Inflammatory &

Immunologic
Disorders
 Immunity
 The specific response of the body to
invasion by microorganisms and
foreign protein and, with the other
defenses of the body, constitutes an
essential protective mechanism.
IMMUNE SYSTEM
A complex network of
specialized cells and
organs that defend the
body against attack
from foreign pathogens.
Functions of Immune System
1. Defending and protecting the
body from infection by bacteria,
viruses, fungi and parasites
2. Removing & destroying
damaged / dead cells
3. Identifying and destroying
malignant cells, thereby
preventing their development
into tumors
Components of Human Immune System
Immune System Components

1. Human Blood
 RBC

 Platelets

 WBC

2. Lymphoid system
 WBC’s (leukocytes)
Leukocytes : principal cells involved in immune
response
1. Granulocytes: relatively short life-span; key
defenders during acute inflammation and
infection
2. Monocytes: largest of WBC and mature to
become Macrophage which is important in the
fight against chronic infections
3. Lymphocytes: principal effectors and
regulators of specific immune response
 Lymphocytes
 Monitor the body for cancerous
cells in the process known as
Immune Surveillance.

3 Types:
1. T lymphocytes
2. B lymphocytes
3. Natural killer Cells
0.5-1 % 60-70% 2-4 % 3-8 % 2-4 % 20-25 %
 2. Lymphoid System
 Lymphocytes concentrate in lymphoid
tissues (scattered in connective tissue,
mucosa and bone marrow), which include:
 Primary lymphoid organs
• Thymus
• Bone Marrow
 Secondary lymphoid organs
• Spleen
• Lymph Nodes
• Tonsils
• Peripheral lymphoid tissues
 Lymph Nodes
• Most numerous &
distributed
throughout
• Filter foreign
products or
antigens from the
lymph vessels
• Store and
proliferate
lymphocytes &
macrophage
 Lymphoid Organs
 Several other
organs contribute to
lymphatic function:
Spleen
Thymus
Tonsils
Peyer’s patches
 Spleen
Largest lymphoid organ
 Located on the upper left
quadrant of the abdomen.
 Filters blood.
 Destroys worn-out blood cells.
 Stores blood and breakdown
products of RBC for future use
 Thymus
 Located in the superior anterior
mediastinal cavity beneath the sternum
 Reaches maximum size at puberty and
begins to atrophy slowly
 Site for maturation and differentiation of T
cells
 Produces hormones
(like thymosin) to stimulate
formation of lymphocytes
Tonsils
 Small masses of lymphoid tissue
around the pharynx.
 Trap and remove bacteria and other
foreign materials.

Peyer’s Patches
• Found in the wall of the small intestine.
• Resemble tonsils in structure.
• Capture and destroy bacteria in the
intestine.
 Bodily Response
1. Non-specific Inflammatory Response
 Occurs when first-line defense are

breached
 It consists of barriers that are nonspecific

and have no memory. (i.e. Repeat

exposures to the same microorganism does
not enhance their response.)
2. Specific Immune Response
 occurs with the introduction of foreign
substances, or antigens, into the body.
 SPECIFIC immune response has MEMORY.
 An overview of the body’s defenses.

The Immune System

Adaptive (specific) defense

Innate (nonspecific) defense mechanisms
mechanisms

First line of defense Second line of defense Third line of defense

• Skin • Phagocytic cells • Lymphocytes-B cells and T cells

• Mucous membranes • Natural killer cells • Antibodies
• Secretions of skin • Antimicrobial proteins • Macrophages and other
and mucous • The inflammatory antigen-presenting cells
membranes response
• Fever

© 2018 Pearson Education, Ltd.

 1. Non Specific
Inflammatory Response
First line of defense

Physical Barriers
1. Skin and Mucous
Membranes .
2. “Flushing” mechanisms
a. Salivary flow
b. Coughing & Sneezing
c. Urination
d. Lacrimation
e. Ciliary action
 Second Line of Defense

Chemical Mediators
• Histamine - Vasodilation, increased permeability of
blood vessels
• Kinins - Vasodilation, increased permeability of
blood vessels
• Prostaglandins- Intensity histamine and kinin effect
• Leukotrienes- Increased permeability of blood
vessels, phagocytic attachment
Phagocytosis
 Inflammatory Response -
Second Line of Defense
 Triggered when body tissues are injured.
 Produces four cardinal signs:
Redness (Rubor)
Heat (Calor)
Swelling (Tumor)
Pain (Dolor)
 Results in a chain of events leading to
protection and healing.
 Functions of the
Inflammatory Response
 Prevents spread of
damaging agents.
 Disposes of cell debris and
pathogens.
 Sets the stage for repair
Steps in the Inflammatory Response

s
2. Specific Immune
Response
Third Line of Defense
Properties of Specific Immune Response

 Antigen specific – recognizes and acts

against particular foreign substances.
 Systemic – not restricted to the initial
infection site.
 Has memory – recognizes and mounts a
stronger attack on previously encountered
pathogens
 Recognition of self – typically directed
against materials recognized as foreign
and not directed against the self
Antibodies (Immunoglobulins)
(Igs)

 Soluble proteins secreted by B

cells (plasma cells).
 Carried in blood plasma.
 Capable of binding specifically
to an antigen.
 2 Types of Immune Response
1. Humoral Immune Response
- “Antibody-mediated” produced by B
lymphocytes
- Antigens usually activate B cells to
produce antibodies
- Attack Mechanism:
 Precipitation
 Neutralization
 Complement fixation
 Agglutination or clumping
Figure 17.8
 2. Cell-Mediated Immune
Response
 Antigens such as viral infected cells, cancer
cells and foreign tissue activate T cells which
is the primary agent in cellular response
 Antigens must be presented by macrophages
to an immunocompetent T cell (antigen
presentation).
 T cells must recognize nonself and self
(double recognition).
 After antigen binding, clones form as with B
cells, but different classes of cells are
produced.
 T Cell Clones
1. Cytotoxic T cells (CD8 cells)
 Specialize in killing infected cells.
 Insert a toxic chemical (perforin).
2. Helper T cells (CD4 cells)
 Recruit other cells to fight the invaders.
 Interact directly with B cells.
3. Suppressor T cells (CD8 cells)
 Release chemicals to suppress the activity of T and B cells
 Stop the immune response to prevent uncontrolled activity
 Properties of Immunity
• Specificity – activated by and responds to
a specific antigen
• Versatility – is ready to confront any
antigen at any time
• Memory – “remembers” any antigen it
has encountered
• Tolerance – responds to foreign
substances but ignores normal tissues
Common Diagnostic Test For
Immune System &
Inflammatory Dxs
1.ESR (Erythrocyte Sedimentation
Rate)
 Measures rate of RBC settling from
plasma.
2.RBC Count
 Determines actual number of formed
elements in relation to volume.
3.Total WBC Count
 Establishes quantity and maturity of
WBC
4. ANA (Antinuclear Antibody)
 Use to detect &/or screen several
connected tissue disorders (SLE &
Scleroderma).
 Use to detect anti-nucleoprotoien fxs
 (+) at a titer of 1:20 or 1:40
 Does not confirm a disease
5. Anti Double-Stranded DNA
Antibodies
 To confirm a diagnosis of SLE
6. Complement Assays
 Use to detect immuno-mediated disease
and genetic complement deficiency.
 total complement – Obstructive jaundice,
thyrioditis, acute rheumatic fever, etc.
 would indicate SLE, Glomerunephritis,
hypogammaglobulinemia or rejecting
allograft.
7. C-Reactive Protein Test
 Evaluate inflammatory disease and severity
of condition where there is tissue necrosis.
8. Human Leukocyte Antigen (HLA)
 Identifies a group of antigens present
on the surface of all nucleated cells,
but mostly detected in lymphocytes.
9. RAST (Radioallergosorbent Test)
 Measures immunoglobulin (Ig)E in serum
and identifies specific allergens that
cause rash, asthma, hay fever, drug
reactions and other atopic complaints.
10.Rheumatoid Factor Test
 Most useful immunologic test for
confirming RA.
 Care of Client
with
Immunological
Health Problems
 Allergies
 abnormal response of immune system to
an allergen
 Allergens are introduced by contact,
inhalation or ingestion
 Causes: plants, animals, chemicals, dust,
food, drugs, cosmetics, pests, perfumes
 Initial exposure to an allergen is required
to produce sensitization
 Hypersensitivity reactions are classified
by the type of immune response and its
time of response
ALLERGIES
 Types of
Hypersensitivity
Reactions
 1. Type I: IgE-Mediated
Hypersensitivity Rxn
• Produce immediate reaction; local or
systemic
• Occurs when allergen interacts with
IgE bound to mast cells & basophils
• Prompts release of histamine and other
chemicals
Example: Allergic asthma, Allergic
rhinitis(hay fever), Urticaria, Allergic
conjunctivitis, Acute anaphylaxis
 2. Type II: Cytotoxic
Hypersensitivity Rxn
 Characterized by IgG or IgM antibodies
reacting to foreign tissues or cells.
 Usually immediate responses.
 Includes hemolytic transfusion reaction of
incompatible blood type.
 Lysis of blood cells occurs by complement
system.
 Symptoms include fever, chills, low back pain,
hypotension, tachycardia, n/v, urticaria, red
colored urine, shock, renal failure.
 Examples: Rh incompatibility; hemolytic
anemia, drug-induced hemolysis.
Rh Incompatibility
 3. Type III: Immune Complex-
Mediated Rxn
• Intermediate reaction (6-24 hr)
• Results from the formation of IgG or
IgM antibody-antigen complexes that
circulate in the blood.
• Complexes adhere to walls of vessels
and cause inflammation that lead to
intravascular, synovial, endocardial
or other organ complications
• Includes autoimmune conditions
Antigen-Antibody Complex
Vessel Rupture
 4. Type IV: Delayed Type
Hypersensitivity Rxn
• Cell-mediated rather than antibody mediated
• Onset 24 to 48 hours after exposure to antigen.
• Results from exaggerated interaction bet.
antigen & normal cell-mediated mechanism.
• Examples: contact dermatitis, TB skin testing,
tissue transplant or graft rejection
• Symptoms are specific to the type of response:
• Dermatitis – e.g. poison ivy : redness,

