Infection/Immunity/Dermatitis Flashcards
Inflammation of the lung parenchyma
-infection is constantly a possibility;
Respiratory open airway
Pneumonia
Acute Bacterial Pneumonia Legionnaires' disease Primary Atypical Pneumonia Viral pneumonia Aspiration Pneumonia Pneumocystis carinii Pneumonia
Types of Pneumonia
Productive cough chills fever cough sputum rust or purulent Hear crackles; possible pleural rub pneumoccocal (strep) 70%, staphaureus; necrosis lung absess or empyema (pus pocket) Throcyntesis or chest tube aspirate fluid out
Acute Bacterial Pneumonia
-(Chest) pleuritic pain; increase change on inspiration
Moisture (swimming in pond) HVAC; duct work; broncho pneumonia Legionella pneumophila (bug found in H2O) gradual onset (up to 2 days after exposure) Dry cough dyspnea malaise chills fever Head ache possible confusion anorexia and diarrhea
Legionnaires’s Disease; pneumonia
Mycoplasma pneumoniae Verigitis or bronchitis, typically young adults living in close quarters 10% viral mild HA fever Malaise Fatigue muscle aching dry cough
Viral pneumonia
Asp. of gastric contents emergency surgery depressed cough or gag impaired swallowing stroke pts. @ risk
Aspiration pneumonia
PCP Abrupt onset includes fever tachycardia SOB dry, non-productive cough ***HIV
Pneumocystis carinii Pneumonia
*Chest Xray; pneumonia dx & rule-out
*Computed tomography; detailed image needed
*Sputum gram stain; tells you what its positive for and to determine broad spectrum antibiotics
*Sputum C&S; culture and sensitivity; what bug is it and drug it’s most susceptible to. (resistant)
*CBC; complete blood count
*Serology testing; detect antibodies to toxins, identify affecting organism
*Pulse oximetry; Sat %
*ABG; arterial blood gases
*Fiberoptic bronchoscopy; some reason pt needs o2.
(bronch tem; look and see whats going on. poss to suck all sputum out and get a specimen).
Diagnostics Pneumonia/Infection
Cough Excess mucus production Dyspnea Hemoptysis Chest pain Fever Decreased appetite Malaise Cyanosis
Symptoms of Pneumonia/Infection
*Pain and Fever Control; treat at 38.5 or greater in hosp.; Tylenol or Motrin
Risk with increase fever; seizures
*Fluids; loosen secretions; have insensible fluid loss; need extra
*Rest
*O2; Sat%
*Chest PT; loosen up secretions; ABX
*Urinary Tract Infection;
What is it? ureuritis, prostatitis, cystistis, pleulonephritis (upper and ureters; 2nd most common in children)
*An infection that can include urethra bladder, ureters, and/or kidneys
*Infecting agent
*Escherichia coli; most common (in stool) Females wipe front to back
*Staphylococcus sapophyticus; 10-15%
*Proteu
*Klebsiella
*Pseudomonas; these 3 have to do with catheterizations
Treatment of Pneumonia/Infections
Dysuria Pyuria Frequency Hematuria Urgency Suprapubic discomfort Nocturia
Urinary Tract Infection
Symptoms
- urinalysis; mid stream or clean catch
- urine gram stain; what type of bacteria?
- urine culture and sensitivity; susceptibility
- WBC with differential; increase infection; leukocytosis
- Intravenous pyelography; contrast, structure elevation, anything unusual there
- Voiding cystourethrography; taking a look while your voiding
- Cystoscopy; up urethra; direct visualization to bladder
- Pelvic/prostate exam; manual exam; determine cystocele, enlarged prostate or rectocele
- Renal/bladder ultrasound; detect pyelonephritis or renal scaring
Diagnostics of Infection/UTI
ABX
Encourage fluids; flush system
Administer analgesics
Treatment of UTI infection
Is a highly contagious, viral respiratory disease referred to as “the flu”
Influenza or “the flu”
Coryza; inflammation of the nasal mucous membrane lining assoc with nasal discharge. Cough; dry Substernal burning Sore throat Fever and Chills Muscle Aches Malaise Fatigue
Symptoms of the Flu
Based on Hx; where u been, with who? Clinical Findings Community Outbreaks Chest Xrays WBC; decreased bc viral CBC; rule out pneumonia 30% mortality rate Prevention; vaccine No aspirin for children: Reye Syndrome (2 to 3 weeks after onset of flu)
Diagnostics for the Flu
myocarditis
encephalitis
Guillian Barre; neuromuscular disorder; loss function top to bottom. recover bottom to top
Complications of the flu
- Antivirals;
- amantadine (5 day prophylactic), rimantidine (preventing), Zanamivir (prophylactic; can give bronchospasms, no COPD patients)
- oseltamivir (PO), ribavirin (inhalant); decrease severity of the flu, 7 days if you have it.
