Immunology

1. NCM 212 – IMMUNOLOGY
OUTLINE
I. Autoimmunity
II. Kawasaki Disease
III. Multiple Myeloma
IV. Hypersensitivity
V. Influenza
VI. Signs and Symptoms of Influenza
VII. Ebola Hemorrhagic Fever
AUTOIMMUNITY
- Production of antibodies against the tissues of your
own body
- the immune system wasn’t able to identify the self-
antigen from the other antigen, thus they will keep on
attacking the body’s own tissues
- it produces autoimmune diseases or hypersensitivity
reaction
- the exact cause of autoimmune disorder is still
unknown
- Theory: some microorganisms or drugs / medications
may trigger changes that confuse our immune system
THEORIES OF EFFECTS/CAUSES OF IMMUNITY:
- Failure to display self-antigens- Macrophage,
dendritic cell, MHC
- Presence of genetic abnormalities (idiopathic)
- Self-reactive clones of T cells and B cells (if activated
then continuously they are going to react to the body)
LUPUS ERYTHEMATOSUS
- collection of autoimmune diseases, in which the
human immune system becomes hyperactive and
attacks normal, healthy tissues
- umbrella of autoimmune diseases
- may manifest as systemic diseases or in a purely
cutaneous form or localized (ex. DLE-Discoid lupus
erythematosus)
- Affects the Joint, skin, kidneys, blood cells, linings of
the heart and lungs
Notes:
- Lupus = “wolf” (Latin)
- Erythematosus - “reddened”
- Attributed to the 13th-century physician Gregorius
[Rogerious] who used it to describe erosive facial
lesions that were a reminiscent of a wolf’s bite
CLASSIFICATION:
- Most common types of lupus are these 4 ff:
1. DISCOID LUPUS ERYTHEMATOSUS
- focuses only on the skin CUTANEOUS IN NATURE
- Chronic skin condition of sores with inflamed
(painful, swelling) and scarring
- Flaking of lesions
- face, ears scalp; other body areas at times
- lesions develop as red and inflamed; it’s like a
inflamed patch with scaling and crusty
- lighter in color with a ring
- darker than the normal skin
3 DIVISIONS/LOCATION:
- Localized
o Skin lesions localized above the neck,
scalp, bridge of the nose, cheeks,
lower lip and ears
- Generalized
o affects head down to the thorax
- Childhood Discoid Lupus Erythematosus
o Low frequency of photosensitivity and
a higher progression of SLE
o clinical presentation and course is
similar to those in adults with SLE
2. DRUG-INDUCED LUPUS ERYTHEMATOSUS
- Brought about the triggering factor → medication
- Stop the medication then the lupus also stops
MEDICATIONS THAT MAY CAUSE LUPUS:
- Hydralazine (Apresoline): Antihypertensive drug-
less commonly used due to side effects
- Procainamide: Anti-arrhythmic drug
- Isoniazid (INH): Anti-tb drug
- Chlorpromazine (Thorazine):
Antipsychotic/neuroleptic drug- old generation anti-
psych drugs
- Penicillin: Antibiotic
Note: there are 38 drugs that can induce lupus
3. NEONATAL LUPUS ERYTHEMATOSUS
- If the mother has SLE

2. - infants have no skin lesions at birth due to antibody
IgG lesions develop during the first weeks of life
- usually benign and self-limited (going to heal on its
own)
4. SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
(COMMON)
- An autoimmune disorder, non-contagious, chronic,
progressive inflammatory disease of the connective
tissue
- Remission (state of the absence of the disease),
may mga months or year na walang manifestation sa
disease but if nasa
- exacerbation phase (flare-up) this is the time na
severe ang manifestations (BISAYA: dukloy, tukar)
- Prevalent in young women (adolescents as young as
15 -40 years old)
- Women are affected 8 times than men
- In one study, since women have 2 X chromosomes,
so we have the potential set of genes, this leads to
more estrogen. The immune system may become
abnormally activated by progesterone during lupus.
- Ratio of 100 in 100,000
- 1 to 295 in black women
- no treatment:; but there drugs available to control the
manifestations, especially during exacerbation
RISK FACTORS
- Genetic abnormality
o SLE does run in families, no single causal
gene identified
- Viral infection
o No specific antigen can be consistently
linked to the disease
- Medications
o drug-induced lupus erythematosus is a
reversible condition that usually occurs in
people treated for a long term illness; DLE
mimic SLE
SIGNS AND SYMPTOMS
- Arthritis (initial manifestation, inflamed) to
arthralgia
o Arthralgia = joint paints; early manifestation
of SLE
- Weakness, fever, fatigue (initial manifestation of
SLE), weight loss
- Photosensitivity from the sun (very evident in the
skin → face, neck, chest, shoulder, arm)
- Butterfly rash/malar rash (evident in the face →
cheeks, nose redness)
- Skin lesions
CHARACTERISTICS OF SKIN LESIONS:
- Margins are bright red
- May extend beyond the hairline
- May occur in the exposed part of the neck
- May spread to the mucous membranes and other
tissues of the body
- Do not ulcerate (di lulubog), but cause degeneration
and atrophy (gradually decline in vigor or mag shrink)
of tissues involved
SYSTEMIC INVOLVEMENT OF OTHER ORGANS
- Lupus nephritis

3. - Pleuritis
- Pericarditis- inflammation of the linings of the heart
- Peritonitis - inflammation in the inner lining of the
abdomen (peritoneum)
- Neuritis - general term for the inflammation of the
nerve
- Anemia
- Serositis - inflammation of the serous tissues of the
body
- Serous tissue = lining of the lungs (pleura), heart
(pericardium) and inner lining of the abdomen/GI
(peritoneum), kidney
RAYNAUD’S PHENOMENON
- a condition in which cool temperature or strong
emotion cause blood vessel spasms that block blood
flow to the fingers, toes, ears and nose
DIAGNOSTIC CRITERIA: SOAP BRAIN MD
- Serositis: Pleuritis or pericarditis or peritonitis
- Oral ulcers
- Arthritis- initial manifestations
- Photosensitivity
- Blood: There may be hematologic disorders;
hemolytic; manifestations of pt with SLE: anemia,
low RBC count, leukopenia, lymphopenia,
thrombocytopenia (worst cases)
- “Penia” low levels
- Renal disorder- renal failure because of nephritis
- Antinuclear antibody ANA/Antinuclear Factor:
Diagnostic exam to confirm/diagnose SLE
-
- HIV - confirmatory test is western blot assay
- Immunologic disorder
- Neurologic disorder: affect the brain, due to serositis
- Malar rash
- Discoid rash
DIAGNOSTIC EXAMS:
- Medical history
- Complete physical exam
- Laboratory tests
o CBC (thrombocytopenia, anemia)
o ESR (erythrocyte sedimentation rate) - can
signal na autoimmune disease
o U/A
o Blood chemistries

