LYMPHATIC SYSTEM
⮚ To protect the body against pathogens
and other foreign material
⮚ To return tissue fluid to the blood to
maintain blood volume.
STRUCTURES of the LYMPHATIC SYSTEM
1. B-Bone marrow
2. L-Lymph nodes
3. T-Thymus
4. S-Spleen
5. T-Tonsils
LYMPH- the water found within lymphatic
vessels.
LYMPHATIC VESSELS- collects tissue fluid and
proteins.
LYMPHATIC TISSUE- a hemopoeitic tissue
that produces some lymphocytes and in which
lymphocytes are mature and are activated.
BONE MARROW
⮚ Lymphocytes -are produced from stem
cells in the RBM then migrate to lymph
nodes and nodules, to the spleen and to
the thymus.
⮚ Lymphocytes – become activated and
proliferated in response to infection.
Types of LYMPHOCYTES
B cells
-produced in RBM; migrate to spleen, lymph
nodes
– produce antibodies that incapacitate the
antigen.
- produce antibodies that will attack an antigen.
T cells
⮚ Attack foreign or abnormal cells and
regulate cell mediated immunity.
⮚ destroy the target cells through the
release of lymphokines.
⮚ It attacks the antigen directly.
⮚ are license to KILL, HELP and SUPPRESS
⮚ KILLER T cells- they bind to surface of
the invading cell, disrupt the membrane
and destroy it by altering its internal
environment
⮚ HELPER T CELLS/CD4 T CELLS-
stimulate the B cells to synthesize and
secrete immunoglobulin (proteins with
known antibody activity
⮚ SUPPRESSOR T CELLS- reduce
humoral response.
Natural Killer Cells
-destroy foreign cells by rupturing their cell
membranes
LYMPH NODES/NODULES
⮚ Are masses of lymphatic tissue and
distributed along lymphatic vessels
throughout the body
⮚ They filter lymphatic fluid which drains
from body tissues later returns to the
blood as plasma
⮚ Remove bacteria and toxins from
the circulatory system. (Infectious
agents can be spread by the lymphatic
system.
⮚ Cervical, axillary, Inguinal lymph
nodes
LYMPH NODES
▪ are found along the pathways of lymph
vessels and the lymph flows through
these nodes on its way to Subclavian
veins.
▪ LYMPH enters a NODE through
severa
▪ LYMPH VESSELS. As the LYPMH
passes through the LYMPH NODE,
bacteria and other foreign materials are
phahocytized by MACROPHAGE.
LYMPH NODULES
▪ are small masses of lymphatic tissue
just beneath of all mucous membranes
▪ ex: Peyer’s Patches in the small
intestines, and Tonsils in the pharynx.
Nodes- are usually larger, 10-20mm in length
and are encapsulated.
Nodules- range from a fraction of millimeter to
several millimeters in length and do not have
capsules.
THYMUS GLAND
 ⮚ Located in the MEDIASTINUM (between
the lung) secretes a group of hormones
that enable the lymphocytes to develop
into mature T cells
⮚ Produced T lymphocytes or T CELLS
⮚ Located inferior to the Thyroid
gland
⮚ Malignant cells, organ transplant are
recognized as foreign and usually
destroyed.
ANTIBODY
-an immunoglobulin produced by the
lymphocytes in response to foreign antigen

SPLEEN
TWO COMPONENTS OF IMMUNITY
⮚ Located in the Upper left Quadrant of
1. INNATE (INBORN) IMMUNITY
the abdominal cavity just below the
- is non-specific, responses are always the
diaphragm
same, does not create memory and does not
⮚ The largest lymphatic organ, the spleen
become more efficient.
functions as a reservoir for blood
-consist of Barriers, defensive cells, and
⮚ Contains plasma cells that produce
chemical defenses
antibodies to foreign antigens
⮚ Cells in the splenic tissue called
1. BARRIERS
MACROPHAGE- that phagocytized
● Unbroken stratum corneum of the
pathogens and other foreign materials in
epidermis of the skin- is an excellent
the blood
barrier to all kinds of pathogens.
⮚ Stores platelets and destroy them when
● SEBUM-has fatty acids that limits the
they are no longer needed.
growths of bacteria on the skin.
TONSILS
● Cells in the epidermis- produce
⮚ Consist of lymphoid tissue and also
defensins which are anti microbial
produced lymphocytes
chemicals
⮚ The location of tonsils allows them to
● Mucous membrane of respiratory,
guard the body against airborne and
digestive, urinary and reproductive are
ingested pathogens.
good barriers
IMMUNITY
● Ciliated epithelium of the URT- dust and
⮚ the ability to destroy pathogens or
pathogens are trapped on the mucus
other foreign material to prevent
● Cilia- sweep the mucus to the pharynx
further infectious disease
and it is swallowed.