induration, lesions, weeping, urticaria

• Positive TB skin test: redenning, induration of

>5mm at 72 hours
Allergic Reaction
 LATEX ALLERGY
 A reaction to contact with latex, producing
allergic dermatitis, immediate hypersensitivity
or anaphylaxis
 Source of allergic reaction is due to the
proteins in the natural rubber and the chemicals
used in the processing of latex
 Causes: latex exposure through
 Cutaneous route
 Mucosal route
 Intravascular
 Intrauterine device
 Internal contact through surgery
Latex Allergy
Nursing Assessment
 Assess high risk individuals
 Acquired sensitivity with repeated
exposures
 Employees required to use gloves often
 Spina bifida clients
 Clients with history of multiple
surgeries when young.
 3 Manifestations of Latex
Allergy
1. Allergic Contact Dermatitis – most common
 Symptoms: dry, itchy red rash on hands and fingers,
blisters, weeping, swelling
2. Immediate Hypersensitivity
 Develops within 5-30 mins. from exposure and
diminish when exposure removes
 Symptoms: immediate itching, intense swelling of
fingers/hand and may proceed to anaphylaxis
3. Anaphylaxis
 Symptoms: local/generalized itching, rhinitis,
urticaria, conjunctivitis, asthma, GI complaints,
tachycardia, hypotension, cardiac arrest
 Monitor respiratory and cardiac status, level of
consciousness
 Nursing Management
 Primary treatment is removal of the
irritant
 Educate client on the causes of
reaction and to avoid future contact
 Use mild soap and emollient creams on
affected area
 Medications include topical steroids,
antihistamines, vasopressors
 Anaphylaxis
 Serious and life-threatening allergic
reaction when an antigen is introduced
to a highly sensitive individual.
 A type 1 allergic reaction and
considered a medical emergency
 Categorized as local or systemic
 Systemic reaction may lead to
anaphylactic shock when widespread
vasodilation occurs
 Pathophysiology
 Antigen reacts with IgE which is
bound to mast cells and basophils
 Reaction causes mast cells to
release histamines and other
chemical mediators
 Mast cells also release packets
containing chemical mediators,
which attracts neutrophils &
eosinophils.
 Local reactions:
 urticaria, vasodilation, edema, erythema
 Systemic reactions:
 Respiratory – bronchoconstriction, air
hunger, stridor, wheezing & barking
cough.
 Cardiovascular – hypotension,
tachycardia, impaired tissue perfusion
 Gastrointestinal – nausea and vomiting
 Nursing Assessment
 Assess vital signs, lung sounds, heart
sounds, respiratory status, skin,
presence of edema and history of past
allergies
 Diagnostic Test:
 Complete Blood count (CBC)
 Arterial Blood Gas (ABG)
 Blood type and Crossmatch
 Radioallergosorbent test (RAST)
 Immune Complex/Complement Assay
 Nursing Management
 Patent airway is the highest priority
 Maintain an IV line for access to emergency
drugs
 Medications include antihistamine, epinephrine,
vasopressors (dopamine) and corticosteroids
 Administer oxygen as needed.
 Monitor vital signs frequently (every 15 mins.)
 Preventive measures against shock
 Urticaria
 Described as an itchy rash that may be recurrent
1. Acute urticaria – subsides over several hours
 Solar urticaria

 Delayed pressure urticaria – occurs after 1-4hrs.

 Aquagenic urticaria – ordinary water

2. Chronic urticaria – persist over 6 weeks

 Caused by massive release from mast cells in the

superficial layers of skin and is a vascular reaction
of the skin
 Assessment
 Symptom analysis of the onset, duration, and
possible causes and skin examination to
determine distribution.
 Signs and symptoms:
 Single or multiple areas of raised, blanched
central wheals surrounded by a red flare that
is highly pruritic.
 May occur anywhere with size ranging from
1-2mm to 15-20cm.
 Diagnostic test: scratch or intradermal tests
for allergy testing, IgE level, eosinophil level
 Nursing Management
 Medications include:
 Anti-histamines and H2 receptor

antagonist to reduce itching and prevent

prolonged symptoms
 Corticosteroids and topical sunscreens

may be recommended
 Cool moist compress to control the itch
 Increase fluids and use of skin lubricants
 Avoid harsh soaps
 Frequent bathing and products with alcohol
should be recommended.
 Angioedema
 Angioedema refers to swelling that
occurs in the tissue just below the
surface of the skin, most often around
the lips and eyes.
 It generally results from an allergic
reaction to either a food or medication.
 There are two basic types of
angioedema:
 Hereditary angioedema (HAE), which is
genetic and tends to recur
 Acquired angioedema (AAE)
 Angioedema can take from minutes to hours
to develop. In most cases, angioedema is
mild.
 Severe angioedema can cause the throat or
tongue to swell, cutting off the airway, and
can be life-threatening.
 Common symptoms of angioedema include:
 Sudden appearance of swelling, especially near
the eyes and lips, but also on the hands, feet, and
the inside of the throat
 Burning, painful, swollen areas; sometimes itchy
 Hoarseness, tight or swollen throat, breathing
trouble
 Discolored patches or rash on the hands, feet,
face, or genitals
 What Causes It???
 An angioedema reaction (AAE in
particular) may be caused by allergies
to foods, dyes, or pollen, or in reaction
to certain medications.
 Foods that commonly cause allergies
include shellfish, dairy, and nuts.
 Drugs that often spark allergic
reactions include (NSAIDs, such as
ibuprofen), antihypertensive
medication, aspirin, and antibiotics.
Prevention
 Eliminate any known or suspected
triggers. Allergy testing may help identify
inciting agents.
 Treatment Plan
 First priority is to ensure that the airway is
open and breathing is not impaired.
 Identifying and removing the trigger
factors as well as relieving other
symptoms
 Frequent attacks may require ongoing
treatment, perhaps with an allergist,
dermatologist to avoid recurrences.
 Management
 Drug Therapies
 For mild cases, use over-the-counter
antihistamines, such as Benadryl, Alavert,
or Claritin. Note that Benadryl often
causes drowsiness.
 For severe cases, doctor may prescribe
corticosteroids to reduce swelling and
itching, or be given a shot of epinephrine.
 Mild attacks tend to clear up within 4 days
with or without medication.
Allergic Rhinitis (Hay fever)
 Anallergic reaction to pollen which
causes inflammation and irritation to
the lining of the eyes, nose and throat.
 Pollen from trees and grass is a
common allergen and can affect
sufferers at specific times of the year.
 Known as “seasonal allergic rhinitis”,
because of the time when pollen
sensitivity occurs.
 Assessment
 Hay fever causes itchy, watery, red
eyes (known as seasonal allergic
conjunctivitis, or “allergic eyes”),
frequent sneezing and a constantly
dripping nose.
 Struggle to breathe through their
nose properly
 Itchy sensation in the nose, ears
and back of the throat.
 Management
 Desensitization such as injections or
drops under the tongue (sublingual
therapy). To date, the most effective
treatment is a course of injection
immunotherapy for grass pollen
allergy, which can have long lasting
benefits
 Allergen avoidance by wearing dark
glasses outdoors helps prevent pollen
settling on the eyes and limits the eyes
response to the sun.
 One mode of treatment is an
antihistamine, usually in tablet form.
Most effective for an itching, sneezing
and runny nose but less so for a blocked
nose.

