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IMMUNOLOGY
IMMUNOLOGY
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OBJECTIVES Discuss topics in detail in
relation the concept
Evaluate students learning
through quizzes, recitations and
homeworks
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Definition of Terms
Infection/control
Immunity/immune systemAllergies/Hypersensitivities
Viral Infections
Bacterial Infections
Disorders in Adults
SCOPE OF DICUSSION
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IMMUNOLOGY
VIRAL INFECTIONS
Rubella
Rubeola
Varicella
H. Zoster
Variola
Poliomyelitis
HPV
Rabies
Meningitis
Mumps
Infectious Mononucleosis
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IMMUNOLOGY
BACTERIAL INFECTIONS
Streptococcal- Impetigo
Staphylococcal- Diphtheria, Pertussis,
Anthrax, Tetanus, Lyme disease
Scabies
Lice
Ascariasis.Pinworms
Candidiasis
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IMMUNOLOGY
OTHERS
GBS
Osteomyelitis
AIDS
Gonorrhea,Trichomoniasis
Hepatitis
Acne,Furuncles,Carbuncles, Psoriasis
Salmonella
Typhoid, Dysentery, Asthma
DM
MS
Addisons Disease
Ulcerative Colitis
Glomerulonephritis
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Terminology
1. Immunity
2. Immunization
3. Immnunocompetence4. Immunocyte
5. Immunodeficiency
6. Immunoglobulins7. Immunodepression
8. Agglutination
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Terminology
9.Antibody
10. Antigen
11. Complement12. Interferon
13. Lymphokines
14. Opsonization15. Memory Cells
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Terminology
16.B cells
17. Helper T cells
18. Cytotoxic T cells
19. Phagocytic cells
20. Suppressor T cells
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Anatomy of the Immune System
FIGURE OF THE BONE
MARROW
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Anatomy of the Immune System
B cells
T-cells
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Immune System Response
Non Specific Defense
Specific Defense
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Non-Specific Defense
This relates to reactions
that include anatomic and
chemical barriers such as the
Skin and mucous membranes
This is is also considerednon-selective.
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Non-Specific Response
I. Mechanical Protection
II. Chemical Protection
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Antimicrobial Substances
I. Interferons
II. Complement System
III. Natural KillerCells
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Phagocytosis
1.Neutrophils
2. Macrophages
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Phagocytosis
Mechanisms
1. Chemotaxis
2. Adherence
3. Ingestion
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Inflammation
4 Classic Signs
1. Pain
2. Sweling
3. Redness
4. Heat
5. Loss of Function
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Inflammation
3 Stages
1. Vasodilation and Increased
Capillary Permeability
2. Phagocyte Migration
3. Tissue Repair
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Fever
Occurs during infection and
inflammation
Intensifies the effects ofinterferons
Inhibits growth of some
microbes
Designates infectious process
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Specific Defense
I. Humoral Immune Response
II. Cell-Mediated Immune
Response
III. Combined Cellular and
Humoral Response
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Specific Response
II. Cell-Mediated Response
a. Activation, proliferation,
differentiation of T Cells
b. Elimination of the foreign Ag
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Specific Response
III. Combined Cellular and
Humoral Response
a. Recognition stage
b. Proliferation stage
c. Response staged. Effector stage
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Properties of the Immune Response
1. Diversity
2. Specificity
3. Recognition
4. Memory
5. Action
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Antibodies
1. IgG
2. IgM
3. IgA
4. IgD
5. IgE
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Antibodies
Properties:
1. Agglutination
2. Precipitation
3. Neutralization
4. Lysis
5. Opsonization
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Factors Affecting the Immune
Response
1. Age
2. Emotional Stress
3. Sex
4. Diet
5. Drugs
6. Medical Treatment
7. Presence of other illness
8. Environment
9. Immunization History
10. Cultural Practices
11. Heredity12. Rest, exercise, personal habits
13. Inadequate defenses
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Types of Immunity
ACTIVE
Natural
Artificial
PASSIVE
Natural
Artificial
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Diagnostic Tests
1. WBC
2. WBC Differential
3. ESR
4. Culture and Sensitivity
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Contagious
Disease that is
transferred easily
from person to
person direct orindirect and through
intermediary means
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INFECTIOUS
Diseases developed
through several
factors such as :
in hosts resistance
Microbes inoculation
microorganisms
mechanism of
resistance
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Infectious Disease Process
Infectious agent
-bacteria
-fungi
-viruses
-rickettsiae
-protozoa
Reservoir
-People
-Equipment
-Water
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Infectious Disease Process
Portal of exit
-Respiratory tract
-GI tract -GU tract
-Open lesions
-from bloodstream
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Infectious Disease Process
Portal of entry
