this is a ppt for subject Immunologic response in Medical-surgical Nursing

1. NCM 112
(Immunologic
Disturbances
Concept)
1st Semester
SY 2011-20SY 2022-2012 OLATA,
RN,MN, PH.D.

3. Hypersensitivities
Hypersensivity is a state of altered
reactivity in which a previously sensitized
immune system reacts in an excessive or
inappropriate way with resultant tissue
damage and pathology.

4. Four Basic Types of
Hypersensitivity
 Type I (immediate) hypersensitivity
(anaphylactic) reactions
 Type II (cytotoxic) reactions
 Type III (immune complex-mediated) reactions
 Type IV (delayed) hypersensitivity reactions

5. Type I: Immediate
mast cell – a constituent
of connective tissue
containing large
basophilic granules that
contain heparin,
serotonin, bradykinin,
and histamine)
Hay fever – an acute,
seasonal, allergic
rhinitis stimulated by
tree, grass, or weed
pollen.
Reaction of IgE antibody on
mast cells with antigen,
which results in release of
mediators.
Clinical Examples: hay
fever, allergic asthma,
anaphylaxis

6. Hay Fever
Hay fever –
an acute,
seasonal,
allergic
rhinitis
stimulated by
tree, grass,
or weed
pollen.
Please turn
to Slide 11

7. Type II: Cytotoxic
Goodpasture’s syndrome – (Ernest Goodpasture- american
pathologist – a chronic relapsing pulmonary hemosiderosis,
usually as-
sociated with glomerulonephritis and characterized by a
cough with hemoptysis, dyspnea, anemia, and progressive
renal failure.
Hemosiderosis – an increased deposition of iron in a variety
of tissues, usually in the form of hemosiderin and usually
without tissue damage.
Myasthenia gravis – an abnormal condition characterized
by chronic fatigability and muscle weakness, especially in
the face and throat. It is caused by the inability of receptors
at the myoneural junction to depolarize because of the
deficiency of acetylcoline. The onset of symptoms is usually
gradual, with ptosis of the upper eyelids, diplopia, and
weakness of the facial muscles. The weakness may then
extend to other muscles innervated by the cranial nerves,
particularly the respiratory muscles. Muscular exertion
aggravates the symptoms, which typically vary over the
course of the day. Treatment consists of anticholinesterase
drugs usually administered before meals. The edrophonium
test is used to determine the optimal maintenance dose.
Myasthenic crisis may require emergency respiratory
assistance.
Ptosis – an abnormal condition of one or both upper eyelids
in which the eyelid droops because of a congenital or
acquired weakness of the levator muscle or paralysis of the
third cranial nerve.
Reaction of IgG with host
cell membrane or antigen
absorbed by host cell
membrane.
Clinical Examples:
autoimmune hemolytic
anemia, Goodpasture’s
syndrome, Myasthenia
gravis

8. Goodpasture’s Syndrome
Goodpasture’s syndrome – (Ernest
Goodpasture- american pathologist – a
chronic relapsing pulmonary
hemosiderosis, usually asso
ciated with glomerulonephritis and
characterized by a cough with
hemoptysis, dyspnea, anemia, and
progressive renal failure.
Hemosiderosis – an increased
deposition of iron in a variety of tissues,
usually in the form of hemosiderin and
usually without tissue damage.

9. Myasthenia gravis
Myasthenia gravis – an abnormal
condition characterized by chronic
fatigability and muscle weakness,
especially in the face and throat. It is
caused by the inability of receptors at
the myoneural junction to depolarize
because of the deficiency of
acetylcoline. The onset of symptoms
is usually gradual, with ptosis of the
upper eyelids, diplopia, and weakness
of the facial muscles. The weakness
may then extend to other muscles
innervated by the cranial nerves,
particularly the respiratory muscles.
Muscular exertion aggravates the
symptoms, which typically vary over
the course of the day. Treatment
consists of anticholinesterase drugs
usually administered before meals.
The edrophonium test is used to
determine the optimal maintenance
dose. Myasthenic crisis may require
emergency respiratory assistance.
Ptosis – an abnormal condition of one
or both upper eyelids in which the
eyelid droops because of a congenital
or acquired weakness of the levator
muscle or paralysis of the third cranial
nerve.