 Use of a nasal-spray containing a topical

steroid is a more effective option and
will have greater effect at relieving
symptoms, especially if a blocked nose
is a problem.
 Acquired Immunodeficiency
Syndrome
• Last stage of Human Immunodeficiency Virus infection
• Immunodeficiency – state in which client’s immune
system is incompetent or unable to respond effectively
• Diagnosis:
- CD4 count of less than 200 cells/mm
- Two opportunistic pathogens
- presence of AIDS defining malignancy
• Transmission:
- Unprotected sexual activity: vaginal, anal or oral
- Blood to blood contact : needle prick, blood transfusion
- Perinatal: placental , via breast milk
• Classification of HIV
a. Category A: asymptomatic, primary HIV
or persistent generalized lymphadenopathy
b. Category B: symptomatic
c. Category C: AIDS-defining characteristics

• Two primary human immunodeficiency virus

• HIV-1 : prototype virus, mostly in the US

• HIV-2: primarily limited to West Africa

 The Structure of HIV

HIV is a retrovirus, which carries its genetic

information in RNA; on entry into the body the
virus infects cells which have the CD4 antigen
(T helper cells)
 Pathophysiology
Virus invades cell with CD4 antigen
Virus sheds protein coat and reveal its RNA
Viral RNA converted with
reverse transcriptase to viral DNA
Viral DNA integrates with host cell DNA

Virus remains latent Virus actively replicates

causing lysis of host cell
 Major Effects
 The viral number increases (Viral load)
 Viral load is the no. of circulating HIV per milliliter
 Less than 10,000 = low risk
 10,000 – 100,000 = moderate risk
 Greater than 100,000 = high risk
 Infected CD4 cells die
 If virus remains inactive, antibodies are
produced and detectable in 6 wks - 6mos.
infection
 Competent immune system = 650-1,200 cells/mm3
 Suppressed immune system = 500 - 200 cells/mm3
 AIDS: indicator values = less than 200 cells/mm3
 Classification of HIV infection
1. Category A
- primary HIV infection: (-) antibody test
- Asymptomatic: no disease process
- Persistent generalized lymphadenopathy for
more than 3 months; influenza-like symptoms
- CD4 T cell count greater than 500/mm3
2. Category B
- positive antibody test
- symptomatic: oral thrush, candidiasis, general
malaise, fever, fatigue, night sweats weight loss
or diarrhea
- CD4 T cell count between 200-499/mm3
3. Category C
- positive antibody test
- AIDS – defining conditions (
pneumocystis carinii pneumonia,
cytomegalovirus, tuberculosis, kaposi
sarcoma, lymphomas, dementia complex,
wasting syndrome)
- CD4 T cell counts of less than 200/mm3
 Assessment
 Signs and Symptoms:
 Flu-like illness lasting days to weeks from infection
 Fever, sore throat, joint and muscle pain,
headache, rash and swollen lymph nodes
 General malaise, fatigue, night sweats,
unintentional weight loss, diarrhea, oral lesions,
candidiasis,
 AIDS- Dementia Complex – dementia with
cognitive, behavioral and motor deficits
Symptoms include: impaired concentration,
forgetfulness, apathy, confusion, hallucinations,
personality changes, unsteady gait, leg
tremors,motor difficulties
 Diagnostic Test
 ELISA (enzyme-linked immunosorbent assay)
 Western Blot test
 HIV viral load – high > 100,000
 CBC – anemia, leukopenia, thrombocytopenia
 CD4 cell count – low < 200/mm3
 Diagnostic for opportunistic infections:
• TB Skin Tests
• MRI of brain, lymphomas
• Cultures
• Pap smears
 Management
 Medications:
 Nucleoside analogs – inhibits action of viral reverse
transcriptase ; e.g. Zidovudine
 Protease inhibitors – inhibits the viral enzyme
protease; e.g. Saquinavir
 Non-nucleoside reverse transcriptase inhibitors
- removal of the transcriptase enzyme of the virus
- e.g. Nevirapine
 Chemotherapy drugs
 Antibiotics for infections
 Analgesics for pain and discomforts
 Antiemetics and Antidiarrheals
 Nursing Interventions
 Monitor weight and nutritional status
 Educate on the side-effects of
medications
 Maintain proper oral care
 Avoid GI irritant foods
 Treat infections promptly
 Teach on safe sex practice and avoid
contamination of body fluids
 Standard precaution always instituted
AUTOIMMUNE DISORDERS
• When the immune system’s ability to
recognize self is impaired and
immune defense are directed against
normal host tissue
• Characteristics:
– Genetics play a role
– Frequently associated with an abnormal
stressors, either physical or
psychological
– Has periods of remission and
exacerbation
 Diagnostic Exams
1. Antinuclear Antibody- test for antibodies to
autoantibodies; highly sensitive in SLE
2. Rheumatoid Factor – test for macroglobulin
found in pts. with RA
3. Erythrocyte Sedimentation Rate
- test to determine the rate at which RBCs fall
out of the unclotted blood
4. Synovial Fluid Analysis – analyzed for its
several components: color, turbidity, viscosity,
WBC count; arthrocentesis is performed
5. Radiologic Studies – rule out skeletal changes
and differentiate soft tissue injury
 Rheumatoid Arthritis
• A Chronic, progressive, systemic disease with
inflammation of joints and deformity
• Incidence is 3x greater in women than men
• Onset usually occurs in middle-age (30-60 yrs)
but can develop at any age
• Unknown etiology: related to autoimmune process
• Systemic Complications include:
– Extrasynovial rheumatoid nodules
– Vasculitis
– anemia
Pathophysiology
Exposure to viral pathogen –
inflammatory response-- IgG
formed --autoantibodies are
produced against IgG -- immune
complex results in chronic
inflammation --
Destruction of articular cartilage
--synovial membrane hypertrophy
and blood supply is occluded --
Necrosis --vascular granulation
tissue (pannus)-- destruction of
bone --
Fibrous adhesion and bony
ankylosis occurs -- joint
instability and deformities occur
 Assessment
• Initial symptoms: anorexia, weight loss, fever
• Tenderness, swelling, redness of joints
• Morning stiffness lasting for at least 1 hr.
• Decreased ROM, impaired ability to perform ADLs
• Joint deformities
1. Swan Neck
2. Ulnar Drift
3. Boutonneire’s
deformities
Rheumatoid Nodules – firm, non-
tender subcutaneous masses found
on extension surface of forearm
 Diagnostic Test
• X-ray: reveal narrowing of joint space, bone
erosion and deformities in progressive disease
• Rheumatoid Factor : positive in 80% of patients
• CBC: evidence of normochromic anemia
• Erythrocyte sedimentation rate: elevated
• Synovial fluid analysis: increased WBC, increased
turbidity, decreased viscosity
 Management
1. Medications
a. NSAIDs – used early in the disease to relieve pain
and inflammation
b. Systemic corticosteroids- for long term use when
NSAIDs are no longer effective
2. Collaborate with physical therapists
a. Isotonic exercises
b. Passive range of motion
c. TENS (Transcutaneous electrical nerve stimulation)
3. Surgery
a. Synovectomy (removal of synovial membrane)
b. Total joint replacement
c. Arthrodesis – joint fusion
 Nursing Interventions
• Pain relief measures:
– massage, proper positioning in bed
– hot and cold application for 15 mins
– Paraffin dips
– Firm mattress for sleeping
• Emphasize rest to decrease joint stress
– Pace activities, splints for hands and wrists,
relaxation technique, guided imagery
 Systemic Lupus
Erythematosus
• Chronic progressive inflammatory & autoimmune
disease characterized by remission and
exacerbation
• Prognosis improves with early diagnosis and
treatment
• Affects connective tissue of body organs
• Disease progression varies depending on organ
involvement
• Women of child-bearing age is more susceptible
• Etiology is unknown but may be
attributed to exposure of UV rays,
genetic defect or hormonal imbalance
• Classification:
a. Drug-induced lupus
- hydralazine, isoniazid, antiepileptic
b. Discoid lupus
– limited to skin involvement
c. Systemic lupus
– musculoskeletal, lungs, kidneys, CNS,
cardiovascular, hematological system
involvement
 Pathophysiology
• Body produces auto-antibodies,
specifically against DNA, secondary to
hyperactivity of B cells
• Auto-antibodies combine with antigens
to form immune complexes which
trigger the inflammatory response
• Chronic inflammation destroys
connective tissue and leads to tissue
necrosis
 Signs and Symptoms
• General Symptoms: fever, malaise, fatigue,
weakness, weight loss
• Integumentary: alopecia, butterfly rash,
petechiae, photosensitivity and ecchymosis
• Respiratory : pleural effusion and pleuritis
• Renal : glomerulonephritis, renal failure
• Cardiovascular : pericarditis
• Musculoskeletal : polyarthralgia, arthritis
• Neurologic : seizures, cognitive disabilities
• Hematological: anemia, leukopenia,
thrombocytopenia
• Gastrointestinal: painless oral ulcers, pancreatitis
 Nursing Assessment
• Health history
• Complete Drug history
• Nutrition
• Skin assessment
• Respiratory
• Renal
• Neurologic
• Cardiovascular
• MSK
• Hematologic
 Diagnostic Findings:
• X-ray: will not show degenerative changes or
bone deformities
• CBC: anemia, leukocytopenia, thrombocytopenia
• Serum ANA: 90% positive not exclusive for SLE
• Anti-DNA antibody: positive, definitive for SLE
• Serum Complete levels : decreased
• ESR: elevated
• Urinalysis: proteinuria and hematuria
• BUN and creatinine clearance : elevated
 Management
1. Medications:
a. NSAIDS – treatment of joint pain
b. Corticosteroids – reduce inflammatory
process
c. Anti-malarials – decrease disease activity
d. Immunosuppressive drugs – used during
acute life-threatening exacerbations only
2. Prevent factors that trigger exacerbation:
a. Pregnancy
b. Exposure to UV rays
c. Medications
 Nursing Intervention
• Monitor skin integrity – keep skin clean and
dry, use mild soaps and lotions
• Provide/Instruct proper oral care
• Instruct the importance of proper nutrition
• Promote adequate sleep and rest
• Apply warm packs to relieve joint pain and
stiffness
• Protection from sun and UV rays exposure
• Suggest alternative hairstyle, scarves and
wigs to cover areas of alopecia
 Systemic Sclerosis
(Scleroderma)
• Generalized, chronic, autoimmune disorder of
connective tissue characterized by hardening and
thickening of the skin and other organs.
• With periods of remission & exacerbations.
• Affects 3-4 times more in women
• Unknown etiology
• Due to overproduction of collagen leads to fibrosis
and inflammation resulting to damage to affected
area.
• Classifications:
1. Systemic Sclerosis
2. C-R-E-S-T Syndrome
3. Limited
• Collagen is the
main structural
protein in the
extracellular
matrix in the
various connective
tissues in the
body.
 Risk Factors:

• Genetics.
• Environmental triggers. triggered by exposure to
certain viruses, medications or drugs. Repeated
exposure — such as at work — to certain harmful
substances or chemicals also may increase the risk
of scleroderma.
• Immune system problems. In 15 to 20 percent of
cases, a person who has scleroderma also has
symptoms of another autoimmune disease, such as
RA, lupus or Sjogren's syndrome.
 Classifications:
1. Systemic Sclerosis (SS)
- involvement of the skin of fingers,
hands, face, trunk and visceral
organs such as esophagus,
intestines, lungs, heart and kidney
- may progress quickly and life-
threatening
2. CREST syndrome
5 main features:
- Calcinosis
- Raynaud’s syndrome
- Esophageal dfxn
- Sclerodactyly
- Telangiectasia
3. Limited – involvement of skin
on fingers, hands and face; self-
limiting with good prognosis
 Signs & Symptoms
• Skin: shiny, thick skin on fingers, hands
progressing to arms, trunk and face
: hyperpigmentation, non-pitting edema,
calcinosis, telangiectasis
• Vascular : Raynaud’s syndrome
• Musculoskeletal: polyarthralgia and joint
stiffness
• Esophageal: heartburn and dysphagia
• Intestinal: constipation, diarrhea,
malabsorption, abdominal distention
• Cardiac: pericarditis, myocardial
involvement
• Lungs: SOB, interstitial fibrosis,
pulmonary HPN
• Renal: sclerodermal renal crisis –
renal failure
 Diagnostic Test
• ESR: elevated
• Urinalysis: proteinuria
• BUN and Creatinine: elevated
• ANA: positive
• Skin biopsy: dermal collagen thickening
- confirms the diagnosis
• Pulmonary function test: decreased vital capacity
• Barium Swallow: esophageal dysmotility
• X-ray: muscle atrophy, osteopenia, osteolysis
 Management
• Medications:
a. NSAIDs for joint pain
b. H2 blockers and proton pump inhibitors for GI
symptoms
c. Calcium channel blockers to promote vasodilation
d. Anti-emetic for intestinal motility
e. Corticosteroids and immunosuppressive drugs
• GI Symptoms
– Remain upright (high-fowler’s) during and after
meals
– Small frequent feedings
– Provide optimal nutrition and weigh weekly
• Raynaud’s syndrome
a. Dress warmly- wear gloves and socks to
warm hands and improve circulation
b. Avoid prolonged exposure to cold
c. Avoid smoking – causes vasoconstriction
• Skin Care
a. Use of moisturizers daily
b. Avoid use of drying soaps
c. Use protective padding – elbow pads
 Gouty Arthritis
• A metabolic disorder marked by increase
serum uric acid levels, deposition of urates in
joints causing inflammation
• Characteristics:
– Acute, painful episodes of monoarticular joint
inflammation lasting for about 10-14 days
– Not all clients with hyperuricemia develops gout
• Classifications:
– Primary: genetic alteration in purine metabolism
– Secondary: hyperuricemia secondary to disease
state or medications
 RISK FACTORS
1. Excess consumption of alcohol
2. Injuries
3. High stress period
4. Diuretic medications
 Pathophysiology
• Overabundant accumulation and subsequent
deposition of uric acid occurs in two ways
– Increase production of uric acid (10%)
• Inherited enzyme defects
• Certain disease conditions
a. myeloproliferative and lymphopoliferative disorders
b. hemolytic anemias
c. psoriasis
– Underexcretion of uric acid (90%)
• Renal and Endocrine disorders
• Medications and chemicals
a. diuretics c. pyrazinamide
b. ethanol d. lead
 Increase levels of uric acid
Initiate inflammatory response
Sodium urates are deposited
Phagocytosis of urate crystals
Cell death
Release of lysozymes enzymes
Chronic inflammation
Cartilage and bone destruction
Formation of tophi
 Assessment
A. Acute Gout Arthritis
- affects one joint, often the
metatarsophalangeal joint called PODAGRA
- sudden onset of severe, crushing pain
- joints appear red or dusky, swollen,
edematous and extremely tender to touch
- pruritus or skin ulceration
B. Chronic Tophaceous Gout
- tophi: hard, movable, nodules with irregular
surfaces occur in synovium, olecranon bursa
or achille’s tendon (most common)
- produce bone erosion and deformities
 Diagnostic Test
• Serum uric acid levels: elevated (>7.5mg/dl)
• Increased WBC and ESR during acute
episodes
• 24 hr. urine to evaluate uric acid excretion
– Levels correlate with increased serum uric acid
levels if there is overproduction of uric acid
– In under-excretion of uric acid, serum levels will
increase while 24hr urine levels will be decreased
• Synovial fluid analysis
– WBC increased
– Positive for urate crystals
 Management
• Medications:
a. Narcotic analgesics and NSAIDs to relieve pain
and swelling associated with acute attacks
* Aspirin is contraindicated since it interferes
with the excretion of uric acid
b. Colchicine- effective in treatment of acute
attacks; given IV to increase response and
decrease nausea & vomiting
c. Uricosuric drugs: Probenecid (Benemid) –
interferes with tubular reabsorption of uric acid
d. Allopurinol (Zyloprim) – prevents the conversion of
hypoxantine and xanthine to uric acid
 Nursing Interventions
• Increase fluid intake to 2-3L/day to decrease
incidence of kidney stones
• Dietary modifications – limit foods high in
purine such as organ meats, anchovies,
sardines, shellfish, chocolate, meat extracts
• Strict bedrest for 24hrs after acute attack
• Provide bed cradle to relieve pressure from
linens at affected area
• Assist with weight reduction
• Limiting intake of alcohol to moderate level
 Sjogren’s Syndrome
• A chronic inflammatory autoimmune process
that affects the lacrimal and salivary glands
• Seen most commonly in RA but can be seen in
SLE and other connective tissue disorders
• Primary Sjogren’s: gland inflammation
• Secondary Sjogren’s: associated with other
connective tissue disorders
• Etiology: unknown, include several factors:
– Genetic predisposition, immunologic, infectious and
hormonal
PATHOPHYSIOLOGY
- Antibodies at exocrine glands are
produced leading to disturbed function of
affected tissue
- Lymphocytes are found infiltrating on
tissues causing damage
DIAGNOSTIC TEST
• CBC: mild anemia, leukopenia in 30% of patient
• ESR: elevated (90%)
• RF: positive (75%-90%)
• ANA: positive in 70% of patients
• Schirmer’s tearing test
• Salivary gland biopsy, radiologic salivary scan and
salivary flow testing
 Signs & Symtoms
• Ocular: decrease tear formation, photophobia
• Oral: xerostomia , mucosal ulcers, stomatitis,
Salivary gland enlargement
• Nasal dryness, epistaxis, nasal ulcers
• Hoarseness, recurrent otitis media, pneumonia
• Renal: renal tubular acidosis
• Skin: xeroderma, urticaria, purpura
• Neuro: seizures, sensory & motor neuropathy
• Reproductive: vaginal dryness, dyspareunia
 Management
Dryness of the eyes
• artificial tears, eye-lubricant ointments
• Cyclosporine eyedrops (Restasis) reduce
the inflammation of the tear glands
improving their function.
Dry mouth
• drink plenty of fluids and good dental care
• sugarless lemon drops or glycerin swabs.
• Saliva stimulants - pilocarpine (Salagen)
and cevimeline (Evoxac). These
medications should be avoided by people
with certain heart diseases, asthma, or
glaucoma.
 Management
• Dryness in the passages of the nose.
– Saltwater (saline) nasal sprays
• Vaginal lubricant should be considered for
sexual intercourse.
• Serious complications, such as vasculitis,
can require immune-suppressant
medications, including cortisone,
(prednisone and others) and/or
azathioprine (Imuran) or cyclophosphamide
(Cytoxan).
 Polyarteritis Nodosa
• Rare autoimmune disease featuring spontaneous
inflammation of the arteries (arteritis).
• Common areas of involvement include the
muscles, joints, intestines, nerves, kidneys, and
skin.
• Poor function or pain in these organs can be a
symptom. Poor blood supply to the bowels can
cause abdominal pain. Fatigue, weight loss, fever
are common.
• Most common in middle-age people.
• Unknown cause, but it has been reported after
hepatitis B infection.
Polyarteritis Nodosa
 Pathophysiology