⮚ this ability is important because the
● HCL- destroy most pathogens that enter
body is exposed to pathogens.
the stomach
● Lysozyme- an enzyme found in saliva
IMMUNOCOMPETENCE- the ability of the cells
and tears that inhibits the growth of
to distinguished between foreign matter and
bacteria in the oral cavity.
what belongs to the body.
ANTIGENS
2. DEFENSIVE CELLS
⮚ are foreign substances which stimulates a. Phagocytes- macrophages, neutrophils,
an immune responses eosinophils- use intracellular enzymes and
⮚ Human cells have their own antigens chemicals such as hydrogen peroxide to destroy
that identify all the cells in an individual ingested pathogens.
as “self”. When antigens are FOREIGN b. Langerhans cell and other dendritic
or “NON SELF”, they maybe cells- activates lymphocytes
recognized and DESTROYED c. Natural killer cells- found in RBM, spleen
⮚ Bacteria, viruses, fungi and protozoa are and lymph nodes that destroy foreign cells by
all foreign antigens that activates rupturing their cell membranes
immune response.
d. Basophils and mast cells- produce
histamine and leukotrines as part of
inflammation.
Histamines- causes vasodilation and make
capillaries more permeable. (Absorbent, spongy,
leaky)
Leukotrienes – increase capillary permeability
and attract phagocytic cells to the area.
3. CHEMICAL DEFENSES
-chemicals that helps the body resist the
infection which include interferon (alpha, beta
and gamma interferon), Complement, and
Inflammation.
INTERFERON
⮚ Blocks the reproduction of virus.
⮚ Virus must be inside the living cell to
reproduce, since the interferon cannot
prevent the entry of viruses into the
cells, it blocks their reproduction.
Complement proteins lyse foreign cells-
⮚ attract WBC’s and contribute to the
inflammation. They are involve in the
lysis of cellular antigens.
Inflammation
⮚ The purpose of inflammation is to
contain the damage, keep it from
spreading, eliminate the cause, and
permit repair of the tissues.
⮚ a response to damage of any kind:
microbial, chemical or physical.
⮚ Basophils and mast cells release
histamine and leukotrienes which affects
the blood vessels
⮚ Vasodilation increases blood flow to the
damage area and capillaries become
more permeable and tissue fluid and
WBC collect on the site.
⮚ Four signs of Inflammation
⮚ REDNESS- from greater blood flow
⮚ HEAT-from the blood and increase
metabolic activity
⮚ SWELLING-from accumulation of tissue
fluid and
⮚ PAIN- from damage itself and swelling
due to compression of nerve endings,
injury to nerve endings
CELL RESPONSE
Neutrophils- first to be launched at the site of
tissue injury
Monocytes- Perform phagocytosis in chronic
tissue injury
Lymphocytes- responsible for immune
response
2. ADAPTIVE IMMUNITY
⮚ responds to any foreign antigen
⮚ very specific, may involve antibodies
and responses are more efficient
⮚ it is carried out by T cells, B cells
and machrophages
⮚ consist of CELL mediated and antibody
mediated immunity.
T CELLS/LYMPHOCYTES
⮚ produced in the thymus and RBM
⮚ they require hormone of the thymus for
maturity
⮚ migrate to the spleen, lymph node and
nodules
⮚ Attack foreign or abnormal cells and
regulate cell mediated immunity.
⮚ The job of T cells is to destroy the
target cells through the release of
lymphokines.
⮚ It attacks the antigen directly.
⮚ are license to KILL, HELP and SUPPRESS
⮚ KILLER T cells- they bind to surface of
the invading cell, disrupt the membrane
and destroy it by altering its internal
environment
⮚ HELPER T CELLS/CD4 T CELLS-
stimulate the B cells to synthesize
and secrete immunoglobulin (proteins
with known antibody activity
⮚ SUPPRESSOR T CELLS- reduce
humoral response.
B-CELLS/LYMPHOCYTES
⮚ produced in the embryonic bone
marrow; migrate into the spleen, lymph
node and nodules
 ⮚ produce antibodies that incapacitate the
antigen.
⮚ - produce antibodies that will attack an
antigen.
NOTE: Antigen must be recognized first as
foreign. This is accomplished by B cells or
Helper T cells.