4. o Complement levels (C3)- increase of
complement indicates inflammatory
response.
- Anti-nuclear antibodies/ANA or ANF
- The ANA test measures the pattern and amount of
antibody which can attack the body’s tissues as if
they were foreign material
- Anti-double-stranded DNA → confirmatory test for
ANA
TREATMENT
- NSAIDs: - pain, arthralgia, fever
- Antimicrobials:
- Antibiotic for prophylaxis
- For inflammatory process
- Corticosteroid:
- Inflammation
- Immunosuppressive:
- address the problem of the Suppressor cell (they
don’t know when to stop)
- Alternative therapies
○ Special diet- alpha sprout (triggers SLE)
○ Nutritional supplement
○ Fish oils- rich in Omega-3, decreases
symptoms of SLE
○ Ointments and creams-
○ Chiropractors
○ sunscreens
○ exercise and rest,
○ stress reduction,
○ Family planning
○ yearly influenza and pneumococcal
vaccination
○ Compliance to medication
WHAT TO AVOID:
- Aromatic amines present in cleaning agents and hair
dyes
- Silicone and silica dust
- Alfalfa sprouts due to their high L-canavanine
- content
- Hydrazines found in some mushrooms and in
tobacco smoke
- Tartrazines found as preservatives in food dyes
- Ultraviolet light
- Excess alcohol
MEDICATIONS
- Anti-inflammatory analgesics: NSAIDs and Aspirin
- Antimalarial drug: Hydroxychloroquine
(Plaquenil/Hydroxychloroquine) managing
cutaneous problems and musculoskeletal for pain,
and mild manifestations of SLE
- Corticosteroids (Prednisone) in high doses
- Topical corticosteroids for rashes or cutaneous
manifestations given in low oral doses
- Cytotoxic agents or antineoplastic
OTHER MANAGEMENT
- Kidney dialysis- because of lupus nephritis
- Total hip replacement (Total Hip Arthroplasty) →
done for arthralgia or arthritis, prosthesis 95% of
people with SLE undergo THR
- Plasmapheresis- similar with dialysis
- Filters plasma
KAWASAKI DISEASE
- AKA Kawasaki Syndrome, Lymph Node Syndrome,
Mucocutaneous Lymph Node Syndrome, Infantile
polyarteritis nodosa
- A form of a condition called VASCULITIS wherein
there is inflammation of the blood vessels
- Also called mucocutaneous lymph node syndrome
because it also affects lymph nodes, skin, and the
mucous membranes inside the mouth, nose and
throat
- First described in 1967 by Tomisaku Kawasaki in
Japan
- Prevalent in male children under 5 years old
Kawasaki Disease is also known as NECROTIZING
VASCULITIS/NECROTIZING ANGEITITIS
CHARACTERISTICS:
- Necrosis (tissue death)
- Fibrosis (fibrotic scarring)
- Proliferation of cells (associated with inflammation)
CLASSIFICATION
1. Systemic Vasculitis
- Inflammatory conditions affecting both veins and
arteries
- Caused by proliferation of cells
2. Medium Sized Vessel Vasculitis
- Affecting medium and small sized blood vessel
found beneath the skin
3. Primary Childhood Vasculitis
- Affecting children under 18
- Predominantly in medium sized vessel but it is
more on children
ETIOLOGY
- UNKNOWN (idiopathic)
Viral Infections:
- Adenoviruses - cause flu-like symptoms,
pneumonia, bronchitis, conjunctivitis, sore eyes
- Enteroviruses - coxaqi virus (causes polio, HFMD→
hand, foot, mouth disease)
- Rhinoviruses - URTI upper respiratory infection,
ear/nose infections
- Coronaviruses - respiratory problems, pneumonia
RISK FACTORS
- Genetic
o Children with parents who have kawasaki
disease are more likely to acquire later in
life
o 1960s- first reported of a case on Kawasaki
- Infection
- Toxic Substances