• Inflammation caused by deranged

immunologic processes results in
disruption of the blood vessel walls

• The affected blood vessels may

narrow as a result of injury or may
develop aneurysms especially at
vessels branching
 Diagnostic Test
• ERS - elevated
• WBC count and platelet count can be elevated,
while RBC count is decreased (anemia).
• Hepatitis B virus testing (for either antigen
and antibody) can be found in 10%-20% of
patients
• Urine testing can show protein and RBC’s
• The diagnosis of polyarteritis nodosa is
confirmed by a biopsy of involved tissue that
reveals the inflamed blood vessels (vasculitis).
• Angiogram – to detect vasculitis
 The American College of Rheumatology established
criteria for the classification of PAN

• Weight loss greater than/equal to 4 kg

• Livedo reticularis (a mottled purplish skin discoloration
over the extremities or torso)
• Testicular pain or tenderness
• Muscle pain, weakness, or leg tenderness
• Nerve disease / peripheral neuropathy
• Diastolic blood pressure greater than 90mm Hg
• Elevated kidney blood tests (BUN greater than 40 mg/dl
or Creatinine greater than 1.5 mg/dl)
• Hep B virus tests positive
• Arteriogram showing the arteries that are dilated
(aneurysms) or constricted by the blood vessel
inflammation
• Biopsy of tissue showing the arteritis
 Management
• Goal of Treatment - Decrease the
inflammation of the arteries by
suppressing the immune system.
• Medications
– High-dose intravenous and oral cortisone
medications (prednisone,) immunosuppressive
drugs (cyclophosphamide (Cytoxan) or
azathioprine (Imuran).)
• When hepatitis B is present.
– antiviral medications (vidarabine and
interferon-alpha).
 Fibromyalgia
• Condition of muscles and joints characterized
by fatigue, diffused muscle pain and stiffness
resulting in chronic pain without evidence of
arthritis.
• Characteristics:
a. Condition may be precipitated or
aggravated by stress or exertion
b. Onset is usually gradual, but it can occur
suddenly
c. Cause: unknown etiology, may be associated
with endocrine disorders, and disturbances
in sleep.
 Pathophysiology
• Suggested various possible causes:
a. Neuro-hormonal disturbances
b. Antecedent physical trauma
c. Viral infection
d. Immune dysregulation
e. Heightened sensitivity to pain
• Lacks the characteristics of arthritis such
as inflammation or structural changes.
• Inappropriate levels of neurotransmitters
have been investigated.
 Assessment
• Signs and Symptoms
– Muscle pain: localized or generalized, common in
neck, shoulders, lower back and hips
– Fatigue, headache, muscle spasm, paresthesias
– Sleep disturbance
– Irritable bowel syndrome
• Diagnostic tests:
– Complete physical exam
– Test to rule out osteoarthritis or rheumatoid
arthritis is performed
 Management
• Medications:
a. NSAIDs - to relieve pain
b. TCAs – for sleep disturbances e.g. Amitriptyline
c. Cyclobenzaprine (Hexent) – to relieve muscle
tension and spasm
• Regular exercise includes stretching, aerobic
activity, muscle strengthening
• Instruct on importance of rest
• Promote stress management
• Suggest a regular sleeping pattern
• Provide pain relief measures e.g. acupuncture
 CARE OF CLIENT WITH
INTEGUMENTARY SYSTEM
DISORDER
 Overview:
Skin is the largest sensory organ of the body
with a surface area of 15-20 feet and weight
9 lbs.
Functions:
- first line of defense against infection
- protects underlying tissues and organs
from injury
- maintains normal body temperature
- detects touch, pressure, pain stimulus
- excretes salt, water and organic waste
• Layers
1. Epidermis – outermost layer
2. Dermis – inner layer
3. Hypodermis – subcutaneous layer
• Epidermal appendages
• Sebaceous – associated with hair follicles that
open onto the skin surface where
sebum is released
• Eccrine – produce sweat and play important
role in thermoregulation
• Apocrine – secrete substance that becomes
odiferous when altered by skin surface
bacteria
• Hair & Nails – nonviable protein-end product
found on skin surfaces; horny scales of
epidermis
1. Macule, Patch
 Flat, non-palpable skin color change.
 Macule : <1cm
 Patch : >1cm
 Examples ; Freckles, flat moles, petechiae,
vitiligo, Port wine stains, ecchymosis