When foreign substances invade the body, two
types of immune responses are possible:
TYPES OF IMMUNE RESPONSES
1. CELL MEDIATED IMMUNITY
⮚ the T cells respond directly to antigen
(bacteria or toxins). This response
involves destruction of the target cells
(such as virus infected cells and cancer
cells) through the secretion of
lymphokines/cytokines (lymph proteins)
⮚ ex. of cell mediated immunity are
rejection of transplanted organs and
delayed immune responses that fight
disease.
⮚ Does not involve antibodies; is effective
against intracellular pathogens ,
malignant cells and graft of foreign
tissues
⮚ HELPER T cells/Macrophage recognize
the foreign antigen, are antigen specific,
and begin to divide to form different
groups of T cells.
⮚ MEMORY T cells will remember the
specific foreign antigen
⮚ CYTOTOXIC (KILLER) T Cells destroy
the foreign cells by disrupting cell
membrane and thus prevent the viruses
from reproduction. And capable produce
cytokines to attract macrophages.
MACHROPHAGE-capable of phagocytosis
pathogen, dead and damage cells.
2. HUMORAL IMMUNITY/Antibody
Mediated
⮚ B-cells act to recognized and
destroy the antigen.
⮚ B cells are responsible for humoral or
immunoglobulin mediated immunity.
⮚ B cells originate in the bone marrow and
mature into plasma cells that produce
antibodies
⮚ Antibodies destroy bacteria and viruses
thereby preventing from entering host
cell.
⮚ Involves antibody production
⮚ Effective against pathogens and foreign
cells
⮚ B cells and Helper T cells recognized the
foreign antigen; the B cells are antigen
specific and begin to divide.
⮚ Memory B cells will remember the
specific foreign antigen.
⮚ Other B cells become plasma cells that
produce antigen specific antibodies.
⮚ An antigen-antibody complex is formed
which attract macrophage
(Opsonization)
⮚ Complement
ANTIBODY
-an immunoglobulin produced by the
lymphocytes in response to foreign
antigen
-an antibody is specific to an antigen
-antibodies include agglutinins, bacteriolysis,
opsonins and precipitin.
Five Classes of Antibodies
(Immunoglobulins)
1. IgG
⮚ The most abundant antibodies, makes
up about 80% of plasma antibodies.
⮚ It appears in ALL BODY FLUIDS and is
the major antibacterial and antiviral
antibody.
⮚ Can cross the placenta, responsible for
immunity in the newborn
⮚ Neutralizes toxins and viruses
⮚ 600-1600mg/dl
2. IgA
⮚ Found mainly in body secretions such as
saliva, tears, bile, colostrum, mucus of
the respiratory, digestive and urinary
tracts
⮚ Adds protection against enteric viruses
in the breastfeed infant
 ⮚ 200-500mg/100ml
3. IgM
⮚ The first immunoglobulin produced
during an immune response.
⮚ First to appear in fetal life
⮚ First to form during viral or bacterial
infection
⮚ The largest of the immunoglobulins in
molecular size to cross membrane
barriers usually present in the vascular
system.
⮚ Second most abundant antibodies
⮚ 60-200mg/ml.
4. IgE
⮚ The antibody involved in immediate
hypersensitivity reactions, or allergic
reactions that develops in minutes of
exposure to an antigen
⮚ Stimulates the release of mast cell
granules which contain histamine and
heparin.
⮚ Present in amount, too small to measure
5. IgD
⮚ Possibly a regulatory antibody, acts as
an antigen receptor of B cells.
⮚ Present in plasma and is easily broken
down. It’s the predominant antibody on
the surface of B cells and is mainly an
antigen receptor.
⮚ Present in amount, too small to
measure.
Types of Antigen-Antibody Reaction
1. Agglutination- means “clumping” where the
antibodies bind to bacterial cells and they are
easily phagocytized by macrophage.
- Type A person needs a transfusion to replace
blood loss in hemorrhage. If the person were
receive type B blood. Type A recipient has anti-B
antibodies that would bind to the type B antigen
of the RBC. The type B RBC would first clump,
then rupture (hemolysis) defeating the purpose
of the transfusion.
2. Precipitation- antibodies react with soluble
antigens resulting in an insoluble complex which
then precipitates (hasten)
3. Neutralization- antibodies combine with all
the toxin
4. Lysis- antibodies attack all membrane and
cause cell rupture.
5. Opsonization- antibodies coat bacteria and
increase susceptibility to phagocytosis. The
antigen is “labeled” for phagocytosis by
macrophage and neutrophils
Immune response serves three functions:
1. Defense- involves resisting infection
2. Homeostasis- involves removing worn out
“self-components”
3. Surveillance- deals with the identification
and destruction of mutant cells.