10. Type III: Immune complex-
mediated
Systemic lupus
erythematosus - is a
chronic, progressive,
inflammatory
connective tissue
disorder that can
cause major body
organs and systems
to fail.
RA - connective
tissue disorder
The clinical
manifestations are
caused by immune
complexes that lodge
in joint spaces
followed by
destruction of tissue,
and later scarring and
fibrous changes.
Formation of immune complex
of antigen and antibody, which
deposits in walls of blood
vessels and results in
complement release and
inflammation.
Clinical Examples: serum
sickness, vasculitis, systemic
lupus erythematosus,
rheumatoid arthritis

11. Type IV: Delayed
Sarcoidosis – a chronic disorder of
unknown origin characterized by
the formation of tubercles of
nonnecrotizing epithelioid tissue.
Common sites are the lungs,
spleen, liver, skin, mucus
membranes, and lacrimal and
salivary glands.
The lesions usually disappear
over a period of months or years
but progress to widespread
granulomatous inflammation and
fibrosis.
Granuloma – a chronic
inflammatory lesion characterized
by an accumulation of
macrophages; epitheloid
macrophages, with or without
lymphocytes; and giant cells into a
discrete granule. Granulomas may
resolve spontaneouly, remain
static, become gangrenous,
spread, or act as a focus of
infection.
Reaction of sensitized T
cells with antigen and
release of lymphokines,
which activate macrophages
and induce inflammation.
Clinical Examples: Poison
ivy, graft rejection,
tuberculosis, sarcoidosis

12. Anaphylaxis
 It is a clinical response to an immediate (type I
hypersensitivity) immunologic reaction
between a specific antigen and an antibody.
 The reaction results from IgE antibody.

13.  The most dramatic example of a type I
hypersensitivity reaction, is a rapid, systemic,
simultaneous occurrence after reactions in
multiple organs.
 It generally occurs within seconds to minutes
of exposure to an allergen.
 Many substances can trigger anaphylaxis in a
susceptible person.

14. Pathophysiology
 An antigen attaches to the IgE antibody fixed
to the surface membrane of mast cells and
basophils, causing these target cells to
become activated.

15. Common Agents that Cause
Anaphylaxis
Protamine sulfate – a
heparin antagonist
derived from fish
sperm. It is
prescribed to diminish
or reverse the
anticoagulant effect of
heparin, particularly in
cases of heparin
overdosage.
 Antibiotics (penicillin,
cephalosporins, tetracycline,
sulfonamides, streptomycin,
vancomycin, chloramphenicol,
amphotericin B., etc.
 Adrenocorticotropic hormone,
insulin, vasopressin, protamine
 Allergen extracts, muscle
relaxants, hydrocortisone,
vaccines, local anesthetics
(lidocaine, procaine)

16. Cryoprecipitate – a
preparation rich in
factor VIII needed
to restore normal
coagulation in
hemophilia. It is
collected from fresh
human plasma that
has been frozen
and thawed.
Hemophilia -
 Whole blood, cryoprecipitate,
immune serum globulin
 Radiocontrast media
 Opiates
 Foods (shellfish, eggs,
legumes, nuts, grains, berries,
preservatives)

17.  Insect bites (hymenoptera: bees, wasps,
hornets)
 Fire ants
 Snake venom
 Other agents (pollens, exercise, heat/cold)

18. Assessment
Clinical manifestations
Onset
 Feeling of uneasiness
 Apprehension
 Weakness
 Feeling of impending doom

19. Dilated or congested
blood vessels produce
red skin, or erythema, the
most common sign of
skin irritation and
inflammation.
When pressure is applied
directly to the skin,
erythema blanches
momentarily, but purpura
does not.
 Generalized pruritus
 Urticaria
 Erythema
 Angioedema of the
eyes, lips or tongue

20. Pathophysiology
Histamine and other chemical mediators
cause bronchoconstriction, mucosal edema,
and excess mucus.

21. Respiratory Assessment
 Congestion
 Rhinorrhea
 Dyspnea
 Increasing respiratory distress with audible
wheezing, crackles, and diminished breath
sounds
 Laryngeal edema-feeling of having a “lump in
the throat,” hoarseness, and stridor(a crowing
sound).

22. Complications
 Respiratory failure secondary to laryngeal
edema
 Hypoxemia(insufficient oxygenation of blood)
secondary to suffocation and lower airway
bronchoconstriction.
 Hypercapnia(increased CO2 in blood)

23. Cardiovascular Assessment
Rationale:
Due to
chemical
mediators,
which cause
vasodilation
and
increased
capillary
permeability
with
resultant
leakage of
intravascular
fluids.
 Hypotension
 A rapid, weak, possibly irregular
pulse

24. Assessment
70% of
death can be
caused by
respiratory
failure
and/or by
shock and
cardiac
dysrhythmia
s.
 Syncope and diaphoresis
 Anxiety, confusion, loss of
consciousness
 Dysrhythmias, shock, and cardiac
arrest – due to decrease in
intravascular volume.

25. Interventions
Epinephrine
- an agent
that
constricts
blood
vessels,
increases
myocardial
contraction,
and dilates
the
bronchioles.
Emergency Respiratory
Management
 Initiate CPR
 Epinephrine: 0.2 – 0.5 mL, to be
given subcutaneously with
symptoms of systemic anaphylaxis.
The same dose may be repeated
every 15 to 20 minutes if needed.

26. Interventions
Antihistamin
es
(Benadryl)
An agent
that blocks
the
histamine
receptor site
(H1) in
vascular and
bronchiolar
smooth
muscle.
 Antihistamines (diphenhydramine)
25 to 100 mg, are usually given
intravenously, IM, or orally to treat
angioedema and urticaria.

