Cute si dims J

Immunology
Ms. Jaidee R. Rojas

• Cytoplasm – type of organelle and fluid-filled por7on of the cells that holds the organelles
together.
• Descrip4on of types of WBC (white blood cells):
o Neutrophils
§ mul7-lobed nucleus specifically three.
§ pale red, blue cytoplasm.
§ it has li>le dots when seen at the microscope called granules.
o Eosinophils
§ Bi-lobed nucleus.
§ the only colored pink cytoplasm.
§ it has granules.
o basophils
§ bi-lobed nucleus
§ purplish-black cytoplasm
§ it has granules.
• note: neutrophils + eosinophils + basophiles they will be called as
granulocytes because all of them has granules present.
o Lymphocytes
§ Large spherical nucleus
§ Thin rim with a color of pale-blue cytoplasm
§ Agranulocytes (no granules present)
o Monocytes
§ Kidney shaped nucleus
§ Abundant pale blue cytoplasm
§ Agranulocytes (no granules present)
• Defini4on of terms (basic concepts)
o Immune system – collec7on of organs, cells, 7ssues, and molecules that mediate
the immune response.
o Immune response – the coordinated response of the components of the immune
system to a foreign agent or organism
o Immunity – the body’s specific protec7ve response to a foreign agent or organism
§ Immunity = protec7on
o Immunopathology – study of disease result in dysfunc7ons within the immune
system.
• Immune system
o Green peas in the body is called the lympha4c nodes
o Lympha7c system it is part of the immune system.
§ Complementary to circulatory system in which they work together.
§ Func4on of lympha4c system:
• It fights infec7on.
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• Removes the waste products.

• Drains excessive fluids and proteins, then return them back to the
blood streams.
o Lymphedema complicaAon of post mastectomy in which
there is removal of the tumor, remove the nodes to ensure
no reoccurrence would occur, posiAon the paAent at semi-
fowlers because if there is no nodes then no one will drain
the excessive fluids à edema
o Types of nodes:
§ Adenoids
• It is a lympha7c 7ssue.
• loca4on: upper back of the nose
• func4on: it protects the body against infec7on that enters the nose.
• Largest unit during childhood,
o if the adenoids are inflamed à there is risk for airway
obstruc7on. Mostly occurs during childhood.
o Removal of the adenoids is adenoidectomy a person can live
even without adenoids it is just a small node.
§ Tonsils
• It is a lympha7c 7ssue.
• Loca4on: middle of the nose, mouth, and throat
• Func4on: it protects the body against infec7on that enter the
mouth
o When tonsils are inflamed à risk for airway obstruc7on
o Removal of the tonsils is tonsillectomy.
o a person can live without tonsils.
§ Peyer patches
• Loca4on: small intes7nes specifically at the ileum.
• Func4on: it protects the body against infec7on that could be found
within the G.I tract.
• Kupffer cells
o Can be found at the liver of the pa7ent.
o Organ structures
§ Thymus
• Bu>erfly shaped organ
• Loca4on: Infront of the lungs by the sternum
• Func4on: responsible for the produc7on and matura7on of T-cells
• It is the most ac7ve organ because it produces thousands of T-cells
and largest
• Development of thymus:
o Childhood: it will con7nuously produce T-cells.
o Puberty: it will shrink in size
o Adulthood: it will con7nuously shrink à become fats
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§ Spleen
• Loca4on: leQ upper abdominal quadrant (LUQ) beneath the
diaphragm
• Largest internal organ of the immune system
• Highly vascular organ 25% that came from the heart will go to the
spleen for cleaning to ensure that the blood cells are cleansed as
they circulate the body.
o Parts of spleen that works for filtering and cleansing.
§ Red pulp – for filtering and cleansing; site where the
old and damaged cells are destroyed.
§ White pulp – contains massive amounts of
lymphocytes for protec7on.
o Enlargement of the spleen is called splenomegaly.
§ Normal size of the spleen: 170g à 1.8kg when there
is damage or injury.
§ Removal of the spleen is splenectomy and when the
spleen is removed the paAent is risk for infecAon thus
the doctors would prescribed anAbioAcs
§ Bones
• Parts of the bones
o Long part of the bone is called compact bones or known as
the diaphysis when cut in half there is the yellow bone
marrow which is a fats.
o The ends of the bones is called spongy bones or known as
the epiphysis when cut in half there is the red bone marrow
in which it contains the actual RBC makes it red in color
o Connects the compact and spongy bones is called
metaphysis, when a person gets taller the metaphysis
stretches in length and when the person stops growing,
during x-ray there will be the epiphyseal plate indicator that
the metaphysis is hardened also known as the best height.
• Hematopoiesis producAon of the RBC
o Process:
§ Stem cells it is the starAng cells its funcAon is to mature to other cell types
known as the hemocytoblast à produces two daughter cells à separates
in to (1) myeloid stem cell and (2) lymphoid stem cell.
§ Myeloid stem cell à it will produce 4 daughter cells such as
megakaryoblast if there is “blast” it is considered as immature cell type and
non-funcAonal; can’t be used, proerythroblast, myeloblasts, monoblast
• Megakaryoblast à megakaryocytes if it is “cyte” it is fully
funcAonal à PLATELETS used for cloNng.
• Proerythroblast à reAculocytes à ERYTHROCYTES or RBC
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• Myeloblast or known as immature WBC à produces the following:

o BASOPHILS
o NEUTROPHILS
o EOSINOPHILS
• Monoblast à monocytes à MACROPHAGES
§ Lymphoid stem cells à lymphoblast à produces two natural killer cells
(large granular lymphocytes) and small lymphocytes.
• Small lymphocytes à (1) T-lymphocytes stored in the thymus, (2)
B-lymphocytes stored in the bone marrow.
• Types of immune response
o 2 types
§ Innate the first responders and will go to the site of infec3on first.
• Non-specific they cannot iden3fy from one pathogen to another pathogen; “I
don’t know you but I will kill you.”
• Fast it can be known as the fever-response when there is possible infec3on in
which increased temperature à kills the infec3on
• Has no memory
• Physical and chemical barriers
o Physical barriers: skin, and mucus membranes
o Chemical barriers: sweat, saliva, and tears.
• Involved in innate response:
o Polymorphonuclear – it is known as neutrophils most
abundant circulaAng white blood cells which is 60-70%
§ Phagocytosis – engulfing of the pathogens à lowers
the pH level of the pathogen à increased acidity à
kills the pathogens.
§ if the neutrophils keep on engulfing pathogens there
will be self-destruc7on that will occur, along with
that the neutrophils will also die.
o Eosinophils – responsible for killing the parasi7c infec7ons.
o Basophils – responsible for allergic response and it secretes
the histamine and other inflammatory molecules such as
leukotrienes like montelukast; exclusively found in the
blood.
o Mast cells – involved in the allergic response and it secretes
histamine and other inflammatory molecules such as
leukotrienes; found in the 4ssues.
o Monocytes or macrophages – it is a phagocy7c cell kills the
pathogens through engulfing process and found in the
4ssue.
o Dendri4c cells – it has finger-like projec7ons it is the anAgen
or prototypical anAgen presenAng cell it will travel body
cells to find the an7bodies.
o Natural killer cells – it can iden7fy cancer cells.
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§ Adap4ve back-up responders

• Highly specific there are specific anAbodies present for every
anAgen.
• Must be ac7vated, takes week it will take Ame to find the perfect
anAbodies to kill the anAgens.
o An<gen presen<ng cell à goes to the site à gets a piece of
that anAgen à it will travel through the anAbodies to see
what compaAble anAbodies to kill that anAgen and it takes
Ame such as days. à an7bodies go to the site and kills the
an7gen.
• Has memory
o Example: such as chicken pox in which once you get varicella
virus it will be remembered by the body does make the body
immune to that specific virus.
• Involved in adap7ve response:
o B – cells – secretes an7bodies.
o T – cells – cytotoxic T cell
§ Types:
• Killer T – cells it kills the pathogens.
• Helper T – cells coordinate the immune
response.
o It releases cytokines as a signal for
blood cells to go the site of infec7on.
• Regulatory T – cells it is known as the
suppressor T-cells.
o It limits the strength of the immune
response especially aQer the
infec7on is resolved.
o Because without regulatory t-cell
there will be hypersensi7vity.
• Types of immunoglobulins: GAMED
o IgG
§ Most abundant an7bodies
§ If there is placenta involvement and it is the natural adap7ve immunity and
can cross over the placenta
§ Responsible for protec7ng the body against the bacteria, viruses.
§ Involved in chronic infec7on.
§ Innate in chronic infec7on response
o IgA
§ Produced by the mucus membranes.
§ Only an7body can cross the breast milk of the mother bluish white or
colostrum.
§ Sweat, saliva, and tears.
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§ Can be seen in the following:

