this slide contains all the basic information about the immune system disorders. The slides explains anatomy and physiology of immune system well.

1. PRACTICE TEACHING
ON
IMMUNE SYSTEM DISORDERS
Presented By-
Mr. Deepak Patel
M.Sc. Nursing

2. INTRODUCTION
Immune system disorders cause
abnormally low activity, over activity
or misguided activity of immune
system.

3. DEFINITION
An immune system disorder is a
dysfunction of the immune system. These
disorders can be characterized in several
different ways:
• By the components of immune system
affected.
• By whether the immune system is
overactive or underactive.
• By whether the condition is congenital or
acquired.

4. ANATOMY AND PHYSIOLOGY OF
IMMUNE SYSTEM
An immune system is a collection of
biological processes within an organism
that protects against disease by
identifying and killing pathogens and
tumor cells.
IMMUNE SYSTEM

5. ANATOMY AND PHYSIOLOGY OF
IMMUNE SYSTEM
Immunity is defined as the resistance
of an organism to infection, disease or
other unwanted biological invasion.
IMMUNITY

6. CLASSIFICATION OF IMMUNITY
Innate

7. THE BODY’S DEFENCE MECHANISM

8. MECHANISM OF INNATE
IMMUNITY
Epithelial surfaces
• Skin
• GI tract
• Respiratory tract
• Eyes
• Vaginal tract
Chemical secretions
• Oils & sweat
• Lysozymes
• Properdine, leukins,
beta lysine
• HCL and bile
• Cerumen wax
Cellular factors
• Monocytes
• Phagocytes
• Basophils
• Neutrophils
• Eosinophil
• Macrophages
• Inflammatory
reaction
• Fever
• Interferon
• Natural killer cells
• Complement system

9. MECHANISM OF ACQUIRED
IMMUNITY
• Defends against specific foreign
component.
• Based on principle of self & non-self.
• Mediated by antibodies.

11. CELLS OF IMMUNE SYSTEM

13. TYPES OF SPECIFIC IMMUNITY CELLS

14. TYPES OF IMMUNE CELLS

15. TYPES OF ANTIGEN PRESENTING
CELLS (APC)

16. TYPES OF ANTIGEN PRESENTING
CELLS (APC)

17. Professional and Non-Professional
APC

18. MAJOR HISTOCOMPATIBILITY COMPATIBILITY
COMPLEX MOLECULES (MHC) CLASS I & II

19. T-CELL AND B-CELL RECEPTORS
(TCR / BCR)

20. MAJOR HISTOCOMPATIBILITY COMPATIBILITY
COMPLEX MOLECULES (MHC) CLASS I & II

21. ACTIVATION OF T-CELL

22. CYTOTOXIC T-CELL

27. ANATOMY AND PHYSIOLOGY OF
IMMUNE SYSTEM
Any foreign substance which when
enters the body, elicits body’s immune
response is called as antigen.
ANTIGEN

28. ANATOMY AND PHYSIOLOGY OF
IMMUNE SYSTEM
Any foreign substance which when
enters the body, elicits body’s immune
response is called as antigen.
ANTIGEN

29. ANATOMY AND PHYSIOLOGY OF
IMMUNE SYSTEM
Any foreign substance which when
enters the body, elicits body’s immune
response is called as antigen.
ANTIGEN

30. ANATOMY AND PHYSIOLOGY OF
IMMUNE SYSTEM
The substance produced by the body in
response to an antigen are called as
antibodies. A specific antibody is
produced against a specific antigen to
defend the body.
ANTIBODY

31. STRUCTURE OF ANTIBODY

33. CLASSIFICATION OF IMMUNOLIC
DISORDERS
1. IMMUNODEFICIENCY
2. GAMMOPATHY
3. HYPERSENSITIVITY
4. AUTOIMMUNITY

34. 1. IMMUNODEFICIENCY
“Immunodeficiency is a state in which
the immune system’s ability to fight
infectious disease and cancer is
compromised or entirely absent.”
DEFINITION

35. TYPES OF IMMUNODEFICIENCY
• These disorders usually occur from intrinsic, inherited
defects in the immune system. They are usually seen in
infants and young children.
Primary immunodeficiency
• Any factor that interferes with the normal growth or
expression of the immune system can lead to secondary
immunodeficiency. It generally develop later in life.
Immunosuppressive agents, chronic illness are common
cause.
Secondary immunodeficiency