Respiratory tract
Gastrointestinal tract
Genitourinary tract
Direct infection of mucus membrane/
breaks of skin
Parenteral: via blod
Transplacental: mother to fetus
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Infectious Disease Process
Infectious agent Mode of
transmission
Susceptible Host
Portal of entryReservoir
Portal of exit
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Course of infection
1.Incubation
2.Prodromal stage
3.Full stage
4.Convalescence
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Course of infection:
Incubation
Initial contact with an infectious agent
First sign of host infection or symptoms
Prodromal stage Onset of non specific symptoms to the
appearance of the specific symptoms
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Course of infection:
Full stage
Acute stage
ConvalescenceRecovery phase
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INFECTIOUSAGENT
Bacteria
FungiViruses
Rickettsiae
protozoa
RES
ERVOI
RS
People
Equipment
Water
PORTALOF ENTRYmucous membrane
GI tract
GU tract
Respiratory tract
Broken skin
PORTALOF EXIT
Excretions
SecretionsSkin
Droplets
SUSCEPTIBLE HOSTImmunosuppression
Diabetes
Surgery
burns
Elderly
MEANSOF TRANSMISSION
Direct contact
Ingestion
Fomites
Airborne
Employee health
Envtl.sanitation
Disinfection
sterilization
Hand
washing
Control of
excretion and
secretion
Trash &wastedisposal
isolation
Food handlingAirflow
control
Standard
precaution
sterilization
Hand hygiene
Rapid accurate identification of organisms
Wound care
Catheter
care
Aseptictechnique
Recognitionof high risk
pt.
Treatment of underlying
disease
INTERVENTIONS TO BREAK THE CHAIN OF INFECTION
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Modes of Transmission
Direct contact
Person toperson spread
of organism
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Droplet infection
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Airborne transmission
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Vehicle transmission
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Vector - borne transmission
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Prevention of Transmission
Transmission Based Precaution Airborne precaution pt. should be put in a
room w/ negative air pressure and wear face
mask.
Droplet Precaution Nurse should wear a
facemask.
Contact Precaution pt. is placed on a private
room to facilitate hand hygiene and protectionof garments from envtl. contamination.
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Prevention of Transmission
Preventing infection in the hospital.
Nosocomial infection
Disinfecting skin Medical hand washing
Use of disinfectants
Changing infusion sets, caps and soln
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Breaking the Chain of Infection
Medical Asepsis
Standard precautions: HW, gloves, masks,
goggles, shields
Transmission-based precautions: isolation
techniques
Surgical Asepsis
Sterilization Disinfection
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Infection Control and Prevention
CDC
OSHA
WHO
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Preventing Infection in the
Community
Sanitation Techniques
Regulated health practices
Immunization program
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Multiple Sclerosis
chronic, progressive, non-contagious CNS
disease characterized by demyelination of
the myelin sheath
usually occurs between 20-40periods of remissions and exacerbations
unknown cause: thought to be
autoimmune or viralPCF: pregnancy, fatigue, stress, infection
and trauma
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Multiple Sclerosis
Clinical Manifestations:1. fatigue/weakness
2. Ataxia/vertigo
3. Tremors/spasticity of the
4. Paresthesias
5. Blurred vision and diplopia
6. Nystagmus
7. Decreased perception to pain, touch and
temperature
8. Bladder and bowel disturbances
9. abnormal reflexes
10. Emotional changes
11. Memor chan es/confusion
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Multiple Sclerosis
Mgt:
1. Bedrest
2. Eye patch
3. Safety4. Monitor for complications
5. Promote regular elimination
6. Encourage independence7. establish rest/exercise program
8. Assist with the need fro assistive devices
9. Initiate physical and speech therapy
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Multiple Sclerosis
10. Instruct the client to avoid fatigue,
stress, infections
11. Increase OFI, eat a balanced-diet
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Multiple Sclerosis
Medications:
1. Baclofen (Lioresal)
2. Dantrolene (Dantrium)
3. Diazepam (Valium)
4. Betanechol (Urecholine)
5. Carbamazepine (Tegretol)
6. Corticosteroids
7. Oxybutinin Chloride (Ditropan)
8. Propanolol (Inderal) and Chlonazepam
(Klonopin)
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Guillain Barre Syndrome
An acute infectious neuronitis of the
cranial and peripheral nerves
The immune system overreacts to the
infection and destroys the myelin sheathThe syndrome is usually preceded by a
mild respiratory tract infection or
gastroenteritis
Recovery is slow
The major concern is difficulty breathing
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Guillain Barre Syndrome
Clinical Manifestations:
1. Paresthesias
2. Weakness of the lower extremities
3. Gradual progressive weakness of upper
extremities and facial muscles
4. Possible progression to respiratory
failure, cardiac dysrrythmias5. Elevated CHON in the CSF
6. Abnormal EEG
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Guillain Barre Syndrome
Mgt:
1. Symptomatic