27. Interventions
 Insert a small endotracheal tube or perform an
emergency tracheostomy if the extent of upper
airway narrowing requires it.
 Administer O2 to minimize hypoxemia.
 Monitor tissue oxygen saturation using pulse
oximetry. (ABG concentrations are monitored
to determine the adequacy of the
oxygenation.)

28. Interventions
 Use suction to remove excess mucous
secretions, if indicated.
 Assess and record the client’s rate, rhythm,
and depth of respirations, presence of
bronchospasm and abnormal breath sounds.

29.  For severe bronchospasm, Aminophylline, 6
mg/kg intravenously, over 20 to 30 minutes.
Maintenance aminophylline (0.3 – 0.5
mg/kg/hour) is initiated.
 Give an inhaled beta-adrenergic agonist such
as metaproterenol or albuterol every 2-4 hours

30.  For persistent symptoms (after 1 to 2 hours),
corticosteroids are added to prevent the late
recurrence of symptoms.

31. Nurse’s Primary Role
Assessment to detect changes in any body
system and monitoring for adverse effects of
drug therapy.
Observation of the client for fluid overload from
the rapid administration of medications and
intravenous fluids and reporting changes to
the physician immediately.

32. Prevention
 Teach the client with a history of allergic
reactions to avoid allergens whenever possible
and to alert health care personnel about their
specific allergies.
 Advise clients to carry an emergency
anaphylaxis kit with injectible epinephrine.

33. Physicians
and nurses
should be
aware of
common
cross-
reacting
agents e.g.,
penicillin:cep
halosporins
have similar
biochemical
structures.
 Careful history is taken before any
drug or therapeutic agent is given.
 Skin tests should be performed
before the administration of
substances with a highly associated
incidence of anaphylactic reactions,
such as allergenic extracts or horse
serums.

34. Atopic Allergy
Once the
person has
sensitized
IgE, allergic
symptoms
occur on
reexposure
to the
allergen via
degranulatio
n of mast
cells.
Atopic reactions are allergic
manifestations that occur in people
who are genetically predisposed to
respond to a variety of
environmental allergens by forming
immunoglobulin E (IgE).

35.  Allergic asthma - most common
 Allergic rhinitis
 Urticaria – most common
 Eczematous dermatitis

36. Urticaria (“hives”)
 It is essentially anaphylaxis that is limited to
the skin.
 It is characterized by local wheals, erythema of
the skin, and pruritis.

37. Pathophysiology & Etiology
Mononucleo
sis – an
abnormal
increase in
the number
of
mononuclear
leukocytes in
the blood
 Exposure to drugs, transfusions,
insect stings, desensitization
injections, certain foods (eggs,
shellfish, nuts, and berries)
 Viral infection such as hepatitis,
infectious mononucleosis, or
rubella.
 Physical stimuli: cold, sunlight, heat,
vibration, or exercise.

38. Collaborative Management
 Urticaria is self-limiting and will disappear
within 7 to 10 days.
 Treatment is symptomatic: oral antihistamine
(diphenhydramine, 25 to 50 mg every 4 to 6
hours, or hydroxyzine-Vistaril, 25 to 50 mg 3X
a day.

39.  Urticaria with angioedema: corticosteroids
(Prednisone) may be used.

40. Nursing Management
 Help the client identify the allergen that caused
the urticaria and explain strategies for avoiding
exposure to that allergen.
 Help clients suffering from chronic urticaria
(with unknown allergens) to reduce stress in
their lives.
 Teach clients to avoid caffeine, tobacco,
alcohol, and aspirin – tend to exacerbate
symptoms.

41. Allergic Asthma
 Extrinsic asthma – 10% to 20% of the adult
asthmatic population
 Intrinsic asthma – 50% of adult asthmatics

42. Extrinsic Asthma
 It is caused by allergenic exposure (e.g., to
pollens, molds, dust, or animal dander).
 It results in bronchoconstriction, edema, and
increased mucus production.

43. Intrinsic Asthma
 It is precipitated by nonallergenic factors (e.g.,
viral infection, exercise, cold, cigarette smoke,
changes in temperature or humidity, gasoline
fumes, and paint fumes.
 Emotional stress seems to exacerbate an
attack but may not have a primary etiologic
role.

44. Assessment
 Subjective cues: shortness of breath, cough,
and a feeling of tightness or pressure in the
chest.
 Objective cues: DOB, tachypnea,
nonproductive cough, wheezes, anxiety,
increasing respiratory distress, use of
accessory muscle for breathing

45.  Client is sitting or is leaning forward
 Hypertensive
 Dehydrated
 Cannot speak more than a couple of words
without stopping to breathe
 Respirations become increasingly rapid and
shallow

46. Rationale:
PO2 drops
and PCO2
rises
Pulmonary
function test
results are
abnormal
and ABG
tests
indicate
hypoxemia
and
hypercapnia.
 Client experiences fatigue and
becomes cyanotic, confused, and
lethargic.