36. ETIOLOGY OF IMMUNODEFICIENCY
• Primary immunodeficiency disorders may be caused by mutations,
sometimes in a specific gene. Mutation leads to deficiencies if immune
cells.
• e.g.- X-linked a-gamma-globuli-nemia (XLA), common variable
immunodeficiency (CVID), Severe combined immunodeficiency (SCID)
Primary immunodeficiency
• Secondary immunodeficiency disorders happen when an outside source
like a toxic chemical or infection attacks the body.
• E.g.- severe burns, chemotherapy, radiation, Diabetes, malnutrition
• (examples of secondary immunodeficiency diseases- AIDS, cancers of
immune system, leukaemia, viral hepatitis, multiple myeloma)
Secondary immunodeficiency

37. PATHOPHYSIOLOGY
Etiological factors such as genetic mutation or acquired factors- Toxins, Chemotherapy,
Radiation, Chronic illness, Nutritional deficiency
Abnormal or absent production of immune cells as B-cells, T-cells, phagocytic cells or
complement deficiencies.
Insufficient immune cells to fight against infection and tumour.
Recurrent infections, tumour may grow
Inability of the body to ward off infections leading health deterioration.
Immunodeficiency diseases

38. CLINICAL MANIFESTATIONS
Opportunistic infections, frequent and recurrent pneumonia, bronchitis
Sinus infections, ear infections, meningitis and skin infections
Inflammation and infection of internal organs
Blood disorders, such as low platelet count or anemia
Digestive problems such as cramping, anorexia, nausea, diarrhoea
Delayed growth and development, recurrent fungal infections
Oral ulcers and conjunctivitis, skin and mucus membrane infections

39. DIAGNOSTIC EVALUATION
History
taking
Physical
examination
Laboratory
tests
Bone marrow
biopsy
Histopathology
study
Genetic testing

40. MANAGEMENT
1. MEDICAL MANAGEMENT
a. Managaing infections
• Preventing infections
• Treating infections
• Treating symptoms
b. Treatment to boost the immune system
• Immunoglobulin therapy- 400-500 mg/dl IM/IV monthly
• Interferon-gamma therapy
• Growth factors
2. SURGICAL MANAGEMENT
• Stem cell transplantation

41. 2. GAMMOPATHIES
“Gammopathies, also termed
typergammaglobulinemias, are
elevated levels of gamma
globulin in serum resulting from
overproduction.”
DEFINITION

42. TYPES OF GAMMOPATHIES
MONOCLONAL
GAMMOPATHIES
Involves the overproduction of one
class of immunoglobulin's in
response to inappropriate antigenic
stimulation.
POLYCLONAL
GAMMOPATHIES
Involves the over production of
virtually all classes of
immunoglobulin's in response to
inappropriate antigenic stimulation.

43. TYPES OF GAMMOPATHIES
MONOCLONAL
GAMMOPATHIES
Involves the overproduction of one
class of immunoglobulin's in
response to inappropriate antigenic
stimulation.
POLYCLONAL
GAMMOPATHIES
Involves the over production of
virtually all classes of
immunoglobulin's in response to
inappropriate antigenic stimulation.

44. 3. HYPERSENSITIVITY
“A hypersensitivity reaction is defined
as the altered reactivity to a specific
antigen that results in pathologic
reactions upon the exposure of a
sensitized host to that specific
antigen.”
DEFINITION

45. TYPES
Hypersensitivity diseases are broadly divided into
five categories based on the immunologic
mechanism involved in the reactions.
1. TYPE-I (Immediate hypersensitivity)
2. TYPE-II (Antibody mediated hypersensitivity)
3. TYPE-III (Immune complex hypersensitivity disease)
4. TYPE-IV (T-Cell mediated or delayed hypersensitivity)
5. TYPE-V (Stimulatory Hypersensitivity)

46. TYPE-I
Immediate hypersensitivity
Type-I hypersensitivity reaction is an allergic reaction
provoked by re-exposure to a specific type of antigen
referred to as an allergen. The reaction may be either local
or systemic. Symptoms vary from mild irritation to sudden
death from anaphylactic shock.
Exposure may be by ingestion, inhalation, injection or
direct contact. The naïve lymphocytes become primed and
differentiated into an antibody secreting cell and this leads
to class-switching of the antibody to the IgE class.