The unique characteristics of the Immune
System are as follows
Self or Non-Self Recognition
⮚ Normally recognizes host cells as non-
antigenic and responds only to foreign
and potentially harmful agents, living or
non-living as antigens
Antibody Production
⮚ Produces specific antibodies for specific
antigens for destruction.
Memory
⮚ Remembers antigens that have invaded
the body in the past allowing a quicker
response.
Self-Regulation
⮚ Monitors its own performance, turning
itself on when antigens invade and
turning itself off when infection is
eradicated.
IMMUNIZATION- process of rendering an
organism to the effects of specific harmful
substances
TYPES OF IMMUNITY
ACTIVE IMMUNITY
 ❑ Host produces own antibodies in
response to natural antigen or
artificial antigens
PASSIVE IMMUNITY
❑ Host receives natural or artificial
antibodies (serum) produced by
another source
TYPES OF ACTIVE IMMUNITY
NATURAL ACTIVE IMMUNITY
❑ Antibodies formed in the presence
of active infection
❑ Lifelong
ARTIFICIAL ACTIVE IMMUNITY
❑ Antigens administered to stimulate
antibody formation
❑ Many years, reinforced by booster
TYPES OF PASSIVE IMMUNITY
NATURAL PASSIVE IMMUNITY
❑ Antibody from immune mother to
baby through the placenta or
colostrum
❑ 6 MONTHS -1 YEAR
ARTIFICIAL PASSIVE IMMUNITY
❑ Immune serum (antibody) from
animal to human is injected
❑ 2-3 weeks
DIAGNOSTIC TEST
1. Bone marrow aspiration
⮚ Decrease WBC indicates bone marrow
suppression
⮚ Decrease lymphocytes (1500-3000/cu
mm) indicates defective cellular
immunity
2. T-cell (cellular deficiency)
⮚ Cell function can be screened by
delayed hypersensitivity
⮚ Skin testing to common antigen
a. PPD- Purified Protein Derivative
b. DNCB- DinitroChlorobenzene
3. B cell (Humoral Deficiency)
⮚ Electrophoresis- the movement of colloid
(CHON) particles in an electrical field.
⮚ Identifies immunoglobulins IgG, IgA,
IgM in serum
⮚ It assesses the effectiveness of
chemotherapy or radiation therapy,
detects hypogammaglobulinemias and
hypergammaglobulinemias.
4. Specific Antigen- Antibody Test
a. Radioimmunoassay test – consist of the
unknown antigen to the antibody followed by
incubation.
b. Immunoflourescence Test-consist of
attaching fluorescein dye to antibodies and then
mixing with the antigen to be tested
c. Agglutination Test- determines the
presence of antigens located on the surfaces of
RBC’s or microorganisms, the antigen and
antibody react by clumping of cells.
d. Compliment Fixation Test
- a standard amount of complement is added to
a mixture of an antigen and its corresponding
antibody.
-determine the presence of a particular antibody
in the patients’ blood, but it does not indicate if
the infection occurs.
5. Antibody Titer
- determines the level or amount of specific
antibody in the patient’s blood
6. ELISA (Enzyme Linked Immunosorbent Assay)
- designed to screen blood or plasma for the
presence of antibody or human T lymphocytes
virus.