47. Collaborative Management
 Treatment of Asthma centers on the following:
> Control of causative factors
> Treatment of acute episodes
> Maintenance drug therapy

48. Medications
 Beta-adrenergic agents: epinephrine,
isoproterol) which relax bronchial smooth
muscle and inhibit mediator release
 Theophylline and derivatives, which act in a
similar fashion
 Corticosteroids, in some cases

49. Nursing Management
 Monitor fluid intake and output and electrolytes
and administers intravenous fluids to replace
loss.
 Give maintenance therapy with theophylline
and bronchodilators as ordered.
 Administer O2 as ordered to maintain a PO2
value higher than 60 mmHg.

50. TYPE II: Cytotoxic Reactions
 The body makes special autoantibodies
directed against self cells or tissues that have
some form of foreign protein attached to them.
 The autoantibody binds to the self cell and
forms an antigen-antibody complex, or
immune complex.
 The self cell is the destroyed by complement-
mediated lysis.

51. Clinical Examples of Type II
reactions
 Coombs’-positive hemolytic anemias
 Thrombocytopenic purpura
 Hemolytic transfusion reactions
 Hemolytic disease of the new born
 Goodpasture’s syndrome
 Drug-induced hemolytic anemia

52. Variants of Type II Reactions
The antibody
known as
long-acting
thyroid
stimulator
(LATS) is
made to the
thyroid-
stimulating
hormone
receptor on
the thyroid
gland. LATS
binds with the
receptor and
stimulates it,
which results
in the
production of
abnormally
high levels of
thyroxine.
 It occurs when the autoantibody is
made to a receptor.
 Example: Graves disease

53. Myasthenia gravis
 It involves an antireceptor antibody.
 An autoantibody is made to the acetylcholine
receptor on muscle.
 The antibody binds to the receptor at the
neuromuscular junction, which blocks
acetylcholine and thus prevents transmission of
the impulse from the nerve that would stimulate
the muscle.
 The result is profound muscular weakness.

54. Hemolytic Blood Transfusion
Reaction
 A hemolytic BT reaction occurs when a person
is given ABO-incompatible blood. If a client is
transfused with incompatible blood, the
antibodies bind to the antigens on the donor’s
erythrocytes and coat them, and the cells
agglutinate, or clump together.

55.  Agglutination of cells results in blockage of
small blood vessels and capillaries.
 The immune complex activates complement,
which results in destruction of the erythrocytes.
Through this destruction, hemoglobin is
released and the renal tubules are blocked
and acute renal failure results.

56. Prevention
 Ensure that the client who is receiving blood
has recently been typed and crossmatched
and by double-checking the blood before use.

57. Collaborative Management
 Stop the transfusion when the first symptom of
a hemolytic reaction occurs but continue
intravenous administration of normal saline
through new tubing.
 Notify the physician immediately.
 Monitor the client’s vital signs and urinary
output every 15 to 30 minutes.

58.  If symptoms of shock develop, appropriate
intervention is initiated with epinephrine,
intravenous fluids, and oxygen.
 Samples of blood from the client are taken and
sent to the laboratory, and urine is also sent for
determination of hemoglobin.

59.  If there is evidence of renal involvement, a
potent diuretic, such as mannitol is given as
ordered.

60. Drug-Induced Hemolytic
Anemia
 Certain drugs precipitate a type II reaction to
erythrocytes. This occurs by two main
mechanisms:
>Drugs such as penicillin and the
sulfonamides form bonds with the erythrocyte
membrane. Antibodies are made, and the
antigen-antibody reaction leads to clumping
and destruction of erythrocytes.

61. >Methyldopa (Aldomet, Dopamet) and
some other drugs alter the erythrocyte surface
chemically, thereby exposing an antigen that
stimulates and reacts with an autoantibody,
and leads to destruction of the cells.

62. Collaborative Management
Treatment of drug-induced hemolytic anemia
starts with discontinuation of the offending
drug. Otherwise, treatment is symptomatic.
Complications such as hemolytic crisis and
renal failure can be life-threatening.

63. Type III: Immune Complex
Reactions
In a type III reaction, soluble immune
complexes are formed, usually in the setting of
antigen excess. These circulating immune
complexes are then deposited in the vessel
wall, usually of small vessels. Common sites
include the kidneys, skin, joints, and other
small blood vessels. The deposited immune
complex activates complement, and tissue or
vessel damage results.

64. Rheumatoid arthritis
 A connective tissue disorder
 The clinical manifestations are caused by
immune complexes that lodge in joint spaces
followed by destruction of tissue, and later
scarring and fibrous changes.

65. Overview
 It is the second most common connective
tissue disease but is the most destructive to
joints.
 It is chronic, progressive, systemic
inflammatory process that affects primarily
synovial joints.