5. o Bacterial superantigens that are produced
by particular bacteria like streptococcus or
Staphylococcus
SIGNS AND SYMPTOMS
1. FIRST PHASE (Acute phase – 1st 10 days)
- Abrupt onset of fever that lasts 7-14 days
typically described as high spiking and
remittent (remain high throughout)
- Bilateral conjunctivitis
- different with sore eyes because it is not painful and
no muta
- uveitis
- Rashes (cutaneous manifestations)
- Described as diffuse macular, popular
erythematous rash
- Swollen Lymph Nodes
- cervical lymphadenopathy.
- Irritability
- brought about fever
In the Mucosa:
- Red-cracked lips
- Bright red lips
- Vertical cracking
- fissures
- Strawberry Tongue
- Red tongue with spots
- Swollen red skin on hands and feet
2. SECOND PHASE (Sub-acute Phase)
- Begin when the fever have abated (subside); start of
the 2nd phase until 4-6 wks
- Hallmark sign: peeling of the skin or desquamation
of the skin of the lower and upper extremities
o Peeling of the skin
o Diarrhea
o Joint pain
o Abdominal pain and vomiting
o Coronary artery aneurysm
- bulging)
o Acquired heart disease in children
3. THIRD PHASE (Convalescent Phase)
- All clinical signs of the disease have resolved, but
laboratory values have not returned to normal
- Can take up to 6-8 weeks to return to Normal/ Within
3 months of presentation
Beau’s Line
- Deep transverse groove across the nails
- Usually, the resolution is in 3 months (return to
baseline date)
Diagnostic Examinations
- Electrocardiogram (ECG)
- Echocardiography
MEDICAL MANAGEMENT
1. Aspirin (Salicylate therapy)
- Given in high doses during the initial stage or
start of the therapy and lowered once the fever
subsides
2. Cyclophosphamide
3. Ulinastatin
4. Intravenous Immunoglobulins (IVIG)
- Standard treatment of Kawasaki
- Given high doses
- Expensive
- Improvement within 24 hours
5. Corticosteroids
- When symptoms recur, we give this
6. Infliximab
- Immunosuppression
• Repeat Echocardiography
• Cardiac Stress Testing
Nursing intervention
- Monitor pain
- Cardiac monitoring and assessment
- Monitor I&O - if may fever, it may place them at risk
for dehydration
- Plan Periods of rest and activities - allow the child to
have uninterrupted rest, provide soft toys, diversional
activities
- Provide oral care - Kawasaki affects the
mucocutaneous area
- offer cold liquids, ice chips, ice pops or give
soft/bland foods, use soft-bristled toothbrushes (only
when there are no fissures)
NOTE: BE PATIENT.
MULTIPLE MYELOMA
GAMMOPATHY
- Disturbance in the synthesis, problems in the
production of immunoglobulin
- Expect that there will be an abnormal proliferation in
the lmyphoid cells that produce immunoglobulins
- Include macroglobulinemia, Hodgkin’s Disease, and
multiple myeloma
MACROGLOBULINEMIA
- Plasma cell dyscrasia (generic term for the abnormal
condition of the blood) representing or resembling
leukemia with cells of lymphocytic, plasmacytic, or
intermediate morphology which secrete an
immunoglobulin M monoclonal component
- Expect hyperviscosity syndrome - more plasma cells
and more mature antibodies circulating in your

6. system → manifesting weakness, fatigue, bleeding
disorders and visual disturbances
- The peak incidence of this is during the 6th or 7th
decade of life
- The presence of increased levels of macroglobulins
in the circulating blood
- There is diffuse infiltration of bone marrow and also,
in many cases, of the spleen liver, or lymph nodes
HODGKIN’S DISEASE
- is a type of lymphoma, which is a cancer originating
from white blood cells called lymphocytes
- Is characterized by the orderly spread of disease
from one lymph node group to another and by the
development of systemic symptoms with advanced
disease
- Named after Thomas Hodgkin who first described
this abnormality in the lymph system way back in
1832.
- The diagnostic indication used to microscopically
examine the presence of Hodgkin’s disease is the
RS cells - Reed-Sternberg’s cells (characteristic and
histopathologic finding)
MULTIPLE MYELOMA
- A malignant disease of the most mature form of B
lymphocytes, the plasma cell
- Characterized by the proliferation of plasma cell
(subsequent overabundance of monoclonal
paraprotein/M. protein ← from the proliferation of
plasma cell. Present ang M protein sa blood, urine
and has no sepcific fucntion) from BM into the hard
bone tissue causing erosion of the bone
- Unknown cause
- Seen both in men and women and peaks at 60 years
old and above
- Intriguing feature: the antibody-forming cell/plasma
cell are malignant and therefore cause the unusual
manifestation
EFFECTS OF PROLIFERATION OF PLASMA CELL
- Interfere with the normal production of blood cells
o Leukopenia
o Anemia
o Thrombocytopenia
- May cause soft tissue masses/lytic lesions
o Plasmacytomas (refers to malignant
plasma cell tumor growing within the
soft tissues or within the actual
skeleton→ erosion)
THE ORIGIN OF MYELOMA CELL
Video link:
https://www.youtube.com/watch?v=tO39V2N9S_I
RISK FACTORS
- Chronic immune stimulation
- Autoimmune disorder
- Exposure to ionizing radiation
- Occupational exposure to pesticides or herbicides
CLASSIC TRIAD
- Plasmacytosis - there is an unusually large portion of
plasma cells in tissues, exudates, and blood. It can
be classified into two types: cutaneous or systemic
but both have identical skin findings
- Lytic bone lesion (plasmacytomas) - bone lesions or
lytic bone lesions will destroy your bone due to
erosion from cancerous plasma cells build up in the
bone marrow
- M. protein or Bence Jones Protein - found in urine or
blood
SIGNS AND SYMPTOMS
- Characterized by widespread bone destruction
- Bone pain (back ribs)
- Anemia
- Hypercalcemia 9constipation, thirst, altered mental
status, dehydration, confusion, and coma)
- Increase uric acid
- Splenomegaly
- Frequent recurring of infections
- Spontaneous pathologic fractures
- Blood viscosity (due to increased IgA)
COMPLICATIONS
- Bone pain
- Hypercalcemia
- Renal failure - patient will have proliferation of
plasma cells which increases Monoclonal protein
and proteins are usually filtered by your kidneys so
too much protein will affect the kidneys
- Spinal cord compression - because of the
proliferation
- Immunosuppression - due to the chemotherapy
management
CRAB
- C = Calcium (elevated)
- R = renal failure
- A = Anemia
- B = Bone lesions
DIAGNOSTIC TEST
- Bone marrow biopsy (confirmatory exam for Multiple
Myeloma)
- X-ray of bone
- (+) Bence Jones protein in the urine: urine
electrophoresis
- (+) M. protein: serum protein electrophoresis
MANAGEMENT
- Prevent infection - because the patient is
immunocompromised
- Chemotherapy:
o Vincristine (Oncovin), Cyclophosphamide
(Cytoxan)
o Dexamethasone (Decadron) - adjunctt to
chemo
- Thalidomide - oral agent with immunomodulator
properties
- BM Transplant
- Ambulation & adequate hydration - ambulation for
bone pain to prevent bone contractures, hydration