• GI
• Respiratory tract
• Genitourinary
o IgM
§ Largest in size which keeps these an7bodies from travelling.
§ Found in blood and lympha7c fluids.
§ Innate in acute infec7on response.
§
o IgE
§ For allergies response
§ Has basophils, mast cells and less abundant (<1%)
o IgD
§ Least understood an7body
§ B-cells à plasma cells there is involvement of the IgD
• Immunopathology
o Hypersensi4vity
§ Exaggerated immune response such as conAnuous phagocyAc process
during pathologic aWack.
§ 4 types: (First three types are immediate hypersensiAvity because their
reacAon would happen in the first 24 hours)
1. Type I (more on allergic reacAons)
a. IgE an7body mediated hypersensi7vity
i. Sensi4za4on – the first encounter with the
allergens with no symptoms (asymptomaAc) à IgE
bind with basophils and Mast cells it is like Acking
Ame bomb because anyAme s/sx can show up, and
they are just waiAng for the allergens.
ii. The following are the S/SX a^er sensiAzaAon:
1. Bronchospasm – secondary to the smooth
muscle contrac7ons.
2. Hypotension
3. Hypovolemia
a. There is peripheral vasodilaAon in
which there will be increase amount
of histamine in the body thus results
to hypotension and hypovolemia.
4. Erythema – extravasa7on of capillary blood
5. Edema – through fluid shiQing into
interspa7al spaces.
6. Pruritus and hives – when itchiness occurs.
iii. There is signs and symptoms because of the effect
of basophils and mast cells.
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iv. Most dangerous allergic reac7on is anaphylac4c

reac4on, and its medica7on is epinephrine given IV
or IM
b. Allergic rhini7s, allergic conjunc7vi7s, asthma anaphylac7c
reac7on
c. Diagnos4c test:
i. Skin prick test – common sites involved in the upper
arm, forearm or back.
ii. Scratch test
iii. Intradermal test – high risk for false posi7ve test
iv. Blood test allergens specific
d. Management:
i. Treatment will depend on the cause of reac7on.
ii. Preven4ve treatments are most effec7ve form of
management.
2. Type II (cytotoxic; CY toxic)
a. An7gen – an7body complex
i. An7body involved à got confused in binding to an
an7gen à hypersensi7vity (mismatched binding or
accidental binding) Cell lysis à inflamma7on and
phagocytosis à 7ssue damage.
ii. It binds at the cell surface.
b. If bind by mistakes occurs the following occurs:
i. Hemolysis
ii. systemic disorders (myasthenia gravis, rheumaAc
fever, and graves’ disease)
3. Type III (immune complex)
a. An7gen (soluble) – an7body bind by mistakes à deposiAon
in the Assue à complement (C3, and C4) cascades.
i. If there is ac7ve inflamma7on à C3 and C4
decreased because they will go to the site and
decrease in number
b. Autoimmune disorders
i. Rheumatoid arthri7s
ii. SLE
iii. Glomerulonephri7s
4. Type IV – (delayed hypersensiAvity a^er 2-3 days)
a. T-cell mediated immune reac7on.
b. Diagnos4c test:
i. Tuberculin skin test
1. Interpreta7on takes 2-3 days for reac7on to
occur.
ii. contact derma77s
iii. graQs rejec7on
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1. graZs VS host disease