2. Monitor respiratory status
3. Provide respiratory treatments
4. Prepare to initiate respiratory support
5. Monitor cardiac status
6. Assess for complications of immobility
7. Provide support for the client and family
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Addisons Disease
Hyposecretion of the adrenal cortex
hormones
Fatal if left untreated
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Addisons Disease
Clinical Manifestations:
1. lethargy, fatigue, muscle weakness
2. GI disturbances
3. Wt loss4. Menstrual changes in women/impotence in men
5. Hypoglycemia
6. Hyperkalemia
7. Postural Hypotension8. Dehydration
9. Emotional disturbances
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Addisons Disease
Mgt:
1. Monitor VS/ I and O
2. Monitor blood glucose and K levels
3. Administer glucocorticoids or
mineralocorticoid medications as
prescribed
4. Observe for Addisonian crisis caused bystress, infection, trauma, trauma or
surgery
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Addisons Disease
Mgt:
1. Avoid individuals with infection
2. Diet:
3. Avoid strenuous exercise and stressful
situations
4. Need for life-long glucocorticoid therapy
5. Avoid OTC medications6. Wear a medic-alert bracelet
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Diabetes Mellitus
A chronic disorder of impaired
carbohydrate, protein and lipid
metabolism that is caused by a deficiency
or lack of insulinIt has two types (I and II)
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Diabetes Mellitus
Type I: nearly absolute deficiency of
insulin
Complications: Insulin shock,
Hyperglycemia, DKA, Diabetic ComaType II: a relative lack of insulin or
resistance to the action of insulin
HONK, NIDDM
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Diabetes Mellitus
S/sx of Hyperglycemia
Increase in temperature
Dim vision
Thirst
Kussmauls respiration
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Diabetes Mellitus
Diagnostics:
1. FBS
2. RBS
3. PPBS/OGTT
4. HGT
5. Acid Test
6. HBA1C
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Diabetes Mellitus
Clinical Manifestations:
1. 3 Ps
2. Hyperglycemia
3. Wt loss4. Blurred vision
5. Slow wound healing
6. Vaginal infections in women
7. Weakness and paresthesias8. Signs of inadequate circulation to the feet
9. Signs of accelerated atheroslcerosis
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Diabetes Mellitus
Mgt: (Diet)
1. 50 % CHO, 20% CHON, 30% Fats
2. Total number of calories
3. Or as prescribed by AP
4. Incorporate diet into individual client
needs, lifestyle and
cultural/socioeconomic status
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Diabetes Mellitus
Mgt: (Exercise)
1. Lower blood glucose level
2. Reduce cardiovascular risks
3. Improves circulation and muscle tone
4. Decrease total cholesterol and triglycerides5. Wt loss (DM II)
6. Instruct client in dietary adjustments whenexercising
7. Instruct client to monitor blood glucose before
exercising8. Initially, the client who requires insulin should
be instructed to eat a 15-grams CHO snackbefore exercise to prevent hypoglycemia
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Diabetes Mellitus
Oral Hypoglycemics and the What to Dos
1. For DM II
2. Assess VS and serum glucose levels
3. Aspirin, ROH, sufanamides, oral contraceptivesincrease the hypoglycemic effect causing adecrease in blood glucose levels
4. No ROHs with sulfonylureas
5. Inform the client that with DM II, insulin may be
needed during stress, surgery or infection6. Teach client about compliance
7. Wear medic-alert bracelet
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Diabetes Mellitus
Insulin
1. Used to treat DM I and DM II when diet and wt controltherapy have failed
2. Best time given 60-90 minutes ac so that the physiologiceffects of insulin will parallel the absorption of glucose
3. Do not give cold insulin4. Rotate sites
5. RI is the only insulin that can be administered IV in theemergency treatment of DKA
6. Glucocorticoids, thiazide diuretics, thyroid agents, oralcontraceptives and estrogen increase blood glucose
levels7. In stress, illness, infection, insulin should not be withheld
8. The peak of action of insulin is important because of thepossibility of hypoglycemic effects
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Diabetes Mellitus
Complications of Insulin Therapy:
1. Local allergic reactions
2. Lipodystrophy
3. Insulin resistance
4. Dawn Phenomenon
5. Somogyi phenomenon
6. Insulin waning
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Diabetes Mellitus
Acute Complications:
1. Hypoglycemia
2. DKA
3. HHNS
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Diabetes Mellitus
Chronic Complications:
1. Diabetic retinopathy
2. Diabetic nephropathy
3. Diabetic Neuropathy
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Diabetes Mellitus
Mgt:
1. Exercise
2. Diet
3. Lifestyle
4. Medications
5. Foot care
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Diabetes Mellitus
Foot Care:
1. Not to walk barefoot
2. No girdles
3. No smoking
4. No local cold compress
5. Do not soak feet
6. Not to cross legs7. Change socks/stockings daily
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Diabetes Mellitus
8. Wear well-fitted shoes
9. Not elevate legs on a pillow (prolonged)
10. Apply lotion to feet
11. Prevent moisture accumulating between
toes
12. Do not treat corn, blisters or ingrown
nails but see the PODIATRIST13. Cut toe nails straight across
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Ulcerative Colitis
An acute
ulcerative and
inflammatory dse.