7. because of hyper viscosity and possibility of renal
failure
- Medication shown to strengthen bone, controlling
pain and bone fracture: by diminishing osteoclast
activating factor (biphosphates)
o Pamidronate ( Aredia)
o Zoledronic Acid (Zometa)
- Thalidomide (Thalomid): a sedative having an
antimyeloma effect
o Inhibits cytokines (Vascular endothelial
growth factor), IL-6, and tumor necrosis
factor.
o S/E: Fatigue, dizziness, constipation, rash
and
- peripheral neuropathy
- Bone marrow transplant- donor bone marrow cells
repopulate recipient bone marrow (top of the list for
management)
o adult position: prone
o child position: side-lying position
o site of donor: posterior iliac crest
QUESTION AND ANSWER:
1. What is multiple myeloma?
Multiple myeloma is a cancer of plasma cells. Plasma cells
develop from a type of white blood cell made in the bone
marrow and produce large amounts of a specific antibody
(immunoglobulin) that helps the immune system work. When
healthy plasma cells turn into malignant myeloma cells, they
produce a type of abnormal antibody called an M protein,
which is not something the body can use. These M proteins
increase and crowd out healthy functioning antibodies and
lead to symptoms seen with multiple myeloma.
2. What are common signs and symptoms of multiple
myeloma?
Both bone pain and anemia
Common signs and symptoms of multiple myeloma include
anemia (decreased red blood cells) and bone pain. Other
signs of multiple myeloma may include high levels of calcium
in the blood (symptoms include thirst, increased urination,
dehydration, constipation, abdominal pain, loss of appetite),
back pain, numbness, weakness, confusion, dizziness, kidney
problems, and infections. Hair loss is not a symptom of
multiple myeloma but it may be a side effect of treatment for
the disease.
3. What are the risk factors for multiple myeloma?
All of the above (race, gender, age)
4. How is multiple myeloma diagnosed?
Multiple Tests
The diagnosis of multiple myeloma is usually based on the
results of several diagnostic tests. In addition to a patient
history and physical examination, blood and urine tests and a
bone marrow biopsy are the first steps in making a diagnosis.
Other tests that may be used to confirm a diagnosis of multiple
myeloma include X-rays, MRIs, CT scans, and PET scans.
5. What are popular treatments for multiple myeloma?
All of the above
There are many different treatment options for multiple
myeloma which may include chemotherapy, drugs, and stem
cell transplants.
Other treatment options for multiple myeloma include steroids
and targeted agents such as lenalidomide (Revlimid),
thalidomide (Thalomid), and bortezomib (Velcade).
Patients may also be eligible for clinical trials of new treatment
options.
6. Multiple myeloma is a rare disease.
TRUE. Multiple myeloma is a rare disease. Fewer than 1% of
adults in the U.S. are diagnosed with multiple myeloma in their
lifetime. The National Cancer Institute estimates about
118,539 cases of multiple myeloma in the U.S. in 2014. It is
more common in men and people of African-American
descent.
7. What is most dangerous to a patient diagnosed with
multiple myeloma?
Infection is a danger to patients with multiple myeloma.
Healthy plasma cells make antibodies that fight infection. In
multiple myeloma, these cells are abnormal and grow out-of-
control, and the body(s immune system becomes unable to
fight off infection. People who have multiple myeloma get
bacterial and viral infections at a rate 7 times higher than
people who do not have the disease.
8. Effects of proliferation of malignant plasma cell are:
Blood dyscrasia, plasmacytoma, plasmacytosis
9. How is the prognosis determined for a patient with
multiple myeloma?
All of the above (stage of disease, age of patient,
condition of patient)
Several factors determine the prognosis for patients with
multiple myeloma:
- Stage of the disease
- Age of patient
- Health condition of patient at the time of
diagnosis
- Kidney function
- How fast the cancer cells are growing
- Certain chromosome changes
10. Proliferation of plasma cell in the bone marrow will
result to blood dyscrasia.
o TRUE
HYPERSENSITIVITY
- Is also known as allergic reaction
- Refers to excessive, undesirable reactions produced
by normal immune system
- Is any heightened immune response to an antigen
- Hypersensitivity is the overreaction to invaders and
foreign antigen that usually causes problems
○ e.g itching, hives

8. ○ It ranges from those uncomfortability to
severely damaged tissues e.g red blood
cells destruction, anaphylactic shock
- It does not usually occur with the first exposure to
antigen but rather the reaction follows at reexposure
(sensitization)
○ Sensitization is the build up or formation of
the antibodies during the first exposure to
the allergen
- Allergy - damaging immune response by the body to
a substance
- Allergy is an appropriate and often
harmful response of the immune
system to normally harmless
substances. These are actually
damaging immune response by
the body to a substance and what
usually causes your allergy are
your allergen
- The antigen causes the allergy is allergen
- Allergen that causes an allergic reaction
so basically an allergic reaction is a
manifestation of tissue injury resulting from
interaction between an antigen and
antibody
4 TYPES OF HYPERSENSITIVITY
Type I immunoglobulin E (IgE) mediated
hypersensitivity
Type II cytotoxic hypersensitivity
Type III immune complex hypersensitivity
Type IV delayed hypersensitivity
For easy memorization:
A - type I - IgE is also known as Antibody
C - type II - cytotoxic (starts with C)
I - type II - Immune complex (starts with I)
D - type IV - delayed (starts with D)
TYPE I HYPERSENSITIVITY
- Commonly called “allergic reactions”
- Systemic
○ anaphylaxis
- Local or atopic reactions (genetic)
○ Rhinitis (hay fever)
○ Food allergies
○ Bronchial asthma
○ Hives
○ Atopic dermatitis
- is also known as your first rapid
hypersensitivity reactions (mabilisan) ,
immediate or your atopic hypersensitivity
- Immediate hypersensitivity is mediated by IgE
- This is the type of hypersensitivity that usually
brings about antibody ee or your IgE. So the
mechanism of reaction usually involves the
production of IgE in type I. In response to
your certain allergens
Primary Cellular Component
- Mast Cell - In allergic response, mast cells
may not only contribute to the chronic
airway inflammatory response that will
happen during asthma and other
hypersensitivity reactions but also they may
have a central central role in the initiation of
an allergic immune response that is
providing signals inducing IgE synthesis by
lymphocytes.
- Basophils - Responsible for the release of your
cell mediator
○ Cell mediators: histamine and bradykinin
○ Amplified by
■ Platelets
■ Neutrophils
■ Eosinophils
SELECTED PERFORMED COMPONENTS OF
MAST CELL GRANULES
Granule
Component
Activity
Heparin Stimulates the generation of
bradykinin, which causes increased
vascular permeability, vasodilation,
bronchiole constriction, and
increased mucus secretion
Histamine Causes smooth-muscle
contraction, increases vascular
permeability, increases mucus and
tear formation
Serotonin increases vascular permeability,
Causes vasodilation and smooth-
muscle contraction,

