examples of conditions under each type.
*Type 1 Reaction: allergens cause allergic reactions immediately causing smooth muscle contraction, increased vascular permeability, vasodilation, hypotension, increased mucus secretion and itching
-asthma
*Type 2 Reaction: destruction of erythrocytes, platelets, and leukocytes resulting in rapid tissue damage
-transfusion reaction
*Type 3 Reaction: local or systemic reactions on self-cells resulting in tissue damage
-rheumatoid arthritis
*Type 4 Reaction: a delayed allergic reaction which could cause itching, redness, and scaly skin
-contact dermatitis to poison ivy
5. Using the NP, explain the care of a patient with an allergic disorder.
*assessment
-subjective: past health history, medications, family history, diet, lifestyle, cramps, diarrhea, fatigue, cough, itching, burning, stinging, tightness of chest
-objective: rashes, wheals and flares, dryness, scratches, watery eyes, lung sounds, sputum, swelling, sneezing…
-dx: skin tests
*diagnoses
-ineffective airway clearance
-fatigue
-risk for infection
-ineffective tissure perfusion
-readiness to learn
-knowledge deficit
*planning
-reduce exposure to allergen
-treat symptoms
-immunotherapy, if necessary
*implementation:
**drug therapy/ immunotherapy:
-anti-histamine: swelling and itching
-sympathomimetics/decongestants: epinepherine for anaphylactic reactions and minor decongestants for allergic rhinitis
-corticosteroids: relieves allergic rhinitis
-anti-pruritic drugs: itch relief
-mast-cell stabilizers: asthma management
-leukotriene receptor antagonists: blocks leukotriene, a major inflammatory mediator
**patient education: administer epi-pen, self tourniquet, avoid allergen sources, sleep in air-conditioned room, hypoallergenic products, medic-alert bracelet
*evaluation:
-does the patient understand the information presented?
6. List and explain the cardinal principles in the therapeutic management of anaphlaxis. (pg. 230)
1. recognizing signs and symptoms of a reaction
2. maintaining a patent airway
3. using a tourniquet to prevent the spread of the allergen
4. drug administration
5. treatment for shock:
-patent airway
-remove substance, ie: bee sting
-Epinepherine 1:1000: 0.2-0.5 ml SQ, repeating 10-15 min
-Epinepherine 1:10,000: 0.5 ml, 5-10 min
-O2 per NRB on high flow
-recumbent elevate leg
-Benadryl IM/IV
-Histamine H2 blocker
-maintain BP
-corticosteroids
7. Describe the different mediators of the allergic response and resulting clinical outcomes. (Table 14-10)
*histamine: increases vascular permeability, constricts smooth muscle, and stimulates irritant receptors
-edema of airway, constriction of bronchial, swelling, itching, n/v/d, shock
*leukotrienes: contricts bronchial smooth muscle, increases vascular permeability
-bronichial constriction, enhanced histamine effect on smooth muscle
*prostaglandins: stimulates vastodilation and constricts smooth muscle
-wheal and flare reaction, hypotension, and bronchospasm
*platelet-activating factor: stimulates vasodilation and aggregates platelets
-increases pulmonary artery pressure and causes systemic hypotension
*kinins: stimulates slow, sustained smooth muscle contractions, increases vascular permeability, stimulates secretion of mucus, and pain receptors
-angioedema with painful swelling, bronchial constriction
*serotonin: increases vascular permeabiliyy and stimulates smooth muscle contraction
-mucosal edem and bronchial constriction
*anaphylatoxins: stimulates histamine release
8. Briefly explain autoimmunity and the different treatment methods and related nursing care.
**immune response against self
*corticosteroids: suppress immune response
*aphresis: term meaning “separate”, separation of a plasma component thought to be the cause of the disease
-watch for complications of hypotension and citrate (anticoagulant) toxicity
9. Differentiate primary from secondary immunodeficiency disorders and related nursing care.
*immunodeficiency involves deficiency of one or more: phagocytosis, humoral response, cell-mediated response, complement system, or combined humoral and cell-mediated response
-primary: caused by irregular or absent immune cells
-secondary: caused by immunosuppression by illness or treatment, primarily drug-induced
**drug therapy and patient education: avoid crowds, report symptoms of infection, avoid animals and plants, avoid sick people…
Chapter 17 – Fluid, Electrolytes, and Acid-Base Imbalances
1. Review fluid movement in capillaries. (pg. 318)
*capillary hydrostatic pressure: moves water out of capillaries
*intersitial oncotic pressure: moves water out of capillaries
*interstitial hydrostatic pressure: moves water into capillaries
*plasma oncotic pressure: moves water into capillaries
*capillary hydrostatic pressure vs. plasma oncotic pressure
-capillary hydrostatic pressure greater at arterial end-fluid moves out of capillary
plasma oncotic pressure greater at venous end-fluid draws back into capillary
**fluids get pulled by proteins, oncotic pressure is due to proteins
2. Explain the different types of crystalloids and their uses.
*hypotonic
-D5W: replaces water, does not expand ECF
*isotonic
-NaCl (.9% NS): for ECF deficits
-Lactated Ringers (LR): for ECF deficits resulting from bleedings and dehydration from loss of bile
*hypertonic
-Lactated Ringers with D5W: for ECF deficits
-D5.9NS: for ECF deficits with metabolic acidosis
-D5.45NS: maintainence fluid
-D5.2NS: maintainence fluid
*colloids
-albumin: increases oncotic pressure
-blood: increases oxygen carrying capacity
3. Give examples of patient conditions or situations with abnormal fluid dynamics and the pathophysiology.
-hyperglycemia
-hypernatremia
4. Use the NP to provide nursing care of a client with sodium imbalance and water imbalances.
**sodium imbalance
*assessment
-subjective: past medical history, medications, diet, elimination pattern, numbness, tingling, twitching, weakness of muscles
-objective: cold, clammy skin; flushed, dry skin; rapid, weak, thready pulse; hypotension; decreased LOC; restlessness; indifference; confusion and irritability
-dx: serum electrolytes and arterial/venous blood gases
*diagnoses
-risk for injury secondary to abnormal CNS function
*planning
-correct underlying cause and fluid/sodium imbalance
*implementation
-monitor neurological changes, ie: LOC, pupillary response, voluntary movement of extremities…
-monitor cardiovascular changes, ie: JVD, BP, pulse force
*evaluation
-is the underlying cause corrected?
**water imbalance
*assessment
-subjective: past medical history, medications, diet, elimination pattern, numbness, tingling, twitching, weakness of muscles
-objective: poor skin turgor; pitting edema; bounding pulse; rapid, weak, thready pulse; hypo/hypertension; SOB; moist crackles; indifference; restlessness; confusion and irritability; ALOC
-dx: serum electrolytes and arterial/venous blood gases
*diagnoses
-FVE/FVD
-impaired gas exchange
-decreased cardiac output
-risk for impaired skin integrity
-disturbed body image
*planning
-correct underlying cause of deficit/excess
-replace/remove fluids
*implementation
-input and output
-monitor cardiovascular changes, ie: JVD, BP, pulse force
-monitor respiratory changes, ie: SOB, cough, crackles, increased RR
-monitor neurological changes, ie: LOC, pupillary response, voluntary movement of extremities…
-daily weights
-skin care
-monitor IV fluids
*evaluation
-is underlying problem of the imbalance corrected?
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