a. for example
i. you donated a blood and
there is reacAon.
ii. Donated a stem cell and there
is reacAon. Gra^s resistance
disease
iii. DonaAon should be allogenic
which means it should come
from other people.
iv. Transplant rejecAon
o Diffuse connec4ve 4ssue disease
§ Rheumatoid arthri4s
• Autoimmune disease of unknown origin (idiopathic)
• Cause inflamma7on of the joins
• Female having 3x more at risk than males.
• Onset occurs between third and sixth decades of life.
• Risk factors:
o Gene7cs
o Obesity
o Smoking
• Synovium joints à damage in the synovium joints Rheumatoid
arthri4s
o Membrane or lining of the joins for lubrica7on.
o
• Car4lage à osteoarthri4s (wear and tear; not an autoimmune
disease)
o Can be seen at the bones and shock absorber.
o Unilateral affecta7ons or localized pain felt by the pa7ent.
• Note: RA and OA is different in nature as RA is autoimmune disease
while OA is not.
• Stages of Rheumatoid arthri4s: (synoviAs à pannus à fibrous
ankylosis à bony ankylosis)
o Synovi4s
§ Inflamma7on in the synovium
o Pannus
§ There is fibrous 7ssue forma7on it is a thickened
Assue.
o Fibrous ankylosis
§ Ankylosis is known as the fusion of the joints using
the fibrous.
o Bony ankylosis
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§ permanently fused bones and permanent

immobility
§ Most severe stage
• Diagnos4c test (there is no single confirmatory test to iden3fy the exact
autoimmune disease)
o An4nuclear an4body (ANA)
§ Iden7fy the number of autoan7bodies and these are
the anAbodies that binds by mistake.
o Rheumatoid factor
§ Iden7fy the number of autoan7bodies.
o Erythrocyte sedimenta4on (ESR)
§ Iden7fy the amount of inflamma7on.
o An4-cyclic citrullinated pep4de an4body (an4-CCP)
§ It talks about the RA.
§ It iden7fies the specific an7body that can be found
in the joints of the pa7ent.
o C-reac4ve protein test
§ Partner of the ESR which helps iden7fy the
inflamma7on.
o Complement test (C3, C4) test.
§ It is lower in number.
o CBC, Serum chemistry
o X-ray of joints, direct. Arthroscopy
o Synovial fluid aspirate/biopsy
• Signs and symptoms
o Symmetric joint pain
o Morning joint s7ffness las7ng longer than 1 hour.
o Small joints of hands, wrists, and feet à knees, shoulders,
hips, elbows, ankles, cervical spine
o red, hot, swollen painful joints.
o Extra-ar4cular (symptoms located outside the joints)
features:
§ Fever
§ Weight, fa7gue earliest sign
§ Anemia, lymph node enlargement, and Raynaud’s
phenomenon (mamumuA ang daliri due to lack of
blood flow or cyanosis)
RA Proximal IP Distal IP
Boutonniere Flexed hyperextend
deformity
Swan neck hyperextend flexed
deformity
OA Proximal IP Distal IP
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Heberden’s Bony swelling

nodes
Bouchard’s Bony swelling
nodes

o Ulnar devia4on = ulnar driQs

o Rheumatoid nodules that grow in the arms of the pa7ent
with chronic RA but it is sAll idiopathic and known to be so^
Assue swelling and generally painless.
• Medica4on management
o NSAIDs – it causes GI ulcers.
§ Ibuprofen
§ Naproxen
o Cor4costeroids – it is not the standard DOC because of so
many adverse effects such as hyperglycemia, osteoporosis,
skin bruising, immunosuppression.
§ Dexamethasone
§ Methylprednisolone
§ Prednisone
o Disease modifying an4-rheuma4c drugs
§ Hydroxychloroquine not the DOC because of its
Irreversible reAnopathy (pagkabulag) adverse effect
§ Methotrexate – STANDARD TREATMENT FOR RA
§ Sulfasalazine
• Surgical management
o Reconstruc4ve surgery
o Synovectomy – surgical removal of synovium not
recommended for paAent with RA since it does not have
cure and it can reoccur anyAme.
o Arthrodesis – surgical fusion of the joints when inflamed
joints are moved it can be painful for the pt. thus with the
fusion of the joints it lessen the pain and for palliaAve
purposes to relieve the symptoms of pain.
o Arthroplasty – surgical replacement of the joints and
changed to prosthe7c which can me (1) metal, (2) ceramic
or (3) plas7c depending on the needs of the paAent.
• Nursing management
o Priority: acute and chronic pain
§ Provide variety of comfort measure
§ Applica7on of heat and cold to reduce the pain
§ Posi7on changes every 2 hours – to reduce the
immobility.
§ Suppor7ve pillows and splints to reduce deformity.
§ Relaxa7on technique
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o Administer medica7on as prescribed.