- aspirin, acetaminophen, NSAIDS, to relieve fever and aches
Treatment of Flu; Antivirals
Acute bacterial infection of the dermis and underlying connective tissue
Cellulitis
Inflammation
Pain
Warmth
Redness
Swelling
***enlarged lymph nodes
-irregular shape, but well defined borders.
-Normal flora on body then break in skin, get an infection.
-ABX-10 day course
-@ risk for sepsis and osteomyelitis (inf. in the bone) and arthritis
Symptoms of Cellulitis
WBC; elevated; bacterial
Blood cultures; possibly, systemic infection
Diagnostics of Cellulitis
Maintain adequate hydration Administer antipyretics, ABX Administer pain medication as needed Maintain bedrest Encourage adequate nutrition for healing
Treatment for Cellulitis
Peripheral Vascular Disease
Legs up
Peripheral Arterial Disease
Legs down
tinea pedis
athlete’s foot
malnutrition dehydration diabetes PVD, circulatory problem issues tinea pedis
Peripheral neuropathy
disorder of nerve(s) apart from the brain and spinal cord.
Peripheral neuropathy
Inflammation of the mucus membranes of the stomach and small intestine. usually the small bowel.
Gastroenteritis
Increased frequency of stooling. ie. watch out for hypokalemia. Replacing K+ possible
Increased water content of stool.
hx, HA, Malaise, muscle aches
“traveler’s diarrhea” from e coli or campylobacter
“dysentery” from Shigellosis
Viral Rotavirus
norwalk virus
Symptoms of Gastroenteritis
Gram stain
Diagnostic for Gastroenteritis
Fluids ABX Skin Care Weights daily (hydration staus) Must use own bathroom and dishes food prep wash hands clean bathroom
Treatment of Gastroenteritis/teaching
Inflammation of the skin
- response to direct contact with allergen
- Common causes; dyes, perfumes, poison plants, chemicals, metals, acids, alkalis, bromide, chlorine, cosmetics, fabrics, rubber products, coloring agents.
- Nursing practice consideration: Latex
Contact Dermatitis
Allergic contact dermatitis
-Type IV cell mediated.
-Delayed hypersensitivity
-First exposure sensitizes, subsequent exposure manifestations noted.
Irritant contact dermatitis
-Inflammation of the skin from irritants.
*Often forms acids, soaps detergents
*Lesions are similar
Risk Factors
-Allergies, family hx or eczema, burns exposure to plants, chemical metals, frequent hand washing,
Elderly @ risk
Pathophysiology and Etiology
Contact Dermatitis
- Allergic Manifestations
- Erythema
- Edema
- Pruritus
- Vesicles
- Bullae
- Irritant contact dermatitis
- Discrete area of redness at exposure location
Clinical Manifestations
Contact Dermatitis
Allergic Contact Dermatitis
-Symptoms can develop several hours to 3 days after exposure
-Rash takes 2-4 weeks to resolve without treatment
Irritant contact Dermatitis
-Rash usually develops within a few hours of contact, peaks within 24 hours and resolves with removal of the irritant.
Clinical Manifestations
Contact Dermatitis
Hx and pattern of rash gives clues
- Testing;
- patch testing, stays on for 48-72 hr.
- Intradermal
- Scratch
Diagnosis
Contact Dermatitis
- Remove offending agent!