URTICARIA & ANGIOEDEMA
URTICARIA
⮚ AKA “HIVES”
⮚ A lesion that affects the epidermis
ANGIOEDEMA
⮚ A similar lesion but involves deep dermis
and subcutaneous tissues
Acute Urticaria
⮚ Hives that last less than 6 weeks, cause
is determine
Chronic urticarial
⮚ Hives that last longer than 6 weeks,
cause is undetermined
Etiology
SYSTEMIC LUPUS ERTHYMATOSUS
⮚ Ingested substances- foods, food
additives, drugs ⮚ A chronic, anti-inflammatory,
⮚ Infections- virals, bacteria, paracitic autoimmune disorder affecting the
⮚ Physical factors- heat, sun, cold, connective tissues that is most likely
Failure of the immune regulation
pressure, stress
⮚ More WOMEN are affected than men
⮚ Insect tings
(9:1 ratio)
⮚ Hereditary
⮚ 90% cases are women
⮚ Native Americans, Blacks, Hispanics, and
Clinical Manifestation
⮚ Red edematous wheals Asian
⮚ Onset usually between ages of 15 and
⮚ Intense pruritus
45 years, but
⮚ Diffuse swelling with angioedema
⮚ Can occur in childhood or later in life
⮚ Sx may develop within seconds over 1-2
TWO FORMS
hrs and last up to 24-36 hrs
Lab Data DISCOID
⮚ Elevated serum tryptase
⮚ Elevated IgE ⮚ affects only the SKIN and leaves a scar
⮚ Challenge testing to determine physical after healing
cause
SYSTEMIC

⮚ affects multi organs and characterized

Management
by remissions and exacerbations
Acute urticaria
CLINICAL MANIFESTATION
⮚ Identify and eliminate the causative
⮚ BUTTERFLY RASH- Classical sign of
factors
SLE characterized by edema and
⮚ H1 antihistamines erythema
⮚ Ring shaped lesions found in shoulders,
⮚ Epinephrine arms and upper back
⮚ Scaly plaques on the face, scalp,
⮚ Corticosteroids
external ears and neck
PROLONGED URTICARIA ⮚ Alopecia
⮚ Fever, anorexia, weight loss, malaise,
⮚ Elimination of DIET fatigue, NV,
⮚ H1 antihistamines
⮚ H2 antihistamines SYSTEMIC
⮚ TCA CARDIOPULMONARY
⮚ Topical agents to relieve itching ⮚ Cardiopulmonary signs and symptoms
occur in 50% of patients
⮚ Chest pain indicates Pleuritis
Nursing Interventions ⮚ Dypsnea- suggesting parenchymal
infiltration and pneumonitis and effusion
⮚ Administer or teach self administration
⮚ Tachycardia, cyanosis and hypotension
of anti histamines and corticosteroids
indicates Pulmonary embolism and
⮚ Avoid exposure to heat, exercise,
Hemorrhage
sunburn
⮚ Avoid to identified triggers
GASTROINTESTINAL ⮚ This form is mainly treated with
corticosteroids and immunosuppressant
⮚ Bowel impaction drugs.
⮚ Acute abdominal pain
⮚ Spontaneous bacterial peritonitis
⮚ Oral ulcers
Class V is membranous nephritis
RENAL
⮚ is characterized by extreme edema and
■ Nephritis: usually asymptomatic, so protein loss.
always check UA if patient has known or
Class VI Glomerulosclerosis
suspected SLE
⮚ increase in the amount of matrix
■ Occurs early in course of disease-if not
material in the glomeruli
present w/in 1 yr, probably will not
occur. CNS
■ Histologic classification by renal biopsy ⮚ Neurologic disorders- psychosis and
is useful to plan therapy Depression
⮚ TIA/stroke
Nephritis
⮚ Epilepsy
⮚ Infrequent urination indicates renal
⮚ Migraine Headache
failure
⮚ Urinary frequency, painful urination
Hematology- due to circulating antibodies
and bladder spasm indicates UTI
⮚ Hemolytic anemia
⮚ UTI and Renal damage are the leading
⮚ Leukopenia
causes of SLE patients
⮚ Thrombocytopenia

Class I is minimal mesangial Other signs

glomerulonephritis ⮚ Fever
⮚ Weight loss
⮚ is histologically normal on light ⮚ fatigue
microscopy but with mesangial deposits
on electron microscopy. Lab Data
⮚ Mild form
⮚ Can be reversible ⮚ CBC- anemia and decrease wbc count,
⮚ Best prognosis decrease platelet count
⮚ Elevated ESR
Class II Mesangial proliferative lupus ⮚ Urinalysis
nephritis. ⮚ 24hr urine collection for CHON and
⮚ This form typically responds completely creatinine clearance
to treatment with corticosteroids. ⮚ X-ray- hands and wrist, reveal pleurisy
and pneumonitis
⮚ CT scan- brain, abdomen
⮚ Cerebral arteriogram- vasculitis
Class III is focal proliferative nephritis
Nursing Diagnosis
⮚ successfully responds to treatment with
⮚ Pain Related to inflammation of the
high doses of corticosteroids
joints
Class IV diffuse proliferative nephritis ⮚ Powerlessness r/l unpredictable coure of
the disease
 ⮚ Impaired Skin/ Oral Mucous membrane ⮚ Corticosteroids (Mainstay of SLE
integrity r/l to skin and oral lesions treatment)
⮚ Altered Urinary r/t renal involvement ⮚ To rapidly suppress inflammation
⮚ Fatigue r/t chronic inflammatory process ⮚ Usually start with high-dose IV pulse
and convert to PO steroids with goal of
Management tapering and converting to something
Prognosis: else.