9. SENSITIZATION STAGE
no s/sx
Antigen invades the body
↓
Stimulates B lymphocytes
↓
Plasma cells produce IgE
↓
IgE attaches to mast cells in the body tissue
End stage of sensitization stage is the production of the
antibody
SUBSEQUENT RESPONSE:
More of the same allergens invade the body
↓
Allergens binds to the sensitized mast cells
↓
degranulation of the mast cells
↓
Triggers release of chemical mediators
Vasodilation; increase permeability; smooth muscle spasm
A. Anaphylaxis
- Most severe form of type I
- Caused by common allergens
- s/s: itching , apprehension, anasarca,
circumoral edema, wheezing, dyspnea,
signs of vascular collapse of shock
- Can lead to death
Management
- Airway is maintained by ET ir tracheostomy as
necessary
- IV fluids
- Vasopressors - address decrease in BP brought by
anaphylactic shock
- Give epinephrine 1;1,000 solution, 0.3-0.5 ml sq/IM
- Antihistamine: Benadryl IVTT
- Hydrocortisone IVTT - this address inflammation
process
PREVENTION
- Identification of high risk person
- Patient education with allergens if known
- Desensitization - prevention or reduction of
immediate hypersensitivity
reaction by administration of small
doses
B. Urticaria & Angioedema
- Urticaria is usually caused by food allergen:
eggs, fish, nuts, seafoods , meds
- s/s: pruritic lesions with pale,pink wheel on
an erythematous background
Dermatitis medicamentosa - acute allergic reaction (skin)
- Angioedema - form of urticaria but involves
subcutaneous tissue rather than skin
- s/s:hives, swollen lips, periorbital edema
- Mgt: epinephrine, antihistamine,
corticosteroids
C. Atopic allergy
- Less severe form type I
- Reacts to pollen, fungal spores, house dust,
feather
- Common forms:
○ Hay fever (allergic rhinitis)
○ Atopic dermatitis (eczema)
○ Asthma
SEVERE FORM - RH INCOMPATIBILITY
1. Hydrops fetalis (Massive fetal red blood cell
destruction)
2. It causes Severe anemia →→ Fetal heart failure →→
Death of the infant shortly after delivery.
TYPE II CYTOTOXIC HYPERSENSITIVITY
REACTION
- Type 1 I E Type 2- G&M
- IgG or IgM antibodies directed against
target antigens on the surface cells or other
tissue components
- Has a reaction time of minutes - hours
- Ag-Ab reaction activates the complement
system
- Primary Cellular Component:
○ IgM
○ IgG
○ Complement System
Ex. (major cases)
- Mismatched BT reactions-hemolytic
transfusion reaction Ex. type b ka, tapos
ang nabigay sayo is type A
- Hemolytic disease of the newborn; HDN
due to ABO or Rh incompatibility
- Others:
○ Certain drug reactions
■ Antibiotics: #1 is
Penicillin
o Disorders:
o Myasthenia gravis - abnormal
disorder causes weakness in the
skeletal muscle; occurs when
communication between nerve
cells and muscles become
impaired and the body mistakenly
generates antibodies against
normal nerve ending receptors.
o Goodpasture syndrome/anti-
glomerular basement
membrane disease - a rare
autoimmune disease in which
antibodies attack the basement
membrane in the lungs and

10. kidneys it leads to bleeding of the
lungs and kidneys, the antibodies
react to the lungs adenal tissue
since there will be; it will produce a
lung and kidney failure
o Hemolytic anemia - Resulting in
RBC destruction associated with
RH; blood transfusion
incompatibility; destruction of
erythrocytes
Common Type II Hypersensitivities
Common Name Cause Signs and
Symptoms
Hemolytic
disease of the
newborn (HD)
IgG from mother
crosses the
placenta
targeting the
fetus’ RBCs for
destruction
Anemia, edema
enlarged liver or
spleen, hydrops
(Fluid in body
cavity),
Leading to death
of newborn in
severe cases
Hemolytic
Transfusion
reactions (HTR)
IgG and IgM bind
to antigens on
transfused RBCs
targeting Donor
RBCs for
destruction
Fever, Jaundice,
Hypotension,
disseminated
intravascular
coagulation,
possibly leading
to kidney failure
and death
Antigen Attached to foreign cell or tissue
↓
Plasma cells produce IgG or IgM
↓
Antibodies bind to tissue specific antigens
↓
Stimulate Complete activation
↓
Destruction of target cells by lysis phagocytosis or activation
of killer cells
Type 2 Disorders
- Autoimmune Hemolytic Anemia
- Rheumatic Heart disease
- Thrombocytopenia
- Erythroblastosis fetalis
- Goodpasture’s Syndrome
- Graves’ Disease
- Myasthenia Grtavis
TYPE III IMMUNE COMPLEX MEDIATED
HYPERSENSITIVITY REACTION
- AKA Immune Complex Disease - - It involves immune
complexes formed when antigens are bind with
antibodies
- Mediated by the formation of insoluble Ag-Ab
complexes that activates complement.
- Ideally, immune complexes must be removed from the
tissue, it should be kept from accumulating in the
circulation and forming deposits throughout the body
- Complexes are deposited in tissues or vascular
endothelium, as a result, there is an increase in
vascular permeability and tissue injury.
o Tissue injury is brought about by Ag-Ab
complex
Primary Cellular Component:
- IgG
- IgM
- IgA
- Complements
- Neutrophils
Antigen invades body
↓
Binds to antibody in the circulation
↓
Antigen-antibody complexes are formed
↓
Deposited in the membrane of
vessel walls & other tissues
↓
Activates complement system
↓
Enhanced opsonization
↓
Release of chemical mediators Cell lysis
↓
Tissue Damage
TYPE III: DISORDERS
- Serum sickness
- Rheumatoid Arthritis - Because of the nature of the
autoimmune disorder
- Post Streptococcal Glomerulonephritis
- Membranous nephropathy
- Reactive arthritis
- Lupus Nephritis
- Nephritis
SERUM SICKNESS
- Develops 1-3 wks after administration of large
amounts of foreign serum (horse antitetanus toxin)
- s/s: fever, urticaria, rash, lymphadenopathy
- Immune complexes can accumulate in the
glomerulus, blood vessels and joints.
TYPE IV DELAYED HYPERSENSITIVITY REACTIONS
- AKA Cellular Hypersensitivity
- Develop 24 to 72 hours after exposure to antigens
- Primary Cell Component: T-lymphocyte &
macrophage
- Delayed-type hypersensitivity
o Tuberculin test
o Allergic contact dermatitis
o Hypersensitivity pneumonitis
o Tissue / Graft transplant rejection