47. TYPE-I
Immediate hypersensitivity
Some examples of Type-I hypersensitivity-
• Allergic asthma
• Allergic conjunctivitis
• Allergic rhinitis (Hay fever)
• Anaphylaxis
• Angioedema
• Atopic dermatitis (Eczema)
• Urticaria (Hives)
• Eosinophilia

48. TYPE-II
Antibody mediated hypersensitivity
In Type-II hypersensitivity reactions, the antibodies
produced by the immune response bind to antigens on the
patient’s own cell surfaces. The antigens recognized in this
way may either be intrinsic or extrinsic . IgG and IgM
antibodies bind to these antigens to form complexes that
activate the classical pathway of compliment activation,
for eliminating cells presenting foreign antigens. That
mediates inflammation and cause cell lysis and death. This
reaction takes hours to day.

49. TYPE-II
Antibody mediated hypersensitivity
Some examples of Type-II hypersensitivity-
• Autoimmune hemolytic anemia
• Erythroblastosis fetalis
• Pemphigus
• Pernicious anemia
• Transfusion reaction / ABO incompatibility
• Rheumatic fever
• Hemolytic disease of newborn
• Hashimoto’s thyroiditis

50. TYPE-III
Immune complex hypersensitivity
In type-III hypersensitivity reactions, insoluble immune
complexes (aggregations of antigens and IgG and IgM
antibodies) form in the blood and are deposited in various
tissues (typically the skin, kidney and joints).
This deposition of the antibodies may trigger an immune
response according to the classical pathway of
complement activation- for eliminating cells presenting
foreign antigens. There are two stages relating to the
development of the complexes.

51. TYPE-III
Immune complex hypersensitivity
Some examples of type-III hypersensitivity-
• Immune complex glomerulonephritis
• Serum sickness
• Rheumatoid arthritis
• Sub acute bacterial endocarditis
• Symptoms of malaria
• Systemic lupus erythematosus
• arthus reaction
• Farmer’s lung

52. TYPE-IV
T-Cell Mediated / Delayed Hypersensitivity
Type-IV hypersensitivity reactions are often called delayed
type as the reaction takes two to three days to develop.
Unlike the other types, it is not antibody mediated but
rather it is a type of cell mediated response.
CD8+ cytotoxic T cells and CD4+ helper cells recognize
antigen in a complex with either Type-I or Type-II major
Histocompatibility complex (MHC-I/II). The antigen
presenting cells in this case are macrophages which
secrete IL-1 which stimulates the proliferation of further
CD4+ T cells.

53. TYPE-IV
T-Cell Mediated / Delayed Hypersensitivity
Some examples of Type-IV hypersensitivity-
• Contact dermatitis (poison ivy rash)
• Temporal arthritis
• Symptoms of leprosy
• Symptoms of tuberculosis
• Transplant rejection / tissue graft rejection
• Coeliac disease

54. TYPE-V
STIMULATORY HYPERSENSITIVITY
In Type-V stimulatory hypersensitivity, antibodies are
made against a particular hormone receptor on a hormone
producing cell. This leads to the overstimulation of those
hormone-producing cells.
An example is Graves’ disease where antibodies are made
against thyroid-stimulating hormone receptors of thyroid
cells. The binding of the antibodies to the TSH receptors
results in constant stimulation of the thyroid leading to
hyperthyroidism.

55. ETIOLOGY
• Genetic factors
• Lack of certain enzymes
• Exposure to allergens

56. Common allergens associated
with hypersensitivity
Proteins
• Foreign serum
• Vaccines
• Virus and
bacteria
Plant Pollens
• Rye grass
• Ragweed
• Timothy grass
• Birch trees
Drugs
• Penicillin
• Sulphonamides
• Local
anaesthetics
• Salicylates

57. Common allergens associated
with hypersensitivity
Foods
• Nuts
• Seafood
• Eggs
• Peas, beans
• milk
Insect
• Bee venom
• Wasp venom
• Ant venom
• Cockroach
calyx
• Dust
• Mites
Others
• Mould
spores
• Animal hair
and dander
• Latex
• Snake
venom

58. PATHOPHYSIOLOGY

61. CLINICAL MANIFESTATIONS

62. CLINICAL MANIFESTATIONS
• Check out leaflet

63. DIGNOSTIC EVALUATION
HISTORY TAKING
• History of allergic reaction
• Family history of allergy
• Recent exposure to
sensitizing agent
• Changes in living, working
environment
• Characteristic of present
environment
• Symptoms experienced
• Alleviating factors
PHYSAICAL EXAMINATION
• Rashes (location / colour)
• Mouth breathing
• Flaring nares
• Difficulty hearing

64. DIGNOSTIC EVALUATION
DIGNOSTIC TEST FOR
ALLERGENS
• Skin prick test
• Intradermal test
• Radioallergosorbent testing
(RAST)
• Provocation testing
• Eosinophil count
• Patch testing
• Oral food challenges
• Food elimination
LABORATORY TEST
• Complete blood count
• Allergen specific IgE blood
tests
• Histamine and tryptase test
• Cytotoxic test
• Genetic testing