- Apply calamine lotion
- Cool compresses; Burrow’s/Domeboro Solution
- Oatmeal soaks; relieve itching
- caution, tub will be slippery
- Antihistamines; itching/limit cytokines; benadryl
- Topical Corticosteroids; 2x/day (2-3 weeks)
- oral corticosteroids for more than 10% surface area
- never stop taking abruptly
Treatment for Contact Dermatitis
- Referral to allergist
- Other consultations if episode recurrent
- School age children; class environment
- Work environment
Collaboration
Contact Dermatitis
Chief Complaint;
- Onset
- Characteristics
- Course
- Severity
- Precipitating and relieving factors
- Physical examination
Nursing Process: Assessment
Contact Dermatitis
Impaired Skin integrity
Deficient Knowledge
Nursing Diagnosis
Contact Dermatitis
Client’s triggers will be identified and eliminated
Client will remain free from infection
Plan for Contact Dermatitis
Medications, treatments relieve symptoms
Client teaching to relieve irritation of skin
May need to change diet, environment
Remove clothing worn after outside activity
place barrier between allergen and skin
Apply topical corticosteroids for 2-3 weeks
Antihistamines with caution (drowsiness)
Implementation
Contact Dermatitis
Control of dermatitis maintained
No infections occur
Triggers identified and eliminated
Client’s sleep minimally disturbed by itching
Evaluation
Contact Dermatitis
- Altered immune response to an antigen that results
- Response may be bothersome or life threatening
- Classified by type of response, immediate or delayed, organ system, or allergen
Hypersensitivity
characterized by rapid development of symptoms after exposure to an antigen. Anaphylaxis is the most severe form
Type I, or immediate hypersensitivity
Rapid development of symptoms after exposure to an antigen
Ie Anaphylaxis
Involves the rupture of cells targeted by the immune response. A common example is transfusion reactions.
Type II, or cytotoxic hypersensitivity
Involves rupture of cells targeted by the immune response.
Ie. transfusion reactions!
Includes inflammatory response in the targeted tissues that leads to tissue damage. Autoimmune disease often involve this type of reaction.
Type III, or immune complex reaction.
Includes inflammation response in the targeted tissues that lead to tissue damage.
Ie. Autoimmune diseases
Characterized by tissue damage at the site of antigen contact 24-48 hours after exposure. Contact dermatitis is an example.
Type IV, or delayed-type hypersensitivity
Characterized by tissue damage @ the site of antigen contact 24-48 hrs after exposure.
Ie. contact dermatitis
Type I; IgE mediated; Local or Systemic Type II; IgG or IgM; Cytotoxic Type III; Immune complexes (IgG or IgM antibody and antigen) Type IV; Delayed; T-Cell/Macrophage *HIV, Rh. Arthritis Stimulatory (Type V)
Types of hypersensitivity Reactions
Humoral
Stimulating specific targets, antibodies bind to target cell & stimulate. “Turned-on”
Ie. contact with foreign antigen stimulates B cells.
IgE-mediated hypersensitivity; ***poison ivy
-common hypersensitivity. Trigger when allergen interacts with free IgE
-allergens can be ingested in food, injected, inhaled, or absorbed.
*Can be local or systemic (atopic or anaphylactic)
-Local mediators remain confined to a local area
-Allergens cause hay fever, rhinitis, asthma.
-Mosquito bite
-Hives
*Systemic-Mediators are released systemically.
-Anaphylactic shock
(Epi pen, epinephrine into thigh) *acts only to stabilize until get to hospital) Very small window; anaphylactic shock. keep airway open, Remove allergen
Type I
*Release of histamine Leads to
-Vasodilation in small arteries and capillaries
-Increased capillary permeability
-Smooth muscle contraction, (muscle tightens, throat closes up)
-Bronchial constriction; can’t breath, bronch seizing up)
*Most severe form is anaphylaxis!
-commonly assoc. with ABX and more recently Latex.
1st 5/10 mins after 1st time taking med; Abx. systemic; rash on skin
Type I
- Erythema and sometimes angioedema of the eyes, lips or tongue.
- First feelings of uneasiness, apprehension, weakness, and impending doom.
- Pruritus & urticaria
- Edema and swelling, followed rapidly by wheezing, dyspnea, cyanosis, and circulatory collapse requiring immediate emergency treatment.
- Maintenance of airway is a priority; tongue blocked; get out of way of opening.
- ABX reaction possible; take history; hospitalization, 1st time taking abx. bc. no previous exposure
Anaphylaxis
Can be fatal!