11. PDD TEST
- Purified Protein Derivative (PPD); usually done to
check if you have an exposure to tuberculosis; AKA
Mantoux Test
- Results are usually after 24 hours, 48 hours, 72
hours; 3 days monitoring
- A positive PPD = lalapad ang wheel or mamumula
(like in the picture); this indicates that the patient was
exposed to TB (not necessarily may TB ang patient)
CONTACT DERMATITIS
TYPES OF TRANSPLANT REJECTION
Types Description Treatment
Hyperacute
Occurs within
minutes to hours,
days after
transplant
Transplant can't
be saved
Acute
Occurs days to
months after
transplant, with
signs of
inflammation n &
impaired organ
function
Increase immune
suppression by
meds
Chronic
Occurs 4months
to years after
gradual
deterioration of
organ function
NONE, loss of
graft will occur,
requiring
retransplant
TYPE IV: DISORDERS
- Contact dermatitis
- Mantoux test
- Chronic transplant rejection
- Multiple sclerosis
○ Affects the brain and the spinal cord
causing wide range of potential symptoms
(includes problem of vision, movement,
sensation and balance; life-long condition
- Celiac disease
○ Digestive condition; small intestine is
inflamed and unable to nutrients.
- Hashimoto's thyroiditis
○ Opposite of Grave’s disease; may cause
Hypothyroidism; does not only have a
problem with the thyroid gland but with the
immune system as well
○ Considered as autoimmune disease
DELAYED HYPERSENSITIVITY
- SJS
○ o Stevens-Johnson Syndrome
○ o Brought about by medication
○ o Milder form of TEN
- Lyell’s Syndrome/TEN o Toxic Epidermal Necrosis
[Necrolysis]
- Both diseases can be mistaken at times with a
condition called Erythema Multiforme (also caused
by medications; more often a reaction to an infection)
ETIOLOGY
- Idiopathic
- Drug-induced
- Infection
- Malignancy-related
SIGNS AND SYMPTOMS
- Cough
- Fatigue
- Fever and Chills
- Headache
- Muscle and joint pain
- Sore throat
MANAGEMENT
- Fluid Replacement
- Wound Care
- Eye Care
- Pain Medication

12. - Antihistamine
- Antibiotics
- Topical Steroids
- lmmunoglobulin intravenous
- Skin Grafting
HYPERSENSITIVITY REACTION
Type 1 Type 2 Type 3 Type 4
Antibody mediated immunity Cell mediated
Immunity
IgE IgG, IgM T helper cells
(Th1)
Fast
response
(Minutes)
Intermediate Late response
(48-72 hours)
Allergic
Reactions
Body cells
directly
attacked by
antibodi es
Complex
accumul
ation and
destruction
Cell mediate d
cytotoxicity
Asthma
Allergic
rhinitis
Rheumatic
heart disease
Autoimmune
hemolytic
anemia
Rheumatoid
arthritis
Poststreptoc
occal
glomerulone
phritis
Transplant
rejection
Contact
dermatitis
QUESTION AND ANSWER
1. True/false: An anaphylactic reaction can be as
simple as developing a rash after exposure to an
allergen.
- FALSE. Anaphylaxis typically involves
more than one symptom in more than one
part of the body at the same time. For
instance, a serious reaction could involve
developing a rash and vomiting or diarrhea
after being exposed to an allergen. Other
warning signs of a serious reaction include:
o Swollen throat or swollen areas of
the body
o Wheezing
o Passing out
o Chest tightness
o Trouble breathing
o Hoarse voice
o Trouble swallowing
o Stomach cramping
o Pale or red color to the face and
body
o Feeling of impending doom
o The most dangerous symptoms
are low blood pressure, breathing
difficulty and loss of
consciousness, all of which can be
fatal.
2. True/False: Anaphylaxis can occur from eating
common foods such as milk, eggs, or shellfish.
- TRUE. These common foods may be
harmless substances for most people but
having an allergy to these or any other
foods can trigger an allergic reaction. Foods
that cause the majority of life-threatening
reactions are peanuts, tree nuts (such as
walnuts, cashews, Brazil nuts), shellfish,
fish, milk, and eggs.
3. True/False: If you had a mild allergic reaction to an
allergen in the past, then you are not at risk for a life-
threatening reaction in the future.
- FALSE. While having previous mild
reactions to an allergen is a strong predictor
regarding the intensity of future reactions, a
mild reaction does not guarantee that your
next reaction won't be more serious.
4. True/False: Epinephrine should be given early in
symptoms of anaphylaxis.
- TRUE. Auto injectable epinephrine
(adrenaline) should be given early to help
stop or slow down the reaction from getting
worse. People with a severe allergy or a
history of anaphylaxis should carry
epinephrine with them at all times.
Remember to refill your prescription if your
epinephrine has expired.
5. True/False: Antihistamines and corticosteroids are
good substitutes for epinephrine in treating
anaphylaxis.
- FALSE. Antihistamines and corticosteroids
can sometimes be used in addition to
epinephrine, but these medications are not
a substitute for epinephrine.
6. True/False: Anaphylaxis always requires medical
treatment.
- TRUE. Anaphylaxis requires immediate
treatment. First with an injection of
epinephrine, followed by a trip to a hospital
emergency room. If it isn't treated properly,
anaphylaxis can be fatal. Sometimes
symptoms go away, and then return a few
hours later, so if you have taken
epinephrine and are feeling better, go to the
hospital anyway to make certain your
reaction is under control. Once you've had
an anaphylactic reaction, be sure to tell
your allergist.
7. Symptoms of anaphylaxis can occur:
- EITHER shortly after coming in contact with
an allergen or hours after coming in contact
with an allergen.
- While anaphylaxis typically occurs within
minutes or even seconds after exposure to
an allergen, it is possible for symptoms to
be delayed an hour or more. There are also
cases where symptoms go away only to
return a few hours later.
8. Which of these are not likely to cause anaphylaxis?
- POLLEN. Out of this group, pollen is not
known to cause life-threatening reactions.
Medications, foods, latex and stinging