65. MANAGEMENT
Antihistamines- Benadryl, Allegra
Decongestant- Phenylephrine
Decongestant- Phenylephrine
Mast cell degranulation inhibitor- Cromolyn sodium inhibiter
Corticosteroids – Prednisolone, Dexamethasone
Adrenaline- Epinephrine
Aminophylline- Theophylline

66. MANAGEMENT
Auto transfusion
Rh-Immunoglobin Administration
Protection from known allergen

67. 4. AUTOIMMUNE DISEASES
“Autoimmune diseases are a group of
disorders in which tissue injury is
caused by humoral or cell mediated
immune response to self tissues
(antigens).”
DEFINITION

68. CLASSIFICATION OF
AUTOIMMUNE DISORDERS
• Autoimmune disorders are grouped
into categories according to the body
part or tissue involved.
2. Non
organ
specific
1. Organ
specific

69. CLASSIFICATION OF
AUTOIMMUNE DISORDERS
1. Organ specific
• Autoimmune
haemolytic anemia
• Idiopathic
thrombocytopenic
purpura
Blood
• Rheumatic fever
Heart
• Multiple sclerosis
• Guillain-Barr
syndrome
Central nervous
system

70. CLASSIFICATION OF
AUTOIMMUNE DISORDERS
1. Organ specific
• Myasthenia gravis
Muscle
• Addison’s disease
• Autoimmune thyroiditis
• Grave’s disease
• Hypothyroidism
• Type-I DM
Endocrine system
• Uveitis
Eye

71. CLASSIFICATION OF
AUTOIMMUNE DISORDERS
1. Organ specific
• Pernicious anemia
• Ulcerative collitis
Gastrointestinal
system
• Glomerulonephritis
• Good pasture’s
syndrome
Kidneys
• Pemphigus valgaris
• Psoriasis
Skin

72. CLASSIFICATION OF
AUTOIMMUNE DISORDERS
2. Non-Organ specific
Systemic lupus erythematous
Rheumatoid arthritis
Progressive systemic sclerosis

73. ETIOLOGY
Generally unknown
Some autoimmune diseases
runs in family
(GENETIC FACTORS)
Some autoimmune disorders
are known to triggered by
viral or bacterial infections
(RHEMATIC FEVER,
ARTHRITIS)
Exposure to certain
chemicals and deficiency of
certain enzymes may lead to
autoimmune disease.

74. PATHOPHYSIOLOGY
The various mechanisms of autoimmune diseases
are listed as follows-
1. Bypass of helper T-cell tolerance
2. Emergence of sequestered antigen
3. Imbalance of suppressor helper T-cell function
4. Microbial agents in autoimmunity
5. Molecular mimicry
6. Polyclonal lymphocyte activation

75. PATHOPHYSIOLOGY
1. Bypass of helper T-cell tolerance-
Tolerance of CD4+ helper T-cell is critical to
the prevention of autoimmunity. Therefore
tolerance may be broken if the helper T-cell
is bypasses or substituted.

76. PATHOPHYSIOLOGY
2. EMERGENCE OF SEQUESTERED ANTIGEN
Any antigen-self that is completely
sequestered during development is likely to
be viewed as foreign if introduced into
circulation, an immune response will
develop.
Spermatozoa, myelin basic protein and lens
crystalline fall into this categories of
antigen.

77. PATHOPHYSIOLOGY
3. IMBALANCE OF SUPPRESSOR HELPER
T-cell function- A loss of suppressor T-cell
function will contribute to autoimmunity
and conversely, excessively T-cell help may
drive B-cells to extremely high levels of
autoantibody production.

78. PATHOPHYSIOLOGY
4. MICROBIAL AGENTS IN AUTOIMMUNITY
Microbes may trigger autoimmune reactions in several
ways-
• First viral antigens and autoantigens may become
associated to form immunogenic units and bypass T-
cell tolerance.
• Second, some viruses (EBV) are non-specific,
polyclonal B-cell mitogens and may thus induce
formation of autoantibodies.
• Third, viral infection may result in loss of suppressor
T-cell function.

79. PATHOPHYSIOLOGY
5. MOLECULAR MIMICRY
The infecting microorganisms may trigger an
antibody response by presenting the cross
reacting haptonic determinants in
association with their own carrier to which
helper T-cell are not tolerant. The antibody
so formed may then damage the tissue that
shares cross reacting determinants.