First assess respiratory function Oxygen CPR may be needed. Epinephrine (1: 1000) 0.3 to 0.5 ml IV or SubQ Antihistamines treat angioedema and urticaria. Treat bronchospasm IV fluids Monitor VS (BP/Resp) Treat underlying cause
Anaphylaxis Intervention
Type II (Cytotoxic) hypersensitivity
- IgG or IgM-type antibodies form to a cell-bound antigen
- Antibodies bind with antigen
- (Exogenous or Endogenous Stimulation)
- Examples of exogenous antigen reaction
- foreign tissue or cells
- Drug reaction PO meds
- Withdrawal of antigen stops hemolysis; remove antigen
Type II
Special autoantibodies directed against self cells that have some form of foreign protein attached to them. Self cells destroyed by lysis or phagocytosis. (pacman)
-clinical examples include:
*hemolytic anemia
*thrombocytopenic purpura
*hemolytic transfusion reactions
*Good pasture’s syndrome; body mistakes and generates
lungs to kidneys; lung/renal damage
Type II Cytotoxic Hypersensitivity
Blood Transfusion
*IgG or IgM antibodies attach to a cell-bound antigen
*Complement cascade destroys target cell
Stop Transfusion, if not reaction will be worse.
**Shut off pump if having a reaction!!!
riders, turn beat red; shooting pain, fever, local irritants (10-15 min) usual reaction. Do next set of vitals in 15 mins.
Drug reaction
*Drug forms antigenic complex on blood cell surface.
*Resulting reaction destroys cells leading to hemolytic anemia
*Discontinuing drug stops the reaction
-check for any itching, swelling reaction.
Cell lysis (destruction)
Examples of Type II
- Endogenous antigen forms on surface of tissue
- Reaction destroys the tissue
- Results in autoimmune disorders
- Myasthenia Gravis; disease of myelin sheath tissue. mistake and generates/misfiring nerves or non-firing.
- Severe weakness caused by circulating antibodies that block Acetylcholine receptors @ the post synaptic neuromuscular junction.
- Goodpasture’s syndrome
- The body mistakenly generates antibodies against lung and renal tissue producing lung damage and renal failure.
Examples of Type II
- remove offending drug or blood product.
- Plasmapheresis-fresh plasma
- Treatment is symptomatic
- Complications can be life threatening
- respiratory failure
- Renal failure
- Hemolytic crisis
Treatment of Type II Cytotoxic Reactions
- Results from formation of IgG or IgM antibody-antigen immune complexes in circulatory system
- These circulating complexes usually lodge in small blood vessels.
- Local
- immune complex accumulates in the glomerular basement membrane of the kidneys.
ex. Streptococcal infection or with systemic lupus erythematosus glomerulonephritis - Systemic
- Fever urticaria, rash, arthralgia, lymphadenopathy, myalgia
Type III; Immune complex-mediated
*Serum Sickness; often seen when horse or rabbit serum injected. Self limiting.
*Systemic Lupus Erythematosus (SLE)
-A chronic inflammatory condition that causes disease of the skin, heart, lungs, kidneys, joints & nervous system.
-Multiple treatment modalities.
*Rheumatoid Arthritis; primarily affects synovial joints causing pain and deformity.[Corticosteriods]
-Multiple treatments: medication; harsh on body, carcinogenics; lupus.
Autoimmune diseases are not curable.
1-3 weeks after injection; reaction.
Type III; Immune complex Mediated
- T cell and macrophage mediated rather than antibody mediated; nothing to do with IgG or IgM
- Local collection of lymphocytes and macrophages causes edema, induration, ischemia, and tissue damage at the site (local site)
- Turberculin testing POS have induration and redness in 8-12 hrs. (PPD). Decrease just having reaction with injection negative. Bump positive. (induration) Have to touch
- Contact dermatitis such as poison ivy
- Latex allergy
- Can process to type I reaction (IgE response); unknown Latex allergy and put on; can have IgG response.
- Insect stings
- Organ transplantation rejection.
- Sarcoidosis-Fibrosis in lung tissue; decrease function of organ. Clumping tissue; grows in organ. Brandylonas. genetic; extreme reaction to antigens.
Type IV: Delayed Hypersensitivity Reactions
- Immunotherapy/Desensitization/Allergy shots build IgG.
- Epinephrine
- Corticosteriods & Anti-inflammatory agents can reduce discomfort.
- Histamine blockers: Benadryl of minimal benefit because Histamine is not the main mediator however, can help with sleep and itching.