Petechiae
ecchymosis Port wine stains
2. Papule, Plaque
 Elevated, palpable, solid mass; circumscribed
border.
 Papule : < 0.5cm (Elevated nevi, warts, lichen
planus)
 Plaque : > 0.5cm (actinic keratosis)

mole(nevi) Keratosis
3. Nodule, Tumor
 Elevated, solid, palpable but extends deeper into
the dermis than a papule.
 Nodule : 0.5-2cm – circumscribed
 Tumor : >1-2cm; does not always have short
borders

lipoma
Keratogenous cyst
4. Vesicle, Bulla
 Circumscribed elevated, palpable mass
containing serous fluid.
 Vesicle : <0.5cm
 Bulla : >0.5cm

Herpes simplex

blisters
5. Wheal
 Elevated mass with transient borders,
often irregular.
 Caused by movement of serous fluid into
the dermis.
 Does not contain free fluid in a cavity
6. Pustule
 pus-filled vesicle or bulla

Acne vulgaris
7. Cyst
 Encapsulated fluid-filled or
semisolid mass
 Located in the subcutaneous tissue
or dermis
1. Erosion
 Lossof superficial epidermis
 Does not exceed to the dermis
 Depressed, moist area
candidiasis
2. Ulcer
 Skinloss extending past epidermis
 Necrotic tissue loss
 Bleeding and scarring possible
 Stage 1
 Skin is unbroken but
appears red, no
blanching when pressed
 Stage 2
 Skin is broken, and there
is superficial skin loss
involving the epidermis
alone or also the dermis.
 Stage 3
 Involves epidermis,
dermis and subcutaneous
tissue
 Stage 4
 Involvesthe epidermis,
dermis, subcutaneous
tissue, bone & other
support tissue.
3. Scar (Cicatrix)
 Skin mark left after healing of wound or
lesion
 Young scars : red or purple
 Mature scars : white or glistening
4. Fissure
 Linearcrack in the skin
 May extend to the dermis

Cheilitis
5. Scales
 Flakes secondary to desquamated, dead
epithelium
 Color (silvery, white) & texture (thick
or fine) varies

psoriasis
6. Crust
 Dried residue of serum, blood, or pus on
skin surface
 Large adherent crust is a SCAB.

Dried herpes simplex

7. Keloid
 Hyperthropied scar
secondary to
excessive collagen
formation during
healing
8. Atrophy
 Thin, dry, transparent
appearance of
epidermis
9. Lichenification
 Thickening and roughening and scaling
of the skin
1. Petechia
 Round red or purple macule
secondary to blood
extravasation
 Small : 1-2mm

2. Ecchymosis
 Round or irregular macular
lesion larger than petechia,
secondary to blood
extravasation.
3. Hematoma
 Localized collection of
blood creating an
elevated ecchymosis
 Associated with trauma

4. Cherry Angioma
 Papular and round, red or
purple, noted on trunk,
extremities.
5. Spider angioma
 Red arterial lesion
 has central body with radiating branches
 May blanch with pressure
6. Telangiectasis (Venous
star)
 Shape varies; spiderlike, or linear
 Color : bluish or red
 Does not blanch when pressure is
applied
 Secondary to superficial dilation of
venous vessel and capillaries
 Primary Lesions
Macule - flat, circumscribed
area of altered skin color
Papule-small,circumscribed
elevation of the skin
Nodule - solid lesion that
has distinct edges and
that is usually more
deeply rooted than a
papule.
Vesicle- small,
circumscribed, fluid
containing elevation
Bullae - similar to vesicle but larger
Pustule - A raised lesion filled with pus.
A pustule is usually the result of an
infection, such as acne, impetigo, or
boils.
Wheal - skin elevation caused by
swelling that can be itchy and usually
disappears soon after erupting
Plaque – flat-topped, palpable lesion,
larger than a lichen
Cyst – cavity-lined epithelium
containing fluid, pus or keratin, can be
nodule or papule
 Secondary Lesions
Scale - dry, horny build-up of dead skin
cells that often flakes off the surface of
the skin.
Crust - dried collection of blood, serum,
or pus. Often part of the normal healing
process of many infectious lesions.
Erosion - Lesion that involves loss of the
epidermis.
Ulcer - Lesion that involves loss of the
upper portion of the skin (epidermis)
and part of the lower portion (dermis)
Scar - Discolored, fibrous tissue that
permanently replaces normal skin after
destruction of the dermis.
Lichenification - Rough, thick
epidermis with exaggerated skin lines.
This is often a characteristic of contact
dermatitis and atopic dermatitis.
Fissure - An ulcer that appears as a
deep crack that extends to the dermis
Atrophy - area of skin that has become
very thin and wrinkled
 Diagnostic Test
1. Skin Biopsy – obtain tissue for microscopic
examination; obtain by scalpel excision or
skin punch instrument that removes a small
core of tissue
2. Patch Testing – identifying substance to
which the patient has developed an allergy
by applying the allergen to the skin under
occlusive patches
3. Skin scraping – tissue samples are scraped
from suspected fungal infection with sclapel
and examine microscopically
Diagnostic Test
4. Tzanck’s Smear
– examines cells from blistering skin
conditions such as herpes zoster or
other pemphigus
5. Wood’s Light Examination
- a special lamp that produces long-
wave UV rays (black light) which
result in a characteristic dark purple
fluorescence
- differentiates a epidermal from
dermal lesions
 Benign Conditions
• Acne
- androgen- stimulated
inflammatory disorder of sebaceous
glands resulting in comedones,
papules, pustules, nodules
- caused by increased sebum
production, proliferation of
propriobacterium acnes
- primary sites are face, chest,
upper back and shoulder
• 3 types of acne:
1. Acne vulgaris – common adolescent type
2. Acne conglobata – causes scarring
3. Acne rosacea – chronic form

• Acne is grades as follows:

• Grade1 – comedonal
• Grade 2 – papular lesions on face and
trunk (25 lesions)
• Grade 3 – more than 25 lesions, mild
scarring
• Grade 4 – nodulocystic, inflammatory
nodules with extensive scarring
 Management
• Wash face gently with mild soap and water
• Advise not to squeeze pimples and avoid
friction around face
• Use of water-based hypoallergenic
cosmetics
• Encourage balanced diet
• Medications:
• Benzoyl peroxide – antibacterial and comedolytic
• Topical antibiotics – suppress growth of acne,
decrease comedones, papules, pustules
• Retinoid therapy (Accutane) – inhibits sebum
production and secretion
• Estrogen therapy – anti-androgenic effect in
women taking oral contraceptive pills
 Benign Conditions
• Psoriasis
- chronic epidermal proliferative
disease characterized by erythematous,
dry scaling patches and heavy silvery
surface with periods of remission and
exacerbation
- caused by alteration of cell kinetics
of keratinocytes where cell cycle is
shortened from 311 hrs to 36 hrs with
increase epidermal cells
- life-long process without cure and
exacerbated by infection
(streptococcal pharyngitis, URTI)
 Management
• Topical corticosteroids decrease inflammation
and suppress excessive skin turnover
e.g. calcipotriene (Dovonex)
• Tar preparation
e.g. Anthralin (Dithranol)
• Photochemotherapy – ingestion of oral
photosensitizer (psoralen compound) followed
by ultraviolet A light therapy
- effects: cataract, nausea, malaise
• Oral methotrexate and cyclosporine are used
for severe cases
- hepatotoxicity occur for methotrexate
- hypertension and renal failure may occur
with cyclosporine
• Moisturizers, emollients & oils to soften scales
 Benign Conditions
• Seborrheic keratosis
- caused by proliferation of immature
keratocytes and melanocytes occurring
within the dermis
- characterized by benign plaques
(beige, brown or black) ranging in size
from 3-20 mm with warty surface
- appear as “stuck on” spots usually
present on the face, neck, scalp, back
and upper chest
Management
• Medication treatment is usually not
required except for cosmetic
purposes
• Educate on the use of sunscreen with
SPF over 15, decrease sun exposure
• Corticosteroids cream may be
applied to affected area
• Mainstay of dandruff treatment with
medicated shampoo (selenium
sulfide, salicylic, sulfur, zinc
pyrithione)
 Bacterial Infections
• Cellulitis
- diffuse inflammation of the deep
dermal and subcutaneous tissue
caused by infection of streptococci, ,
H. influenzae, S. aureus
- presents various lesions including
vesicles, bullae, abscess that are
tender, warm, erythematous and
swollen
- S/S: erythema, warmth, edema and
pain, often presented with fever,
chills, malaise and lymphadenopathy
C
E
L
L
U
L
I
T
I
S
 Bacterial Infections
• Folliculitis
- inflamation of the hair follicle caused
by Staphylococcus areus and
Pseudomanas aeruginosa
- commonly seen in beard area of men
and women’s legs from shaving
- appears single or multiple erythemic
papules or pustules
• Furunculosis
Furuncle – deep folliculitis consisting of
pus-filled mass which is painful
Carbuncle – 2 or more confluent furuncles
- tender, circumscribed, erythematous
lesion common in back of neck, axillae,
buttocks area
FOLLICULITIS
FURUNCLE
 Bacterial Infections
• Impetigo
- superficial skin infection initially
seen as erythemic vesicle and
changes to a honey-colored crusted
lesion
- commonly seen in 2-6 yrs., crowded
living, poor hygiene, warm climate
- caused by Staphyloccus areus and
Streptococcus pyogenes
- manifested by extreme itching, red-
macular lesion
- common on face, arm, legs & buttocks
IMPETIGO
 Management
• Topical/Oral antibiotics for small
localized areas given 10-14 days
e.g. penicillinase-resistant penicillin,
cephalosporins, quinolones
• Daily cleansing of antibacterial soap
• Avoid irritating lotions/creams
• Warm compress to reduce inflammation
and promote comfort
• Use clean razors when shaving
• Incision and Drainage for suppurative
lesion may be necessary
 Viral Infections
• Herpes zoster (shingles)
- acute viral infection of the dorsal nerve
root ganglion, caused by the reactivation
of varicella virus during immuno-
compromised state
- skin culture provides definitive diagnosis
- manifested as cluster of vesicles along
peripheral sensory nerves on trunk,
thorax
- symptoms include erythematous lesion,
Itching, burning and severe pain
- fever, headache, malaise may precede
the rash
 Management
• Suppression of pain, inflammation and
infection is the goal of therapy
• NSAIDs or acetaminophen may be used
for pain and fever
• Cool wet compress for comfort measures
• Systemic therapy with acyclovir,
vidarabine and corticosteroids for newly
developing outbreaks
• Prevent the client from scratching or
rubbing the affected area
• Instruct to avoid clients who are at risk:
neonates, pregnant women,
immunocompromised persons
 Viral Infections
• Warts
– virus-induced epidermal tumors and
transmitted by touch and often appear
on hands, periungual regions, and
plantar surface
- most warts resolve in 12-24 months
without treatment
- symptoms include round, raised rough
gray lesions
Types:
1. common (dome-shaped, scaly, irregular)
2. filiform ( thin projections on narrow stalk)
3. flat ( flat-topped, skin-colored papule)
4. plantar ( on surface of feet)
5. venereal ( cauliflower-like on genitals)
WARTS
 Management
• Medications include liquid nitrogen and
topical preparation to be used nightly for
6-8 weeks
• Apply petroleum ointment on
surrounding skin to prevent irritation
• May suggest removal of wart lesion by
snip excision (filiform)
• Educate client since wart is viral in
nature, it may reappear in the same site
or on other areas of the skin
 Fungal Infections
• Infections caused by fungi
(dermatophytes) found on the stratum
corneum, hair and nails
• Caused by excess moisture, contact
with infected person, use of broad-
spectrum antibiotics, immuno-
suppression, malnutrition and disorders
such as diabetes mellitus
• Diagnostic test:
• culture of scraping or microscopic exam
using 10% KOH (potassium hydrogen)
• Wood’s lamp – used UV light; area fluoresces
blue-green in the presence of fungi
 Candidiasis
• Infection caused by Candida
albicans – yeast like fungi that is
part of the normal flora of mucous
membranes
• Includes oral (thrush), vaginal
(vulvovaginitis), diaper area
(perineal), prepuce and glans penis
(balanitis), nail folds (paronychia)
• S/S: bright red lesion, smooth
macules with scaling, elevated
border
 Characteristics:
• Oral thrush: white, milky plaques on oral
mucosa associated with burning
sensation
• Vulvovaginitis: excessive itching, thick,
white, curdy vaginal discharge
• Perineal : erythema, papules, pustules,
and scaling border
• Balanitis: flattened pustules, edema,
scaling, erosion, burning and
tenderness on the penis
• Paronychia : tenderness with creamy
purulent discharge, discolored
• Dermatophyte Infection
1. Tinea capitis (scalp)
- erthyema and scaling of scalp with
patchy hair loss
2. Tinea corporis (body)
- lesions are circular, erythematous, well-
marginated with raised, scaly vesicular
border
3. Tinea cruris (groin and upper thigh)
- sharply demarcated, scaling patches and
extremely pruritic lesion
4. Tinea pedis (foot) “ Athlete’s foot”
- fine, vesiculopustular, scaly, itchy
5. Tinea unguium (nails) “Onychomycosis”
- distal thickening and yellow color nails
TINEA PEDIS TINEA CAPITIS
 Management
• Topical treatments is preferred but some
cases require oral medications such as:
Miconazole (Monistat)
Nystatin ( Mycostatin)
Ketoconazole (Nizoral)
Fluconazole ( Diflucan)
• Avoid sharing personal items
• Dry all skin folds with use of clean towel
• Apply drying powders of topical antiperspirants
to decrease moisture
• Wear light cotton socks and change frequently;
wear sandals or open-toed
• Avoid tight clothing and pantyhose, dry genital
area thoroughly, treat sexual partner
 Parasitic Infestations
• Pediculosis
- infestation of skin/hair by specie of
blood sucking lice
- symptoms: itching, skin excoriation,
erythematous macule or wheals,
blue-gray macules with pediculosis
pubis
• Pediculosis capitis – head lice; common in
school children spread by close contacts by
sharing comb, hats or linens
• Pediculosis pubis – crab louse infest the
genital area, spread by sexual contact
PEDICULOSIS
CORPORIS
 Management
• Antiparasitic preparation:
• Lindane (Kwell) , Permithrin (Nix)
– apply cream/lotion after bath on affected
area, wash off after 8-12 hrs
- apply shampoo to affected hairy areas,
lather for 4-5 mins., rinse and dry
• Manual removal of nits may be performed
using fine-tooth comb
• Washing all infested clothing or linens
with hot water and soak for 20 mins.
• Educate on the mode of transmission and
promote preventive measures
 Parasitic Infestation
• Scabies
- superficial infestation by the itch mite
(Sarcoptes scabier hominis) transmitted
by close personal contact
- common in people who don’t have
access to bathing or laundry facilities
- parasite identified by microscopic
exam of skin scraping
Symptoms:
intense pruritis at night,
small erythematous papules
short wavy burrow lines in the skinfolds
 Management
• Systemic or topical steroids to treat
symptoms of allergic reaction to mites
• Avoid close contact for 24 hrs. after
treatment to prevent transmission
• Machine wash and dry clothing and
linens on hot cycle
• Antiparasitic treatment
• Premethrin (Nix)
- applied thinly to the entire skin and
leave medication for 8-12 hrs. not longer
to prevent irritation
- applied on dry skin since moist skin
increase absorption and possibility of
toxicity
 Allergic Conditions
• Contact dermatitis
- inflammatory conditions caused by
exposure to irritating or allergenic
substance such as:
plants (poison ivy) hair dyes
cosmetics metals
soaps & detergents rubber
Symptoms: itching, burning, erythema
progresses to crusting, fissuring
- chronic type results to lichenification
and pigmentation changes
 Management
• Removal / avoidance of causative agent
• Topical or oral steroids given in tapered
dose to provide anti-inflammatory effect
• Systemic or topical anti-histamine or
calamine preparation for pruritus
• Perform patch test by applying
substance behind ear or inside of wrist
before trying new cosmetics, soaps etc.
• Wash and rinse skin thoroughly when in
contact with potential irritants
 Allergic Conditions
• Exfoliative Dermatitis
- chronic extensive scaling and
inflammation of the skin
- maybe idiopathic or related to pre-
exisitng skin condition, drug reaction
Symptoms:
- patchy erythema with fever, chills;
- skin color changes to scarlet,
desquamates and ooze serous fluids
- pruritus, hair loss and secondary
infection
 Management
• Discontinuation of offending drug or
treatment of underlying condition
• Systemic corticosteroids control most
cases
• Supportive treatment – bed rest, warm
environment and fluid/electrolyte
replacement
• Soothing bath and topical emolients for
symptomatic relief of itch
• Possible use of immunosuppressants –
methotrexate, cyclophosphamide
• Seborrheic Dermatitis
- Acute inflammatory condition
- Affects the scalp, forehead,
eyebrows, eyelashes, nasolabial
folds, axillary and genital areas
- Signs and symptoms:
- Yellow or white plaques that
may scale, crusts with greasy
appearance, pruritus, oozing
and loss of hair
Management
• Medications include selenium
containing shampoo, keratolytic
agents, topical and systemic
cortisone lotions
• Frequent shampooing is
suggested if on the scalp
• Scrupulous skin hygiene and
keeping the skin dry is
imperative
• Atopic Dermatitis (eczema)
- Common inflammatory skin
disorder seen in children and
adults
- Related to cell-mediated
immunity, excessive histamine
sensitivity, increased levels of IgE
- Signs and symptoms:
- Erythema, scaling, pruritus, and
lesions on hands, feet , arms
and legs
Management
• Medications include
antihistamine, softening lotions,
cortisone cream and oral
antibiotics if needed
• Avoid soaps and keep bath to
minimum; use bath oils to
soften skin
• Soft texture clothing is ideal
• Clip fingernails to decrease
injury while scratching
Seborrheic Atopic
 Burns
• Alteration in
skin integrity
resulting in
tissue loss or
injury caused by
heat, chemicals,
electricity or
radiation.
 Types of Burns:
• First-degree burn
(superficial thickness
burn)
• Only epidermis is damaged
• Skin is red and swollen
• Second-degree burn
(partial-thickness burn)
• Epidermis and superficial
part of dermis are damaged
• Skin is red, painful, and
blistered
• Regrowth of the epithelium
can occur
 Types of Burns:
• Third-degree burn (full-
thickness burn)
• Destroys epidermis and dermis;
burned area is painless
• Requires skin grafts, as
regeneration is not possible
• Burned area is blanched (gray-
white) or black
• Fourth-degree burn (full-
thickness burn)
• Extends into deeper tissues (bone,
muscle, tendons)
• Appears dry and leathery
• Requires surgery and grafting
• May require amputation
Causes:
• 1. Thermal burns
• 2. Chemical burns
• 3. Electrical burns
• 4. Radiation burns
 Pathophysiology:
• Burn from any source is a major insult to the
body
• Within several hours, capillary integrity is lost
due to release of chemical mediators of
inflammation
• Fluid passes from intravascular system to
interstitial system causing hypotension and
massive edema
• Loss of IV volume leads to increase blood
viscosity, decrease cardiac output, decrease
perfusion to kidney and activation of RAA
system to increase volume which leads to
retention of water and further edema
Pathophysiology:
• Cells can’t maintain adequate electrolyte shifts
and results in the ff:
• excess Na and water;
• loss of K, Mg, P leading to cardiac dysrhythmias &
altered CNS
• Cortisol is released due to stress and depressed
immune system which intensifies risk for
infection
• SNS is activated, increasing metabolic rate and
oxygen demand; this hypermetabolism lead to a
breakdown of tissue, protein metabolism, fat
wasting
• Fluid shifts back within 24-48 hours and
intravascular overload will then be a concern
 Complications of Burns:
• Immune
• infection with Staphylococcus aureus, septic shock
• Cardiovascular
• blood clots leading to CVA or myocardial infarction,
Heart failure, cardiac arrest, pulmonary edema
• Gastrointestinal
• peptic ulcer, impaction
• Respiratory
• adult respiratory distress syndrome, hypoxia
• Hematological
• burn shock, DIC, anemia
• Renal
• oliguria, renal failure
Nursing Assessment:
1. Symptom analysis of the cause of burn, time
occurred, medical history, medications & allergies
2. Overall general appearance for distress and
amount of pain
3. Depth and extent of burn (% total body surface
area)
4. Cardiac status, respiratory status, airway patency,
hydration status
5. Airway status is essential whenever burn has the
capability of compromising the airway because of
edema
6. Diagnostic test: blood urea nitrogen (BUN),
creatinine clearance, Urine output, CBC,
electrolytes, albumin, bilirubin, ABGs, chest x-ray,
ECG, C&S
• Extent of a burn is estimated
using the Rule of Nines
• Body is divided into 11 areas for
quick estimation
• Each area represents about 9
percent of total body surface area
• The area surrounding the genitals (the
perineum) represents 1 percent of
body surface area
 Totals
4 1 2%
Anterior and posterior
head and neck, 9%