67. Pathophysiology
The pannus is vascular
granulation tissue,
composed of
inflammatory cells, that
erodes articular cartilage
and eventually destroys
bones.
Clients may experience
spontaneous remissions
and exacerbations with
or without treatment.
Bony ankylosis – fixation
of a joint, often in an
abnormal position,
usually resulting from
destruction of articular
cartilage and
subchondral bone, as
occurs in RA. It may also
occur in immobilized
patients when active or
passive range of motion
is not provided.
 The onset of RA is characterized
by synovitis, or inflammation of
the synovial tissue in joints. The
synovium thickens and becomes
hyperemic, fluids accumulates in
the joint space, and a pannus
forms.
 As a result, fibrous adhesions,
bony ankylosis, and calcifications
occur; bone loses density and
secondary osteoporosis occur.

68. Bony Ankylosis
Bony ankylosis –
fixation of a joint,
often in an abnormal
position, usually
resulting from
destruction of
articular cartilage and
subchondral bone, as
occurs in RA. It may
also occur in
immobilized patients
when active or
passive range of
motion is not
provided.

69. These
pathologic
changes
occur late in
the disease
process and
cause life-
threatening
problems.
 In addition to synovial joints, RA
also affects other areas of the body
in which connective tissue is
prevalent.
 If blood vessel involvement occurs,
the organ that is supplied by that
vessel can malfunction and fail.

70. Etiology
 The Immune Complex Hypothesis – states that
unusual antibodies of the immunoglobulin (Ig)
G and/or IgM type (rheumatoid factor) develop
against IgG antigenic determinants to form
complexes that lodge in synovium and other
connective tissues.
 Local and systemic inflammatory responses
result.

71. Predisposing factors
 Genetic predisposition – RA affects people
with a family history of RA two to three times
more often than the rest of the population.
 Female – Some researchers suspect that
female reproductive hormones influence the
development of RA because it affects women
more often that men.

72. Epstein-Barr – the herpesvirus
that causes infectious
mononucleosis and is associated
with nasopharyngeal sarcoma,
Hodgskin’s disease, B-cell
lymphoma, leokoplakia, central
nervous system lymphoma in
Aids, and Burkitt’s lymphom,
especially in immunodeficient
patients such as posttransplant
patients on immunosuppressive
therapy.
Infectious mononucleosis – an
abnormal increase in the number
of mononuclear leukocytes in the
blood.
Sarcoma – a malignant neoplasm
of the soft tissues arising in
fibrous, fatty, muscular, synovial,
vascular, or neural tissue, usually
first manifested as a painless
swelling.
 Viral infection – Researchers
suspect that a virus, such as
Epstein-Barr, may trigger the
autoimmune process.
 Physical and emotional
stresses have been linked to
exacerbations of the disorder
and may be contributing
factors in its development.

73. Epstein-Barr Virus

74. Assessment
 History
> age and sex
> family history
> previous viral infection
> use of oral contraceptives
> client’s ability to cope with physical and
emotional stress

75. Categories of RA
Manifestations
 Early manifestations
 Late manifestations

76. Early manifestations
 Joint
> Inflammation
 Systemic
> Low-grade fever
> Fatigue
> Weakness
> Anorexia
> Paresthesias

77. Late Manifestations
 Joint
> Deformities e.g., swan neck or ulnar
deviation
> Moderate to severe pain and morning
stiffness

78. Swan Neck

79. Ulnar Deviation

80.  Systemic
> Osteoporosis
> Severe fatigue
> Anemia
> Weight loss
> Subcutaneous nodules
> Peripheral neuropathy

81. Osteoporosis

82. Subcutaneous Nodules

83. Peripheral Neuropathy

84. Sjogren’s
syndrome - a
triad of dry
eyes, dry
mouth, and
dry vagina
(immune
complexes
and
inflammatory
cells are
thought to
obstruct
secretory
glands and
ducts.)
> Vasculitis/peripheral neuropathy
> Pericarditis/myocarditis
> Fibrotic lung
disease/pleurisy/pulmonary
hypertension/pneumonitis
> Sjogren’s syndrome
> Renal disease

85. Vasculitis
Neurovasculi
tis, retinal
vasculitis,
uveitis

86. Pericarditis

87. Sjogren’s Syndrome

88. Laboratory Assessment
RF is
valuable in
the early
diagnosis of
RA for
potential
treatment
measures
and
inhibiting the
progression
of the
disease.
RF is
present in
75% of
people with
RA.
 Rheumatoid factor – measures the
presence of unusual antibodies of
the IgG and/or IgM type that
develop in a number of connective
tissue diseases.
> Rose-Waaler test
> Latex agglutination test

89. ANA – Antinuclear
antibodies are produced and
act against the body’s own
DNA and nuclear material
that causes tissue damage
as autoimmune disorders.
ANA titer – elevated levels
are found with RA, SLE,
hepatitis, myasthenia gravis,
pulmonary fibrosis,
Reynaud’s syndrome.
ESR is particularly useful in
connective tissue disease
because the value directly
correlates with the degree of
inflammation and, later, with
the severity of the disease.
 Antinuclear Antibody Titer –
measures the titer of unusual
antibodies that destroy the
nuclei of cells and cause
tissue death.
 ESR – confirms inflammation
or infection anywhere in the
body.