⮚ Commonly used: prednisone,
⮚ No cure for lupus, the recovery hydrocortisone, methylprednisolone, and
improves with early detection and dexamethasone
treatment ⮚ Primarily for CNS/renal
⮚ Poor prognosis for patients who involvement
develop cardiac, renal, or neurologic, ⮚ Mycophenolate mofetil (cellcept)
and severe bacterial complications ⮚ Azathioprine (imuran): requires several
months to be effective, effective in
Pharmacologic
smaller percentage of patients
⮚ NSAIDS-( Ibupropen- )reduce pain and ⮚ Cyclosporine: used in steroid-resistant
inflammation SLE, risk of nephrotoxicity
⮚ Topical Corticosteroids- to reduce ⮚ Cyclophosphamide (cytoxan) Almost all
inflammatory process in skin lesion trials performed on patients with
⮚ Immunosuppressives- to suppress nephritisImmunosuppressive
immune response
NURSING INTERVENTIONS
⮚ Administer analgesic- reduce pain
To Maintain Skin and Mucous Membrane
Non pharmacologic
Integrity
⮚ Avoid direct exposure to sunlight to
⮚ Suggest alternatives hairstyles, scarves
reduce the chance of exacerbation
and wigs to cover significant areas of
-use sunscreen SPF 15- greater
alopecia
-wear protective, light weight clothing
⮚ Encourage good oral hygiene and
long sleeves and hats
inspect mouth for oral ulcers
⮚ Avoid exposure to drugs and chemicals
⮚ Avoid hot or spicy foods that may
(hair spray, coloring agents)
irritate oral ulcers
⮚ Encourage good nutrition, sleep habits
⮚ Apply topical corticosteroids to skin
and exercise rest and relaxation- to
lesions (Triamcinolone, hydrocortisone)
improve general health and to prevent
⮚ Apply topical analgesics to reduce pain
infection
To Reduce Fatigue
For those w/out major organ involvement.
⮚ Pace activity and exercise according to
⮚ NSAIDs: to control pain, swelling, and
body’s tolerance
fever
⮚ Teach relaxation techniques such DBE-
⮚ Caution w/ NSAIDS though. SLE pts
to reduce emotional stress that causes
are at increased risk for aseptic
fatigue.
meningitis
⮚ Antimalarials: Generally to treat
DRUGS That SPARK SLE
fatigue joint pain, skin rashes, and
inflammation of the lungs 1. Procainamide
⮚ Commonly used: Hydroxycholorquine 2. Hydralazine
⮚ Used alone or in combination with other 3. Isoniazide
drugs 4. Methyldopa
 5. Anticonvulsant
6. Penicillins and hormonal contraceptives
IMMUNOLOGIC DISORDERS
IMMUNODEFICIENCIES
⮚ Deficiency in the proper expression of
the immune system response
TWO TYPES
1. PRIMARY Immunodeficiency
⮚ Deficiencies resulting from the improper
development of the immunosuppressive
cells and tissues
⮚ GENETIC disorders seen in CHILDREN
TYPES OF PRIMARY IMMUNODEFICIENCY
1. T-CELL DEFICIENCY/DI GEORGE
SYNDROME (THYMIC HYPOPLASIA)
⮚ A congenital disorder in which the
thymus and the parathyroid glands are
absent at birth
⮚ TG is necessary for normal development
of T lymphocytes
⮚ This disorder have a low number of of T
lymphocytes, limiting their ability to fight
many infections
⮚ Infection begins soon after birth and
recur often.
⮚ PG regulate calcium levels in the blood.
The low calcium levels lead to muscle
spasms (tetany)
Ss/Sx
⮚ Ss of congenital heart disease
⮚ Unusual facial features
⮚ Low set ears
⮚ Wide set eyes
⮚ Muscle spasms
⮚ Hypocalcemia and tetany
Treatment
⮚ Transplantation of stem cells or thymus
tissue can cure immunodeficiency
⮚ Bone marrow transplantation
2. B CELL Deficiency/ (Brutons
Agammaglobulinemia
⮚ A hereditary immunodeficiency due to
abnormality in the X chromosome
resulting to few or no B lymphocytes
and very low levels or absence of
antibodies
⮚ Affects and found only in BOYS
⮚ First 6 months after birth, antibodies
from the mother protects against
infection.
Ss and Sx
⮚ Recurrent infections of the ears, sinuses,
lungs and bones due to bacteria such as
pneumococcus, haemophilus, and
streptococcus.