o Encouraged verbaliza7on of feelings
o If fa4gue…
§ Provide educa7on about fa7gue.
§ Facilitate making of ac7vity/rest schedule.
§ Encourage adequate nutri7on.
§ Encourage adherence to treatment program.
o If impaired mobility…
§ Encourage verbaliza7on regarding limita7ons.
§ Assess need for physical therapy referral.
§ Assist to iden7fy environmental barriers.
§ Encourage intendance in mobility and assist as
needed.
§ Systemic Lupus Erythematosus (SLE)
• Inflammatory autoimmune disorder that affects nearly every organ
in the body.
• More in common to females than males 9 out of 10 are SLE paAents.
• No cure so far. With periods of flare ups/exacerba4ons symptoms
has worsen.) and remission (symptoms disappeared)
• Types of SLE:
o Systemic lupus erythematosus – most common
§ Risk factors.
• Gene7cs has a strong geneAc associaAon
and it a relaAve risk factors.
• Immunologic
• Hormonal high estrogen à increased risk for
SLE.
• Environmental
o Sunlight
o Fluorescent light bulbs
o Viral infec4ons:
- Epstein barr virus,
- cytomegalovirus (CMV), and
- Varicella
o Medica4ons can trigger SLE, such as
the following:
- Procainamide
- Minocycline
- Hydralazine
• Emo7onal stress
• Stress on the body like surgery and
pregnancy
§ Manifesta4on: rash happens symmetrically
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o Cutaneous lupus – limited to the skin.

o Drug induced lupus – caused by drugs.
o Neonatal lupus – affects infants of women who have lupus
• Diagnos4c test:
o An7nuclear an7body ANA test
o Erythrocyte sedimenta7on rate (ESR)
o C-reac7ve protein test
o An7-dsDNA test
o An7-Sm an7body (an7-smith)
§ These two tests are exclusive for lupus.
o Complement test (C3, C4)
o CBC, serum chemistry
• Signs and symptoms per organ
o Lungs
§ Tachypnea
§ Cough
§ Pleural inflamma7on/effusion
o Heart
§ Raynaud’s phenomenon
§ Pericardi7s – COMMON CARDIAC SYMPTOMS OF
SLE
§ Vascular inflamma7on
o Cutaneous/skin
§ Bu>erfly rash over cheeks
§ Erythematous rash to areas exposed to sun.
o kidney
§ Lupus nephri7s
§ Proteinuria
§ Hematuria
o Others/systemic
§ Weight loss
§ Fa7gue
§ Fever infec7on
§ Arthri7s
§ Emo7onal liability
§ Hematologic disorders
§ Neurologic disorders
• Medical management
o Medica7ons.
§ Cor7costeroids
§ An7-malarial hydroxychloroquine
§ NSAIDs
§ Immunosuppressants (methotrexate, azathioprine)
o Dialysis
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• Nursing management
o Improve skin integrity.
o Manage pain and provide comfort.
o Decrease fa7gue.
o For skin rashes
§ Avoid ultrasound rays.
§ Wear maximum protec7on sunscreen in the sun
sunbathing is contraindicated. Spf15
§ Wear protec7ve eye wear.
§ Wear a wide-brimmed hat (has good protecAon of
the paAent than the regular cap) and carry an
umbrella.
o For oral ulcer
§ Instruct the client of the following:
• apply topical ointments as prescribed.
• to rinse the mouth with half strength
hydrogen peroxide three 7mes a day
• avoid spicy and citrusy food.
• Keep ulcerated skin clean and dry.
o For hair loss
§ Instruct the client of the following:
• Scalp hair loss occurs during the
exacerba7on of disease ac7vity.
• Scalp hair loss may be caused by high-dose
cor7costeroids (prednisone)
immunosuppressants drugs. REVERSIBLE
§ Encourage the client to inves7gate ways (e.g.,
scarves, hats, wigs) to conceal hair loss

---Addi7onal management---
§ Plasmapheresis
• Draw and return cycle Blood are removed à remove the anAbodies
à cleansed blood
• Components:
o 55% plasma if inflamed plasma is removed blood volumed
will be reduced therefore administer PNSS and albumin
since it is a plasma expander.
o 45% blood cells
• An7-coagulant: citrate an7coagulant
o Watch out for hypocalcemia.
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§ Immunotherapy
• Ac7va7on or suppression of immune system of the pa7ent.
o Ac<va<on it means boost the immune system of the paAent
such as the following:
§ Monoclonal an7bodies
§ Cytokines (interferons, interleukins)
§ Vaccines to boost the immunity of the paAent, and
any kind of vaccines can strengthen the immunity of
the paAent.
o Suppression of the immune system/immunosuppressant
§ Tacrolimus, azathioprine, cyclosporine,
methotrexate, sulfasalazine, leflunomide usually
used for organ transplant to lessen incompaAbility.
• Nursing management:
o monitor for fever, chills, weakness,
n/v, and dizziness.