13. insects are allergens most likely to cause
anaphylaxis. While rare, there is a chance
of experiencing a serious reaction after
exercising.
9. Epinephrine should be injected into the:
- THIGH. Evidence shows that epinephrine
should be given in the anterior thigh
muscle.
10. If you are at risk for anaphylaxis, the best way to
manage your condition is:
- ALL OF THE ABOVE: avoid allergens
that trigger symptoms, carry auto
injectable epinephrine, know how to use
epinephrine, develop an anaphylaxis
action plan.
- The risk of you or your child suffering a life-
threatening allergic reaction is frightening.
Being prepared for an emergency can help.
Work with your allergist / immunologist to
identify allergens that trigger symptoms so
that you can avoid these allergens. Your
physician can help you develop an action
plan for emergency situations. Know how to
administer epinephrine and teach others
who are in close contact with you or your
child. Last, but not least, keep epinephrine
close by at all times for emergency use.
11. Which of the following are examples of type III
hypersensitivity:
- Rheumatoid arthritis and arthus reaction
12. Type IV hypersensitivity is mediated by:
- T Cells
13. The principal antibodies involved in type II
hypersensitivity are:
- IgG and IgM
14. Jeremy's own body cells and receptors are under
attack by antibodies that his body produced. These
types of antibodies are referred to as:
- Autoantibodies.
15. A 21-year-old woman is stung by a bee. Within 5
minutes she develops severe dyspnea. On her skin
are blotchy areas of erythema. She is given an
injection of epinephrine and improves over the next
30 minutes. She receives therapy over the next year
in which she receives small injections of bee venom.
The most likely goal of this therapy is replacement of
which of the following forms of immunoglobulin on
her mast cells?
- IgE. She has type I hypersensitivity. She
has increased amounts of IgE bound to
perivascular mast cells in her airways.
Upon encounter with a specific antigen, the
antigen binds to IgE and the mast cells
degranulate, releasing vasoactive amines
which mediate the symptoms through
edema. By 'desensitizing' her with injection
of small amounts of the allergen, it is hoped
that there will be gradual replacement of the
IgE with IgG, so that subsequent antigen
encounters will not be life-threatening.
INFLUENZA
- Common called as “flu” - self-limiting
- Sometimes, complications of influenza can be
deadly
- High risk: Young children (5 years old), and Older
Adults (65 years old) like residents of Nursing Home
(reverse isolation), pregnant women, postpartum 2
wks; weak immune system, comorbidities), obese
- viral attacks that attack the respiratory system (nose,
throat, and lungs)
- Common infectious disease or highly contagious
disease brought about the airborne
- Occurs in seasonal weather/epidemic
- Acute manifestations: fever
- Systemic symptoms may appear: Mild fatigue to
respiratory failure to death
3 MAJOR TYPES OF INFLUENZA
- Type A
- Type B
- Type C
Note:
- Type A and B are used in the formulation of vaccines.
Type A Subtypes:
- Hemagglutinin (17 classes)
- Neuraminidase (9 classes)
Note: Present in Swine flu (H1N1)
- Hemagglutinin and neuraminidase are proteins
- Hemagglutinin viral proteins attach to the surface of
the cell or act as a receptor, while the Neuraminidase
detaches
1. Influenza A (H1N1) Virus - Swine Flu
- A subtype of influenza A virus and was the most
common cause of human influenza (flu) in 2009
influenza
- Highly contagious respiratory disease
- In pigs originally, but it transmitted to humans
- How: Through contact with fluids from the pig
MOA- SWINE FLU (Video)
2. Avian Flu H5N1 - Bird Flu
- An infection in birds caused by an influenza virus
- A result of either handling dead infected birds or
from contact with infected fluids (for example
chickens, ducks, and turkeys)
- Started from species of waterfowl found in the wild
- Way back in 1997 on an island in Hong Kong, that
was the time it started infecting humans from
chickens
- A pig with swine flu can not be transmitted through
food, as long as it is cooked or handled properly. Just
do not come in contact with the secretions.
3. Severe Acute Respiratory Syndrome
- Life-threatening viral respiratory illness caused by
coronavirus known as SARS-associated
coronavirus (SARS-CoV)