90. ESR also
monitors a
client’s
response to
anti-
inflammatory
drug
therapy.
ESR Values
20 – 40mm/hr mild inflammation
40 – 70mm/hr moderate
inflammation
70 – 150mm/hr severe inflammation

91. An abnormal
finding is
indicated by
a decrease
in serum
complement
and is seen
in clients
with
vasculitis.
 Serum complement – In an attempt
to destroy the immune complexes,
complement attaches to the
complex. If a large amount of
complement is used in this lytic
process, the concentration of free-
floating complement in the blood
diminishes.

92.  Serum Protein Electrophoresis – In acute
inflammation, the level of alpha globulin is
raised, but in chronic inflammatory conditions
such as RA, the level of gamma globulin is
increased because of the increase in
immunoglobulins.

93.  Immunoglobulins – In chronic inflammation,
IgG is needed to combine with rheumatoid
factor. Thus, in RA the IgG value is typically
elevated.
 CBC is monitored for a low hemoglobin,
hematocrit and RBC. Increase in WBC is
consistent with an inflammatory response.

94.  Radiographic assessment
> X-ray
> CT scan – determines the presence and
degree of cervical spine involvement.

95. Common Nursing Diagnoses
 Chronic pain related to joint inflammation
 Impaired physical mobility related to fatigue,
inflammation, and pain
 Self-care deficit related to fatigue, pain,
stiffness, and joint deformity
 Fatigue related to states of discomfort, sleep
pattern disturbance, and increased energy
requirement to perform ADLs.

96.  Body image disturbance related to effects of
loss of body function.

97. Lupus Erythematosus Overview
The word lupus is the Latin term for “wolf.” In
the mid-19th century, the facial rash that was
seen in clients with the disease was thought to
look like bites caused by a wolf. The rash was
usually red, and thus, the term erythematosus,
a Latin word meaning reddened, was added to
describe it.

98. Classifications of Lupus
 Discoid lupus erythematosus (DLE) – affects
only the skin
 Systemic lupus erythematosus (SLE) – is a
chronic, progressive, inflammatory connective
tissue disorder that can cause major body
organs and systems to fail.

99. SLE
 The condition is potentially fatal, although the
survival rate has dramatically improved.
 It is thought to be an autoimmune process;
that is, abnormal antibodies are produced that
react with the client’s tissues.
 It is characterized by spontaneous remissions
and exacerbations, and the onset may be
acute or insidious.

100. Many clients
with SLE have
some degree of
kidney
involvement-
the leading
cause of death.
Other causes
of death are
cardiac and
CNS
involvement.
Lupus affects
women
between the
ages of 15 and
40 years.
 These antinuclear antibodies (ANA)
primarily affect the deoxyribonucleic
acid (DNA) within the cell nuclei.
 As a result, immune complexes
form in the serum and organ
tissues, which causes inflammation
and damage.
 The complexes invade organs
directly or cause vasculitis, which
deprives the organs of arterial blood
and oxygen.

101. Systemic Lupus Erythematosus
 The clinical manifestations result from immune
complex deposition in the vessels (vasculitis),
the glomeruli (nephritis), the joints
(arthralgia/arthritis), and other organs and
tissues.
 The immune complex is composed of cellular
DNA and anti-DNA antibodies.

102. Collaborative Management
Assessment
History
> sex and age of the client
> family history of lupus or other related
connective tissue disease
> ask if client is pregnant
> client’s reaction to ultraviolet light
> complete medication history

103. Clinical Manifestations
Discoid
lesion – flat
round object:
a disk-
shaped
object or
part
Nephritis –
severe
inflammation
of the
kidney,
caused by
infection,
degenerative
disease, or
disease of
the blood
vessels.
Skin manifestations:
> Inflamed, red rash
> Discoid lesions
Renal manifestations:
> Nephritis

104. Raynaud’s
phenomenon
– on
exposure to
cold or
extreme
stress, the
client
complains of
the
characteristic
red, white
and blue
color
changes and
severe pain
in the digits
caused by
arteriolar
vasospasm.
Cardiovascular manifestations:
> Pericarditis (tachycardia, chest
pain, myocardial ischemia)
> Raynaud’s phenomenon

105. Pulmonary manifestations:
> Pleural effusions (dyspnea, ABG
abnormalities)

106. Neurologic manifestations:
> CNS lupus (psychosis, paresis, seizures,
migraine headaches, cranial nerve palsies.

107. GIT manifestations:
> abdominal pain
Musculoskeletal manifestations:
> joint inflammation
> myositis (inflammation of the muscle tissue,
usually of voluntary muscle.