Type IV: Interventions
-Stimulatory hypersensitivity; antibodies are produced with the property of stimulating specific cell targets (humoral immunity)
-B cell mediated immunity; activated when in contact with antigen can excrete memory cells or antibodies; made in bone marrow.
-Autoantibodies bind to target cell and stimulate cells.
-Excess stimulation of a normal cell surface by an autoantibody, results in a continuous “turned-on” state for the cell.
-May cause uncontrolled secretion of hormone.
*the feedback mechanism is lost. Sends thyroid over stimulations; Grave’s disease; hyperthyroidism
*Grave;’s disease (hyperthyroidism)
eyes popping out of there head.
B cells in plasma generated memory cells provide rapid response to antigen it encounters.
Stimulatory Reaction
Is found in body secretions including tears, saliva, breast milk, and colostrum. It lines mucous membranes and protects body surfaces. Found in secretions of respiratory, GI and GU tract. purpose is to protect mucus membranes from invading organisms.
IgA
Oral
In the gut and respiratory & GI
Is found in plasma and interstitial fluids, it causes symptoms of allergic reactions. It attaches to mast cells and basophils. Assists in defense against parasitic infections, attached to mast cells and help with release of histamine-allergic reactions. Increases during allergic reactions and anaphylaxis.
IgE***
Major immunoglobulin: primary antibody in a secondary immune. important in resistance to infection and passive resistance for a fetus, surveillance antibody. Responsible for antiviral and antibacterial barrier.
IgG
Is found in plasma. It is responsible for primary immune response and forms anibodies to ABO blood antigens. Early reactors to antigens. Produced within 48-72 hrs. from antigen exposure. Produces antibody activity against Rheumatoid factor, gram-negative organisms.
IgM
A state of responsiveness to foreign substances such as microorganisms and tumor proteins.
Immunity
Immune responses serve what function?
- Defense
- Homeostasis
- Surveillance
What type of hypersensitivity reaction is allergic rhinitis?
Type I
Under which of the following classifications of hypersensitivity would systemic lupus erythematosus (SLE) and rheumatoid arthritis be classified?
Type III hypersensitivity
What type of hypersensitivity reaction is the body’s defense against the tubercle bacillus (tuberculosis)?
Type IV
What type of hypersensitivity reaction are hemolytic transfusion reactions (Rh & ABO incompatibility)?
Type II
Human body constantly threatened by
- foreign substances (non-self)
- infectious agents
- abnormal cells
- Function of immune system
- protect body from foreign antigens
- identify and destroy potentially harmful cells
- remove cellular debris
Immunity
Body’s natural or induced response to infection
- immunocompetent clients
- hypersensitivity; overreaction of immune response/allergies
- autoimmune disorders-attack self
- immunodeficiency
- Understanding immune system
- importance of immunizations
- hygiene
- nutrition
- optimize health
Immunity
- Complex network
- Performs several functions
- defends and protects body from infection
- removes and destroys dead/damaged cells
- identifies/destroys malignant cells
- Activated by external agents
- inflammation nonspecific response
- ability to differentiate host from foreign tissue
Immune System
Leukocytes (WBC’s)
- primary cells
- derived from stem cells in bone marrow
- use circulation to transport to site
- normal number: 4,500-10,000 cells/mm3
- Leukoctosis in presence of infection
- Leukopenia
- Leukocytes divided into 3 major Types
- ***granulocytes
- ***monocytes
Components of the Immune System
Granulocytes; 60-80%
- Myeloid stem cells of bone marrow
- Protect body from microorganisms
- Three types
- Neutrophils
- Eosinophils
- Basophils
Types of Leukocytes
Antigen-presenting cells (APC;s) *Initiate immune response *Actively phagocytic Three types *Monocytes *Macrophages *Dendritic cells Phagocytic cells
Types of Luekocytes
Lymphocytes
- Effector and regulator cells of specific responses
- Constantly circulate
- Three types
- T cells
- B cells
- Natural killer cells; lymphnodes, spleen and other lymphoid tissue
Types of Leukocytes
- Provoke specific immune response
- Complete antigens have 2 characteristics
- immunogenicity; ability to stimulate a specific immune response
- specific reactivity; stimulate specific immune system components.
- Primary immune response; sensitizes body
- Secondary immune response; Memory cells; again; ready to fight off infection.