----con7nua7on of the diseases----

§ Primary Sjogren’s syndrome (dry eyes and dry mouth)
• Rare systemic autoimmune disease (failure of lacrimal and salivary
glands.) no tears or salivary producAon therefore there is dry eyes
and dry mouth.
• Predominantly affects middle aged woman.
• OZen manifests with other autoimmune diseases.
o RA
o SLE
o Autoimmune thyroid disease
• Signs and symptoms:
o Dry eyes
o Dry mouth
o Difficulty swallowing
o Pain
o Fa7gue
o Op7c neuri7s
o Trigeminal neuralgia
o Sensory neuropathy
o Raynaud’s phenomenon
o Sleep disturbances
• Diagnos4cs test:
o ANA, CRP, ESR tests
o Tear test – the tear producAon of the paAent
o Slit lamp – it is a ocular test to see the extent of damage
when there is tear problems.
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o Sialogram – inject on salivary gland to measure the salivary

producAon of the paAent.
o Salivary gland biopsy
• Management:
o NO CURE…but has treatments.
§ Ar7ficial eye drop (pilocarpine); topical cyclosporine
§ Suggest small, frequent feeding, avoid spicy, salty, or
irrita7ng food.
§ Avoid smoking, excessive alcohol use.
§ Refer for possible depression or sleep disturbance.
o Punctual occlusion
§ It is a minor procedure.
§ Within minutes
§ Doctor will insert mechanical plugs to block the tear
ducts of the pa7ent to avoid reabsorb of tears of the
paAent to the circulaAon.
§ Scleroderma (thickness and s<ffness)
• Rare autoimmune disease of connec7ve 7ssues of the skin, blood
vessels walls, and internal organs.
• Women affected four 7mes than men; between 25-50 years old
• Two general types:
o Localized: only cutaneous system
o Diffused: systemic sclerosis
• Collagen – it is fibrous 7ssue, and it is a thick 7ssue; its
responsibility is the skin elas7city, hair and joints.
o In the scleroderma it is the overproduc7on of the collagen.
• Diagnos4cs test:
o ANA, ESR, rheumatoid factor
o Scleroderma an7body tes7ng
o CBC, Metabolic panel, urinalysis
o Other tests…to see if there is thickness of the organs.
§ Chest x-ray
§ CT-scan of lungs
§ Electrocardiogram – heart rhythm
§ Echocardiogram – heart structures
§ Skin biopsy
• Other name is stone facies in which there is somehow paralysis in
the face where in the paAent cannot control their faces.
• Leonine facies – usually seen for leprosy pa7ent.
• Signs and symptoms:
o Cutaneous signs:
§ Raynaud’s phenomenon
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§ S7ffness and 7ghtness of skin of fingers, hands,

forearm face
§ Hair loss
§ Lighter or darker skin
§ Ulcers on finger7ps or toes
§ Telangiectasis: small, widened blood vessels
beneath the surface or fingernails.
o Raynaud’s phenomenon
§ White – due to lack of blood flow
§ Blue – due to lack of oxygen
§ Red – when blood flows return.
o Musculoskeletal
§ Joint pain, s7ffness, swelling, numbness
§ Pain in the feet
o Pulmonary
§ Dry cough
§ Shortness of breath
§ Wheezing
o GI
§ Dysphagia, heartburn
§ Bloa7ng
§ Cons7pa7on
§ Diarrhea
o Cardiac
§ Abnormal heart rhythm
§ Fibrosis in the heart
o Kidney or genitourinary
§ Kidney failure
§ Erec7le dysfunc7on
§ Vaginal dryness
• CREST syndrome
o Calcinosis – calcium deposits in the skin
o Raynaud’s phenomenon
o Esophageal dysfunc4on – acid reflux and decrease in
mo7lity of esophagus.
o Sclerodactyly – thickening and 7ghtening of the skin on the
fingers and hands
o Telangiectasis – dila7on of capillaries causing remarks.
• Management:
o Symptoma7c and suppor7ve
o No medica7on is effec7ve in modifying disease process
o Avoid extreme temperature and use lo7on to minimize
dryness.
o Me7culous skin care
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o Support measures to decrease pain and limit disability.