108. Other manifestations
 Fever
 Fatigue
 Anorexia
 Vasculitis

109. Psychosocial Assessment
 Altered body image
 Fear and anxiety
 Withdrawal and depression

110. Psychosocial Nursing
Management
 Assess the client’s feelings about the illness to
identify areas that require intervention.
 Assess the person’s usual coping mechanisms
and support systems before developing a plan
of care.

111. Rheumatic Fever
 Description: Generalized systemic disease
affecting principally the connective tissues.
 Cause: Group A Beta hemolytic streptococci
 Incidence: With familial predisposition-
common in children who belong to low socio-
economic status families and those who are
malnourished.

112.  Diagnosis: It is confirmed by the presence of
antibodies of the causative organisms (titer is
called ASO) and the application of Jone’s
criteria.

113. Jone’s Criteria
 Two (2) major signs or one (1) major sign and
two (2) minor signs suggest Rheumatic Fever.

114. Major Signs
 Migratory polyarthritis – most common
complaint; usually affecting large-weight-
bearing joints which become hot, swollen,
tender, red, and accompanied by fever and
intense pain.

115. Aschoff bodies (Karl A. L. Aschoff,
German Pathologist) tiny rounded
or spindle-shaped nodules
containing multinucleated giant
cells, fibroblasts, and basophilic
cells. They are found in joints,
tendons, the pleura, and the
cardiovascular system of
rheumatic fever patients.
Osler’s nodes (Willian Osler,
American-British physician) tender,
reddish or purplish subcutaneous
nodules of the soft tissue on the
ends of fingers or toes, seen in
subacute bacterial endocarditis
and usually lasting only 1 or 2
days. The nodes represent
bacterial embolisms from the
infected heart valve.
 Carditis – mitral valve is
most often affected;
manifested primarily by
heart murmur.
> tachycardia
> cardiac enlargement
> edema
> dyspnea
> aschoff’s bodies in the
myocardium
> Osler’s nodes

116. Sydenham’s chorea (Thomas
Sydenham, English physician) a
form of chorea associated with
rheumatic fever, usually occurring
during childhood. The cause is
streptococcal infection of the
vascular and perivascular tissues
of the brain. The choreic
movements increase over the first
2 weeks, reach a plateau, and then
diminish.
Saint Vitus’ Dance – a motor
nerve disorder characterized by
irregular involuntary jerky
movements of the limbs and facial
nerves. Historically the condition
was once confused with symptoms
of a dance mania that reportedly
was cured by a pilgrimage to the
shrine of Saint Vitus.
 Sydenham’s chorea/St.
Vitus’ Dance – involves
nerve tissues characterized
by:
> purposeless movements
> muscular weakness-
trouble handling a cup to
drink
> emotional instability
> indistinct speech
It usually occurs during the
convalescent stage and is
not accompanied by

117.  Erythema marginatum – skin rashes which
begin as a small, pink, slightly raised
macules over the trunk and the inner
aspects of the arms and the thighs.
 Subcutaneous nodules – painless, non-
pruritic, freely movable elevations on the
joints, the scalp and along the spine.

118. Minor signs
 Previous streptococcal infection
 Arthritis
 Fever
 Epistaxis
 Prolonged P-R interval
 Leukocytosis
 Elevated ESR

119.  (+) C-reactive protein
 Presence of inactive heart disease
 Signs of inflammation

120. Treatment
 Maintain a balance between the body’s needs
and the supply of blood the weakened heart is
able to deliver.
> Bed rest
> Maintain body alignment
> Diet
> O2 inhalation as ordered
> Medications

121. Bed Rest
 Aim: To reduce cardiac workload
 Length: Promote bed rest until the pulse rate,
hemoglobin level, and C-reactive protein have
become normal.

122. Maintenance of Body Alignment
 Support joints with pillows
 Use bed cradles to protect painful joints from
bthe weight of bed covers
 Avoid sudden, unexpected moves.
 Immobilize joints

123. Diet
 High protein, high caloric, low sodium, high
vitamins and roughage.

124. Medications
 Diuretics
 Steroids
 Digoxin – if with CHF
 Penicillin – given at least for 5 years but
perhaps for life (or until 18 years of age)
 Aspirin for 2 – 3 weeks

125. Aspirin Dosage
 One (1) gram for each year of age until age
ten (10)
 Precaution: must be given with meals or with
milk
 Side effects: tinnitus, nausea, bleeding

126. Prognosis
 It depends primarily on the extent of cardiac
damage (mitral valve is usually affected)
favorable when the first attack occurs when
the child is older and when treatment is
prompt.

127. Serum Sickness
 A complex of symptoms that occurs after the
administration of foreign serum or certain
drugs.
 It is caused by collection of immune
complexes in the walls of vessels in the skin,
joints, and the glomeruli of the kidney.