14. - SARS-CoV1 - November 2002,
Guangdong Province of Southern China -
800+ deaths, 8,400+ cases
- SARS-CoV2 - Wuhan, China, started on
November 2019 and spread to Hong Kong
to 32 other countries
- Saudi calls this MERS (Middle East
Respiratory Syndrome)
- Fever, cough, diarrhea
- Transmitted by close person-to-person contact by
respiratory droplets produced by the infected
person who coughs or sneezes (fecal-oral route)
SIGNS AND SYMPTOMS
STAGE 1: FLU LIKE PRODROME (STARTS: 2 TO 7
DAYS AND LASTS: 3 TO 7 DAYS)
Characteristics:
- Fever (>38C)
- Fatigue
- Headaches
- Chills
- Myalgias
- Malaise
- Anorexia
Less common symptoms:
- Sputum production
- Sore throat
- Coryza - whooping cough
- Nausea and vomiting
- Dizziness
- Diarrhea
- Conjunctivitis (H5N1)
STAGE 2: LOWER RESPIRATORY TRACT PHASE
(STARTS: 3 OR MORE DAYS)
Characteristics:
- Dry cough
- Dyspnea
- Progressive hypoxemia
- Respiratory failure (x-ray: infiltrates)
Note: after 7 days, may abnormalities na
CLINICAL MANIFESTATIONS:
STARCHED - 7 days incubation period
- ST = Sore throat
- A = Aches (body, joints, head)
- R = Runny nose
- C = Chills / cough
- H = High fever / headaches
- E = Easy fatigability
- D = Dry cough
DIAGNOSTIC TEST
- RT-PCR
o Test to detect the definitive number of viral
particles/viral RNA)
- Rapid Antigen Or Antibody Immunoassays
o Test to detect an antigen for any microorganism.
It is generic that is why it is difficult to know if you
have COVID/SARS-Cov1
- Viral Culture
○ tinitignan kung saan na virus siya mag react
- CXR
○ If the result stated ‘infiltrates’ → having an
abnormal area in the lungs; It can be
localized, one/both lungs; Poorly defined
TREATMENT/MANAGEMENT
- Antipyretic - fever
- Analgesics - myalgia
- Increased fluid consumption - dehydration
- Bedrest - energy
- Antiviral agents (Oseltamivir / Zanamivir) - for the
viruses
- Isolation - to prevent further transmission
- Influenza virus quadrivalent (Afluria Quadrivalent,
Fluarix)
- Other antivirals like oseltamivir (Tamiflu) and
zanamivir (Relenza) - Tamiflu was popular before
- Electrolyte replacement - for hydration
- Vaccination - Influenza virus vaccine trivalent -
tatlong klase which fights three strains of the virus,
(Fluad, Fluzone, Flucelvax) can be given to 6 months
and above
- Gives protection from 2 A and 2 B influenza -
Quadrivalent (Allowed in 2 years old and above)
NURSING MANAGEMENT
- Ensure adequate rest
- Proper disposal of wastes used by suspected
patients such as tissues and other disposable items
- Person should wash their hands with soap and water
after touching used tissues and similar waste
- Nurses should try to maintain a distance of 6 feet or
more from the person with a suspected and
confirmed case of H1N1 virus
- Nurses should keep their interactions with ill persons
as brief as possible
- The ill person should be asked to follow good cough
etiquette and hand hygiene and to wear a facemask,
if able, and on is available
- Nurses and other workers who are
immunocompromised or at increased risk of severe
illness from influenza infection should avoid handling
H1N1 patients
- Wear a face mask or N95 respirator or higher filtering
facepiece respirator certified by the Center for
Disease Control and Prevention (CDC) / National
Institute for Occupational Safety and Health (NIOSH)
- Proper disposal of waste

15. EBOLA HEMORRHAGIC FEVER
- A rare and deadly disease caused by infection with
one of the Ebola virus’s strains. Ebola can cause
disease in humans and nonhuman primates (bats,
sick/dead people with ebola virus).
- Etiologic agent: Ebola Virus
- Mainly present in Sub-saharan Africa
- 1976, Ebola River affecting people from time to time
- outbreak
Note:
- Arenviridae infects rodents and humans
- Bunyaviridae infects vertebraes
- Invertebrates
- Filoviridae
- Deadliest ang Ebola, you can die from bleeding
6 SUBTYPES OF EBOLA VIRUS
Most common type:
o The 4 have caused disease in people
- Ebola virus (species of Zaire ebolavirus)
- Sudan virus (species of Sudan ebolavirus)
- Tai Forest virus (species of Tai Forest
ebolavirus, formerly Côte d’Ivoire ebolavirus)
- Bundibugyo virus (species of Bundibugyo
ebolavirus)
The preceding 4 cause disease in humans
- Reston virus (species of Reston ebolavirus)
- not in human
- found in primates and pigs
- Bombali virus (species of Bombali ebolavirus)
- first identified in bats (2018)
- on study it can cause disease animals
○ 2014-2016: 3 Major African Countries
that has an ebola Outbreak
• Guinea
• Libya
• Sierra Leone
▪ 11,000 deaths; 28,000
cases
MODE OF TRANSMISSION
- Direct contact with the blood, body fluids and tissues
of animals affected
- Direct contact with body fluids of a person who is sick
with or has died from EVD
- Gets into the body through broken skin or mucous
membranes
- Sexual contact
- Blood or body fluids (urine, saliva, sweat, feces,
semen, breastmilk)
- Objects (clothes, bedding, medical equipment)
- Infected fruit bats or nonhuman primates
- Semen from a man who recovered from EVD
Note: The ebola virus is still present 10 days post-mortem or
even 10 weeks later
SIGNS AND SYMPTOMS
DRY symptoms - (2-21 days after the contact with virus:
average 8-10 days for the symptoms to appear)
- Fever
- Aches and pains (severe headache and muscle and
joint pain)
- Weakness and fatigue
- Sore throat
- Loss of appetite
WET symptoms
- Abdominal pain, diarrhea, and vomiting
- Unexplained hemorrhaging, bleeding or bruising
- Skin rash
- Red eye
DIAGNOSTIC TEST
Within a few days after symptoms begin:
- Antigen-capture enzyme-linked immunosorbent
assay (ELISA) testing
- IgM ELISA
- Polymerase Chain Reaction (PCR) - detect low
levels of ebola virus
Later in disease course or after recovery:
- IgM and IgG antibodies
Retrospectively in deceased patients:
- Immunohistochemistry testing (Like doing autopsy to
the patient)
- PCR
- Virus isolation (Post-mortem examination that
usually includes the diseased lymphoid organs)

16. MEDICAL MANAGEMENT
- Symptoms of Ebola and complications are treated as
they appear
- Provide intravenous fluids and balancing electrolytes
in the body (For “dry” symptoms)
- Maintain oxygen status and blood pressure
(especially if patient is in “wet” symptoms)
- Treat other infections if they occur
- Drugs: Inmazeb October 2020 and Ebanga
December 2022 (can be used by children)
- ERVEBO - 1st US FDA-approved vaccine December
2019 to treat EVD caused by specie Zaire
PREVENTION
- Practice careful hygiene
- Do not handle items that may have come in contact
with an infected person’s blood or body fluids
- Isolate patients with ebola from other patients
- Practice proper infection control and sterilization
measures
- Wear appropriate personal protective equipment
- Notify health officials if had direct contact with blood
or body fluids of a person who is sick with Ebola