o Spondyloarthropathies (systemic inflammatory disorders of the skeleton)

§ Ankylosing spondyli4s
• Chronic inflammatory disease of the spine
• More common males than females
• Usually diagnosed in the second or third decade of life
• Highly gene7c in nature
• Gene found in pt. with this disease.
o HLA – B27 GENE this is correlaAve only
• Inflamma7on of the sacroiliac joints it is called the spondyli4s.
o When there is inflamma7on of the sacroiliac joints à fusion
of the joints occurs
• Signs and symptoms
o Kyphosis (pagka kuba ng paAent or stoop posture)
o Neck, joint, back, and hip pain
o Difficulty breathing
o Fa7gue
o Loss of appe7te
o Unexplained weight loss
o Abdominal pain; diarrhea
• Complica4ons
o Osteoporosis
o AV defects of the heart
o Pulmonary fibrosis most threatening complica<on because
when kyphosis occurs there is difficulty of the lung’s
expansion.
§ Reac4ve arthri4s
• HANS Reiter’s syndrome
o Conduc4vi4es cant see
o Urethri4s cant pee
o Arthri4s cant bend the knee
• Arthri7s occurs aZer an infec4on (primarily gastrointesAnal or
genitourinary
• Most affect young adult males
§ Psoria4c arthri4s
• Arthri7s associated with psoriasis or skin disease.
• Onset is between 30 to 50 years old
• Men and women are equally affected
• Chronic skin and nail disease; red; scaly rashes
o Addi4onal:
§ Enthesis – part of the bone where the tendons and
ligaments are a>ached.
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• Inflamma7on of the enthesis à psoria7c

arthri7s
• Signs and symptoms
o Fa7gue
o Tenderness, swelling over tendons. PROMINENT FEATURES
o Swollen fingers and toes resemble sausages.
o Reduced ROM
o Nail changes such as piqng or separa7on form nailbed.
§ Medical Managements
• NSAIDs remains first line therapy.
• Methotrexate, sulfasalazine, leflunomide
• Cor7costeroids
• An7-TNF TUMOR NECROSIS FACTORS meds (etanercept, infliximab)
§ Surgical management
• Osteotomy – reshaping of the bones of spine.
• Total joint replacement
§ Nursing management
• Symptoms management and maintenance of op7mal func7oning
• Focusing on physical ac7vity and good posture
• Address psychosocial concerns.
• Metabolic autoimmune disease
o Gout
§ One of the most understood diseases because there are records of gout
pa7ents.
§ Most common form of inflammatory arthri4s
§ Men are three 7mes more commonly affected than females.
§ Risk factors
• Being male (30-50 years)
• Obese
• Co-morbidi7es
o AKI
o Cancer
• Diet high it is mostly the indicator of risk factors to gout as it
increases the purines and fructose.
o Purines
§ Natural chemical compound and humans has
natural purines in the body.
§ Related to the uric acid à uric acid crystals thick,
sharp crystals
§ sources
• internal organs meat (liver, isaw, bopis,
papaitan, red meats)
• seafoods (shrimp, anchovies, and scallops)
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• Alcohol drinking
§ Common loca4on: toes
§ Types of high uric acid:
• Primary hyperuricemia
o Caused by diet and starva7on.
• Secondary hyperuricemia
o Co-morbidi7es (AKI, cancer leukemia, mulAple myeloma)
o DOC: diure7cs thiazide, aspirin, ethanol
§ Diagnos4cs test:
• Arthrocentesis
• Serum uric acid test
o Female: 2.5 – 7.5 mg/dl
o Male: 4.0 – 8.5 mg/dl
• X-ray of the joints
§ Stages of Gout: (asymptomaAc à acute gout à inter-criAcal gout à
chronic gout)
• Asymptoma4c hyperuricemia – there is no symptoms but there is
consistently the uric acid is elevated; presence of uric acid crystals
is s7ll not prominent.
• Acute Gout/Gout flare – it is the first a>ack of gout, and toes will
be the loca7on of the manifesta7on.
o Some paAents will wake up in the middle of the night for
painful joints.
• Inter-cri4cal gout – symptoms disappeared, or the pa7ent became
asymptoma7c for as long as 2 years
o perfect 7me to give medica7on for preven7on purposes.
o Health educa7on of the pa7ent for future a>acks
• Chronic gout/tophaceous gout– con7nuous symptoms or no more
disappearance of the symptoms or re-current a>acks
o Tophi – generally painless can be found in toes, fingers or
ears of the pt.
§ Medical management
• Uricosuric agents: probenecid
• Colchicine (both prevenAons, during aWacks), NSAIDs,
cor7costeroids
• Xanthine oxidase inhibitors (allopurinol – only prevenAon aWacks,
avoid taking vitamin C because it will oversaturate and causes
kidney stones, febuxostat)
• II – 1 receptor antagonist
§ Nursing management
• Advise client to stay hydrated with 2-3 liters of fluids a day, unless
contraindicated, and report any decrease in urine output.
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• Educate client about dietary medica7ons to limit foods high in