128. Common Causes of serum
sickness
 Penicillin and related drugs
 Horse serum antitoxin
 Antilymphocyte globulin
 Antithymocyte globulin (used to suppress the
immune response in organ transplantation.

129. Signs & Symptoms
S/S usually
appear
about 7 to
12 days after
administratio
n of the
causative
agent.
 Fever
 Arthralgia (achy joints)
 Rash
 Lymphadenopathy ( enlarged lymph
node)
 Malaise
 Polyarthritis and nephritis

130. Collaborative management
 Serum sickness is usually self-limiting, and
symptoms subside after several days.
>antihistamines given for pruritus and aspirin
for arthralgias.
>Prednisone is given if symptoms are severe.

131. Type IV: Delayed
Hypersensitivity Reactions
 In a type IV reaction, the important cell is the
T lymphocytes (from a previous exposure)
respond to an antigen by producing and
releasing certain lymphokines (chemical
mediators).

132.  The lymphokines act to recruit, retain, and
activate macrophages that help to destroy
the antigen.
 A type IV response typically occurs hours to
days after exposure rather than immediately.
 It is characterized by an accumulation of
lymphocytes and macrophages. These
events cause edema, ischemia, and tissue
destruction at the site of response.

133. Examples
Positive PPD test. In a client
who had previously been
exposed to tuberculosis, an
intradermal injection of this
agent causes sensitized T cells
to accumulate at the injection
site, release lymphokines, and
recruit and activate
macrophages.
Poison ivy – a climbing vine of
the cashew family that has 3-
part leaves and white berries;
contact with the plant produces
an itchy rash; native to North
America.
 Positive PPD test.
Induration and erythema at
the site of the injection
appear approximately 24 to
48 hours later.
 Contact dermatitis
 Poison ivy skin rashes
 Local response to insect
stings
 Allograft (tissue transplant)
rejections
 Granulomatous diseases in
which the antigen is
unknown e.g., sarcoidosis

135. Overview
 Autoimmunity is a process whereby a host
develops and expresses immunologic
reactivity, especially in the form of antibodies,
against self components. For unknown
reasons, certain cells or tissues of the body
are recognized as nonself or no longer
tolerated as self, and immune reactions to
them occur.

136.  The responses, both antibody and cell
mediated, are similar to normal immune
responses against nonself, although they are
inappropriate and sometimes excessive.
 Not only is the etiology of autoimmunity
uncertain; there is also a lack of consensus as
to which diseases are truly autoimmune.

137. Examples of Autoimmune
diseases
 Diseases that are generally believed to be
autoimmune include:
>SLE
>Polyarthritis nodosa
>Rheumatic arthritis
>Autoimmune hemolytic anemia
>Rheumatic fever
>Hashimoto’s thyroiditis

138. Examples of Connective
tissue disorder
 SLE
 Rheumatoid arthritis
 Scleroderma
 Polyarthritis nodosa

139. Autoimmune Disorders
Systemic or Non-organ-Specific
Disorder Autoantigen Comments
Systemic Lupus
Erythematosus
DNA, DNA
proteins
Autoimmune bodies to a number of entities;
immune complex-mediated damage
Rheumatoid arthritis IgG Immune complex-mediated damage in
joints (arthritis, fibrosis)
Progressive systemic
sclerosis
DNA proteins Autoimmune bodies against nuclear
materials; sclerosis
Mixed connective
tissue disorder
DNA proteins Autoantibodies to ribonucleoprotein

140. Autoimmune Disorders
Organ-specific
Disorder Autoantigen Comments
Autoimmune hemolytic
anemia
Erythrocytes Killing of antibody-coated
erythrocytes
Autoimmune
thrombocytopenic
purpura
Platelets Killing of antibody-coated
platelets or innocent bystander
effect

141. Myasthenia gravis Acetylcholine receptor Blocking of impulse transmission
by autoantibody to acetylcholine
receptor on muscle
Graves’ disease Thyroid-stimulating
hormone receptor
Stimulation by autoantibody to
thyroid-stimulating hormone
receptor
Rheumatic fever Myocardial cells Cross-reaction of antibody with
myocardial cells
Idiopathic Addison’s
disease
Adrenal cell Antibody-and-cell-mediated
adrenal cytotoxicity
Hashimoto’s thyroiditis Thyroid cell surface Antibody-and-cell-mediated
thyroid cytotoxicity

142. Pernicious anemia Intrinsic factor/parietal
cell
Autoantibodies to intrinsic factor,
intrinsic factor/B12 complexes,
and parietal canalicula cells
Goodpasture’s syndrome Basement membrane Anti-glomerular basement
membrane antibodies, which also
cross-react with pulmonary
basement membrane
Glomerulonephritis Glomerular basement
membrane
Autoantibodies and/or immune-
complex-mediated damage
Uveitis Uvea Cell-mediated and humoral damage
Vasculitis Unknown Immune complex-mediated damage