80. PATHOPHYSIOLOGY
6. POLYCLONAL LYMPHOCYTE ACTIVATION
Several microorganisms and their products
are capable of causing polyclonal activation
of B-cells.

81. CLINICAL MANIFESTATIONS

82. DIGNOSTIC EVALUATION
HISTORY TAKING
• History of allergic reaction
• Family history of genetic
disorders, habits
• Recent exposure to
sensitizing agent
• Changes in living, working
environment
• Characteristic of present
environment
• Symptoms experienced
• Alleviating factors
PHYSAICAL EXAMINATION
• Rashes (location / colour)
• Over growth of tissues
• Scaly patchy appearance
• Mouth breathing
• Flaring nares
• Difficulty hearing

83. DIGNOSTIC EVALUATION
LABORATORY TESTS
• Antinuclear antibody tests
• Autoantibody test
• CBC
• C-reactive protein (CRP)
• Erythrocyte sedimentation
rate (ESR)
OTHER PROCEDURES
• Lumber puncture
• Bone marrow biopsy

84. MANAGEMENT
MEDICAL MANAGEMENT
SYSTEMIC
CORTICOSTEROIDS
Initial dose of 60
mg prednisolone
CYTOTOXIC DRUGS
Cyclophosphamide
Azathioprine
methotrexate
ANALGESICS
Ibuprofen

85. NURSING MANAGEMENT OF
IMMUNE SYSTEM DISORDERS
NURSING ASSESSMENT
1. Review record of history of risk factors, constitutional
signs and symptoms recent infections, positive blood
test of immune disorders.
2. Assess and monitor nutritional status, weight, history
of weight loss and serum albumin.
3. Assess immunization status.
4. Investigate the use of medications.
5. Inspect vital signs, mouth for lesions, skin for rash,
bowel pattern, presence of pain and weakness.

86. NURSING DIAGNOSIS
1. Risk for infection related to immunodeficiency,
neutropenia secondary to medications.
Goal- To prevent infection.
Interventions-
a. Administer prescribed medications.
b. Assess the systems thoroughly and notify
physician if abnormal.
c. Maintain cleanliness of the environment .
d. Employ aseptic techniques when performing
invasive procedure.
e. Instruct visitors to wash hands before and after
meeting patients.

87. NURSING DIAGNOSIS
2. Imbalanced nutrition less than body requirements
related to anoxia, secondary to infection.
Goal- To maintain proper nutrition.
Interventions-
a. Monitor nutritional status by daily weighing and
anthropometric measurement.
b. Consult with dietician to develop strategies for
nutritional care.
c. Encourage small, frequent meals as these may
make best use of limited absorption capacity.
d. Continue monitoring weight.
e. After timing of medications to improve intake of
meals.

88. NURSING DIAGNOSIS
3. Impaired oral mucus membrane related to
opportunistic infections secondary to reduced
immune function.
Goal- To maintain skin integrity.
Interventions-
a. Ask about persistent sore throat dysphasia, heart
burn all these symptoms are suggestive or oral
oesophageal candidiasis.
b. Examine mouth for oral candidiasis, a harbour of
infection.
c. After prescribe mouth rinse and antifungal
agents.
d. Provide patient with the soft diet.

89. NURSING DIAGNOSIS
4. Impaired gas exchange related to leukocytes
infiltration of systemic tissue secondary to decreased
mature RBC.
Goal- To maintain adequate oxygenation.
Interventions-
a. Maintain adequate oxygenation and perfusion.
b. Administer nebulization.
c. Watch for sudden change in respiratory functions.
d. Provide bronchodilators.
e. Encourage smoking cessation.
f. Administer medications as prescribed by the
doctor.

90. NURSING DIAGNOSIS
5. Fatigue and activity intolerance related to
anaphylaxis.
Goal- To relieve fatigue and maintain well-being.
Interventions-
a. Evaluate the patients description of fatigue.
b. Determine the possible causes of fatigue.
c. Restrict environmental stimuli.
d. Encourage the patient to maintain a 24 hour
fatigue or activity log for at least 1 week.
e. Teach energy conservation methods collaborate
with occupational therapist.

91. COMPLICATION OF IMMUNE
DISORDER
• Recurrent infections
• Autoimmune disorders
• Damage to heart lungs, nervous system,
digestive system
• Slowed growth
• Increased risk of cancer
• Death from serious infection, anaphylactic
shock
• Rheumatic heart disease
• Heart failure

92. SUMMARY

93. CONCLUSION