purine.
• Promote comfort and reduce pain.
o Fibromyalgia syndrome
§ Chronic pain syndrome
§ Neurogenic in origin over-amplificaAon of pain signals; in which there is so
much pain over small sAmulaAon.
§ More commons in females
§ Signs and symptoms
• Generalized muscle aging
• Chronic fa7gue
• Sleep disturbance
• Cogni7ve disturbances
§ Medical management
• NSAIDs – diffused muscle aching and tenderness
• Tricyclic an7depressant (amitriptyline, nortriptyline)
• Muscle relaxant (cyclobenzaprine)
• Cogni7ve behavioral therapy
§ Nursing management
• Reassure pa7ent fibromyalgia is a real disease.
• Provide psychosocial care
• Good sleep hygiene
• Physical exercise program to maintain movement for paAents such
as cardiovascular exercises
• HIV (human immunodeficiency syndrome)
o Decreased immune system which are prone to infec7on; and it is blood-borne
disease,
o AIDS
§ Most severe form of HIV.
o HIV 1 found on 1981
§ Retrovirus
§ viral RNA (it will use enzyme called reverse transcriptase) à
o HIV 2 found on 1986 on west Africa.
o Viral load – the higher the viral load the more infected the pa7ent; undetectable
viral load it means the paAent can have sexual acAviAes again and also cannot
transmit to other people as long as it is undetectable.
o Transmit HIV:
§ Sperm cell
§ Breast milk
§ Amnio7c fluids
§ Needles
§ BT
o CD4 count – the higher the CD4 count the higher the pa7ent is protected
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§ Normal: 500 – 1500 Cells/mm3

§ Abnormal: <200 cells/mm3 -- AIDS
o Process: STAGES OF HOW HIV PROLIFERATE
§ Aiachment stage – GP120 part of the HIV it is the one that aWaches to the
CD4 receptors.
• HIV enters the body à looks for the Helper T-cells CD4 receptors à
GP120 a>aches to the CD4 receptors.
§ Fusion HIV fuses cell membrane it implies that the HIV can enter the host
cells.
§ Reverse transcrip7on Viral RNA
• From viral RNE à converts to VIRAL DNA using the reverse
transcriptase
§ Integra7on HIV DNA
• HIV DNA à binds to the host DNA à can hijacked the control
center of the cells. Enzyme used is Integrase
§ Replica7on long chains HIV proteins will be produced.
§ Assembly stage: it will separate from the host cells
• HIV proteins + HIV DNA = IMMATURE HIV
§ Budding:
• immature HIV Pushed out of the cells using the enzyme protease
o diagnos4c test
§ An7gen an7body test
§ An7body test
§ Nucleic acid test
§ ELISA – first test to be ordered by the doctor form suspected paAent à
Western blot confirmatory of (+) Elisa test
o Medical management
§ HAART (highly acAve anAretroviral drug therapy)
• Nucleoside Reverse transcrip7on inhibitor such as
o Abacavir
o Lamivudine
o Tenofovir
o Zidovudine (immunosuppression)
• Protease inhibitor
o Ritonavir
o Lopinavir
o Saquinavir
• Non-nucleoside reverse transcrip7on inhibitor
o Efavirenz