Treatment
⮚ Gamma globulin- given throughout life
to help prevent infection
⮚ Antibiotics-to treat bacterial infection
⮚ With treatment, lifespan maybe
unaffected
COMMON VARIABLE IMMUNODEFICIENCY
(CVID)
⮚ Very low antibody levels despite of
normal number of B lymphocytes
⮚ Deficiency in IgA and IgM
⮚ Develops between the age 10-20,
becomes evident to adult person
⮚ Lung infection, autoimmune disorder,
Thyroiditis, and Rheumatoid arthritis
⮚ Diarrhea, Indigestion
⮚ Immunoglobulin lifetime and antibiotics
to treat infections
⮚ Lifespan maybe shortened
Severe Combined Immunodeficiency
Disease
⮚ Complete absence of both cellular and
humoral immunity
⮚ A congenital disease with Low level of
antibodies and low number of T cells
⮚ Gene defect/ hereditary
⮚ Infant may develop pneumonia and
diarrhea at age of 3 months
Treatment
⮚ Antibiotics, immunoglobulin
⮚ Transplantation of stem cells from bone
marrow
 ⮚ Gene therapy- removing of WBC from
the infant, inserting a normal gene into
the cells, and returning the cells to the
infant.
SECONDARY
IMMUNODEFICIENCY/Acquired
1. HIV/AIDS (Acquired
Immunodeficiency Syndrome)
2. Protein Caloric Malnutrition
3. Induced Immunosupression
ALLERGIC REACTIONS
⮚ Results from antigen-antibody reaction
on a sensitized mast cells causing the
release and synthesizes of chemical
mediators.
⮚ The reaction maybe characterized by
inflammation, increase secretions, and
bronchoconstriction
HYPERSENSITIVITY REACTIONS
⮚ The immune system over responds to
the allergen and produces tissue
damage.
Types of Hypersensitivity
Type 1- IgE mediated allergic reactions
Type 2- Cytotoxic reactions
Type 3- Immune complex reaction
Type 4- Cell mediated reactions
ALLERGEN
⮚ The antigenic stimulants that invokes
the reactions.
TYPES OF ALLERGEN
⮚ Inhalants
⮚ Ingestants
⮚ Contactants
⮚ Injectants
⮚ Bacteria
⮚ Self-allergens
GENERAL ETIOLOGIC FACTORS
Hereditary
Congenital
Contact
ANAPHYLAXIS
⮚ an immediate, life threatening systemic
reaction that can occur on exposure to a
particular substance
⮚ It is an acute Type 1 allergic reaction
that causes sudden, rapidly progressive
urticarial (hives) and respiratory
distress.
⮚ A severe reaction may lead to
respiratory obstruction, vascular
collapse, systemic shock and even
DEATH minutes to hours after the first
symptoms occur
⮚ Delayed or persistent reaction may last
up to 24 hours.
Understanding Anaphylaxis
1. Antigen will enter the body
2. Response to antigen
⮚ Immunoglobulins M and G
recognize and bind the antigen
3. Release of chemical mediators
⮚ Activated IgE on basophils promotes
the release of mediators: Histamines,
serotonin, and leukotrienes
4. Respiratory distress
⮚ In the lungs, histamine causes
endothelial cell destruction and fluid will
leak into the Alveoli
5. Deterioration
⮚ Mediators increase vascular permeability
causing the fluid to leak in the blood
vessels
ETIOLOGY
P-enicillin and other antibiotics- the most
common anaphylaxis causing antigen.
A-llergen
S-kin Testing
S-ALICYLATES
I-nsect bites- venom from honeybees and
certain spiders
L-atex and local anesthetics
E-nzymes such as L-asparaginase
F-oods
D-iagnostic chemicals such as contrast media
infusion
H-ormones
 ⮚ In the early stage of anaphylaxis, when
CLINICAL MANIFESTATION the patient remain conscious, give
RESPIRATORY epinephrine IM SC. Massage the
⮚ Laryngeal edema, stridor injection site to speed the drug
⮚ Lump in throat, hoarseness of the voice into the circulation.
⮚ Cough, Dyspnea, ⮚ In severe reaction, when the patient is
⮚ Bronchospasm unconscious, give the drug I.V.- to
⮚ Whezzing prevent vascular collapse
⮚ Effects: it causes Vasoconstriction,
CUTANEOUS Decrease capillary permeability, relaxes
⮚ Urticarial (hives) airway smooth muscle, and inhibits mast
⮚ Angioedema cell mediator release.