Anterior and posterior

upper limbs, 18%

Anterior and posterior

41 2 % 41 2 % trunk, 36%
Anterior
trunk, 18%

Perineum, 1%
9% 9%

Anterior and posterior

lower limbs, 36%

100%

(a) Rule of nines

Criteria for deeming burns
critical (if any one is met):
a) Over 30 percent of body has second-
degree burns
b) Over 10 percent of the body has third-
or fourth-degree burns
c) Third- or fourth-degree burns of the
face, hands, or feet, or genitals
d) Burns affect the airways
e) Circumferential (around the body or
limb) burns have occurred
Nursing Management:

1. Remove all rings and jewelry to avoid

a tourniquet effect on the affected site
2. Flush chemical burn copiously with
water and apply cold compress;
Remove clothing and cover with dry
sheet
3. Administer oxygen if necessary
4. Maintain proper hydration and
encourage high protein and high
calorie diet; monitor input/output
Nursing Management:
• Fluid Replacement (Emergent)
• Parkland Formula
Nursing Management:
5. For superficial thickness, topical
anesthetic creams may be used to relieve
pain and no dressings needed
6. For partial thickness, leave blister intact
7. Small burns may be covered with
antibiotic ointment and non-adherent
dressing to absorb drainage
8. For larger burns cover with silver
sulfadiazine 1%, non-adherent dressing
and bulky dressing to absorb drainage
Nursing Management:
9. Full thickness will not heal on its own and
require skin grafting to heal
10. Use of sterile technique to decrease risk
of infection
11. Monitor pain management needs & treat
pain before debridement
12.Assess for tetanus prophylaxis and
administer tetanus toxoid if needed.
 Skin Cancer
• Risk Factors:
• Fair complexion
• Working outdoors
• Exposure to certain chemical agents
• Long-term immunosuppressive therapy
• Genetic susceptibility
• Multiple dysplastic nevi (larger,
irregular, more numerous, variable
color)
• Large congenital nevi
Most Common Types of
Skin Cancer
1. Basal Cell Carcinoma
2. Squamous Cell Carcinoma
3. Malignant Melanoma
 Malignant Conditions
1. Basal Cell Carcinoma
- most common and least
aggressive
- lesions typically begin as
small nodule with a pearly,
translucent border with
crusting and occasional
ulceration
- appear frequently on sun-
exposed skin, particularly
on face between hairline
and upper lip
 Malignant Conditions
2. Squamous Cell
Carcinoma
- more aggressive type,
slow growing cancer of
atypical squamous cells
and metastasize to
lymphatic system
- common on sun-expose
areas: lips, nose, hands
- appears firm, irregular,
erythemic, thickened scaly
lesion
- may sore and/or bleed
 Malignant Conditions
• Malignant Melanoma
-Most deadly of skin cancers, but
accounts for only 5 percent of skin
cancers
-cancer tumor arising from
melanocytes & metastasize to
different organs
-common sites are back and legs
-precursor: dysplastic nevi,
congenital nevi
- Characteristics: asymmetry,
border irregularity, color variation,
diameter > 6mm, evolve (ABCDE)
Detection of Malignant
Melanoma
• A = Asymmetry
• Two sides of pigmented mole do not match
• B = Border irregularity
• Borders of mole are not smooth
• C = Color
• Different colors in pigmented area
• D = Diameter
• Spot is larger than 6 mm in diameter
• E = Evolution
• One or more of the ABCD characteristics is evolving
Assessment & Management
Diagnostic Test:
Incisional Biopsy – removal of a piece of tissue
to detect malignancy and level of invasion
that determines treatment
Management:
1. Assess all lesions in the body as to its
size, color, shape, texture
2. Avoid contact with chemicals
3. Sun exposure protection
4. Curettage – for small tumors
5. Complete excision – 1-4mm depth
6. Radiation therapy
7. Systemic chemotherapy – for recurrent
metastasis
Thank You!!!
and
GOD Bless!