Antigens
Found in nose, breathing passages, digestive tract, ears,eyes, and vagina. Found in saliva, tears and blood Consists of 10% to 15% of the antibodies. A small number of people do not make IgA antibodies. 1 in 400 don’t make.
IgA; (Ahhh, as in oral)
Found in all body fluids. They are the smallest but most common antibody (75% to 80%) of all the antibodies in the body. Very important in fighting bacterial and viral infections. Only type that can cross the placenta
IgG (little Grandma; all goo in body)
Largest antibody. Found in blood and lymph fluid. First responder to an infection. Cause other immune system cells to destroy foreign substances. 5% to 10% of all the antibodies in the body
IgM (M for mom; largest antibody)
Found in the lungs, skin, and mucous membranes. Cause the body to react against foreign substances such as pollen, fungus spores, and animal dander. Occur in allergic reactions to milk, some medicines, and some poisons. Levels are often high in people with allergies.
IgE (exhale; lungs)
Found in small amounts in the tissues that line the belly or chest. how they work is not clear.
IgD (Dad; belly, chest)
Intracellular pathogens activate T lymphocytes (Armed forces; Army-Tissue/Tents/T-Cells)
- Helper T cell initiate immune system.
- Complement activates
- general inflammatory reaction
- Immune cells secrete cytokines
- Carry messages for immune system function
- cell proliferation, differentiation of cellular actions, produce inflammation, sensitization to pain
- interleukins are a type of cytokine.
- cytotoxic T lymphocytes; attack malignant cells.
respons. for rejection of transplants.
Cell-mediated (cellular) Immune response
Lymph nodes, spleen, thymus, tonsils, lymphoid tissue scattered in connective tissues, mucosa and bone marrow.
- Recovers proteins for vascular system.
- protects bloodstream from invading organism
- Lymph nodes
- Filter foreign products or antigens
- House and support lymphocytes and macrophages
- Spleen
- Thymus gland
- stimuates lymphopoiesis
- Bone marrow
- produces, stores hematopoietic stem cells
- Lymphoid tissures-mucosa-assoc.
- peyer’s patches; gut assoc. largest collection of immune cells
- Tonsils and adenoids
- Protect from inhaled or ingested foreign agents
Lymphoid System
Introduced antigen into body allowing immunity to develop.
- active immunity
- passive immunity; given immunoglobulins. Not long term from someone else;
- Types of vaccines
- killed virus
- toxoid
- live virus
- recombinant
Immunizations
Responses to vaccines;
*local reaction
*systemic reaction
*local allergic reactions
*life-threatening allergic reaction; anaphylaxis
Vaccine Anaphylaxis Treatment
-Epinephrine
-0.01ml/kg up to 0.5ml IM
-Repeat every 10-20 min to total of 3 doses until symptoms subside
-Keep resuscitative equipment immediately
Immunizations
Immune function declines with aging External and internal factors -decrease in immune response -lowered resistance to infections -poor response to immunizations -autoantibodies more common decrease with aging
Normal Changes of Aging
Enzyme Immunoassay Immunoglobulins Polymerase chain reaction Rapid HIV test Radioallergosorbent test (RAST) antigens on I gE in blood Skin allergens Western blot test Complete CBC Complement Enzye-linked immunosorbent assay
Diagnostic tests; immunity
Irritant to the skin; hypersensitivity
Contact Dermatitis
What are some common causes of Contact Dermatitis?
Dyes Latex Cosmetics Poison Plants Acids Different Fabrics
What is usually the cause of irritant Contact Dermatitis?
Chemicals (acids), soaps, detergents
Not a hypersensitivity response
Allergies Fam hx of eczema exposure of plants burns Elderly
Some Risk Factors for Contact Dermatitis
Redness
Edema
Itching
Bullae or Vesicles; rupture, ooze and crust
Clinical Manifestations of Contact Dermatitis
Symptoms develop within several hours to 3 days of exposure to irritant and peaks within 24 hours.
Contact Dermatitis
Removal of Agent Apply calamine lotion cool compress oatmeal bath antihistamines corticosteroids oral corticosteroids
Treatment of contact dermatitis
Onset Characteristic Severity Course Precipitating Factors
Nursing Assessment for Contact Dermatitis
Impaired Skin Integrity
Deficient of Knowledge
Nursing Diagnoses for Contact Dermatitis