⮚ Pruritus DIPHENHYDRAMINE
⮚ Erythema (flushing) ⮚ 50 mg IM IV
⮚ For signs and symptoms of allergy
Cardiovascular ⮚ It blocks the effects of histamines
⮚ Hypotension
⮚ Tachycardia Aminophyline
⮚ Palpitation ⮚ Helps to relieve bronchospasm
⮚ Syncope 2. Oxygen/ETT/Tracheostomy
⮚ Early signs of laryngeal edema (stridor,
Gastrointestinal dyspnea, hoarseness
⮚ Nausea 3. Fluids and vasopressors
⮚ Vomiting ⮚ to correct hypotension and shock
⮚ Diarrhea 4. H1 antihistamines (Benadryl) and H2
⮚ Abdominal pain antihistamines such as ranitidine (Zantac)
⮚ Bloating ⮚ to block the effects of histamine
production
Diagnosis 5. Corticosteroids
⮚ Ineffective airway clearance rt ⮚ to decrease vascular permeability and
laryngeal edema and diminished or it helps in inflammation
bronchospasm process
⮚ Decrease cardiac output related to 6. Additional bronchodilators (albuterol)
vasodilation ⮚ to relax bronchial muscles
⮚ Anxiety rt respiratory distress and Complications
life threatening situation. 1. Cardiovascular collapse
2. Respiratory failure
COLLABORATIVE MANAGEMENT 3. Death

Drug Alert ALLERGIC RHINITIS

⮚ Act fast with anaphylaxis. Epinephrine
injection is the first line of defense
1. Drugs
EPINEPHRINE/Adrenaline
⮚ 1:1000 aqueous solution
⮚ 0.3-0.5 ml SQ/IM
⮚ 0.01ml/kg SC/IM
⮚ Should be repeated 10-20 minutes as
needed if symptom persist
⮚ Inflammation of the nasal mucosa and
the lining the eyelids (conjunctivitis)
caused by inhaled airborne allergen that
triggers an immune response
⮚ The most common allergic reaction
⮚ It can affect anyone at any age
⮚ Most common in young children and
adolescents
ETIOLOGY
 ⮚ Type I hypersensitivity causes
vasodilatation and increased capillary
permeability
⮚ Cause by airborne allergen
Types
a. Seasonal/Hay fever
⮚ it occurs occasionally (spring, fall,
summer) caused by airborne pollens
from trees, grass, weeds or mold.
⮚ Symptoms are episodic
b. Perrenial
⮚ It occurs year round
⮚ Dust mites, mold, cockroaches, house
dust, feathers, fungi, tobacco smoke,
material or industrial chemicals
CLINICAL MANIFESTATIONS
Seasonal/Hay fever
⮚ Sneezing attacks
⮚ Rhinorrhea- profuse watery nasal
discharge
⮚ Nasal obstruction
⮚ Itchiness in the eyes, ears and nose and
throat
⮚ Headache/ sinus pain
Perrenial
⮚ Chronic nasal obstruction which can
obstruct Eustachian tube (children)
Diagnosis: Ineffective breathing pattern rt
nasal obstruction
Diagnostic test
Skin testing
⮚ Confirms hypersensitivity to allergens
Nasal smear
⮚ Increase number of eusinophils suggest
allergic reaction
Rhinoscopy
⮚ Visualization of nasopharynx, useful to
rule out nasal obstruction
Collaborative Management
⮚ Minimize contact with offending allergen
⮚ Dust mite exposure can be reduce by
encasing bed pillows and mattress
⮚ Washing bed linens and stuffed animals
in hot water weekly
H1anti histamines
a. Older Sedating antihistamines
⮚ Inexpensive, OTC, short acting and
effective
⮚ Diphenhydramine (Benadryl)
⮚ Chlorphenamine
⮚ SE: sedation, dry mouth, nausea,
dizziness, blurred vision and
nervousness
⮚ Instruct the pt to avoid driving cars
b. New-Non Sedating/Less Sedating
antihistamine
⮚ Obtained by prescription, more
expensive, long acting and effective
⮚ Loratadine (Claritin)
⮚ Fexofenadine (Allegra)
⮚ Cetirezine
c. Decongestant
⮚ Shrink the nasal mucous membrane by
vasoconstriction
⮚ Do not use otc nasal decongestant
because their effect is short live and has
rebound effect- nasal mucosal edema
d. Anticholinergic agents
⮚ Act as drying agents, inhibits mucous
secretions.
e. Corticosteroids (oral/ intranasal)
⮚ Reduce inflammation of nasal mucosa
⮚ Prevent mediator release
f. Intranasal cromolyn sodium
(Nasalcrom)
⮚ Mast cell stabilizer
⮚ Hinders the release of chemical
mediators
Complications
Allergic asthma
Chronic otitis media, hearing loss
Chronic nasal obstruction, sinusitis