Of the bowel thatresults in poor
absorption of
nutrients
Remissions andexacerbations
PICTURE
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Ulcerative Colitis
Clinical Manifestations:
1. Anorexia
2. Wt loss
3. Malaise4. Abdominal tenderness/cramping
5. Severe diarrhea that may contain blood and
mucus
6. Dehydration7. Electrolye imblance
8. Anemia/ Decreased Vit. K
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Ulcerative Colitis
Mgt:
1. Acute phase: NPO
2. Restrict activities
3. Monitor bowel sounds and for abdominal
tenderness and cramping
4. Monitor stools, noting color, consistency
and the presence or absence of blood5. Monitor for perforation, peritonitis and
hemorrhage
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Ulcerative Colitis
6. Following the acute phase, the diet
progresses from clear liquids to low-
residue diet as tolerated
7. Instruct the client to consume a low-residue, high CHON diet (vitamins and
Iron supplement as prescribed)
8. Instruct to avoid gas forming foods and
milk products
9. NO SMOKING
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Ulcerative Colitis
10. Administer bulk-forming agents such as
psyllium, methylcellulose to decrease
diarrhea
11. Antimicrobials, corticosteroids,immunosuppresants
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Ulcerative Colitis
GROUP ASSIGNMENT
Computerized
Font: Arial, 12
Spacing: Single
+ Bibliography (correct format)
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Glomerulonephritis
Caused by immunological reaction
Ag-AB reaction produced by an infection
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Glomerulonephritis
Complications:
1. Heart failure
2. Hypertensive
encephalopathy
3. Pulmonary edema
4. RF
TYPES:
1.AGN
2.CGN
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Glomerulonephritis
Clinical Manifestations:
1. Hematuria
2. Dark, smoky, cola-colored or red-brown urine
3. Proteinuria
4. Urinary debris
5. Moderately elevated Sp. Gravity
6. Low urinary pH7. Oliguria or anuria
8. Chills/fever
9. Fatigue/weakness
10. Anorexia/ N/V
11. Pallor
12. Edema
13. SOB, ascites, pleural effusion, CHF14. Abdominal, flank pain
15. HPN
16. Increased BUN and creatinine levels
17. Increase ASO titer
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Glomerulonephritis
Mgt:
1. VS monitoring
2. I/O
3. Weigh daily
4. Monitor for edema
5. Monitor for fluid overload, pulmonary edema and CHF6. Restrict fluid intake as ordered by AP
7. Provide a high-calorie and low-CHON diet
8. Restrict Na intake as prescribed if edema is present
9. Bed rest and limited activity
10. Instruct the client to obtain treatment to infections
11. Monitor for s/sx of RF, Heart Failure and hypertensiveencephalopathy
12. Instruct the client to report symptoms of bloody urine,headache and edema
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Hypersensitivities
A. Type I
Severity of symptoms depend on:
1. Amount and route of entrance of
sensitivity dose2. Amount and distribution of IgE Abs
3. Amount and route of entrance of
shocking dose
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Hypersensitivities
I. Anaphylaxis
Consitutes the principle of ABC
Most severe form of Type I
Common antigens: penicillin, insectstings, contrast media used in X-ray
and/or CT Scan, Food e.g. seafoods,
legumes, egg, albumin, strawberries
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Hypersensitivities
Clinical Manifestations:
1. Edema
2. Itching
3. Apprehension
4. Wheezing
5. Dyspnea
6. Signs of vascular response with shock7. DEATH
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Hypersensitivities
Mgt:
1. Position
2. Epinephrine
3. Hydrocortisone4. AIRWAY
5. IV fluids
6. Vasopressors
7. Diphenhydramine HCl8. Emotional Support
9. Medic-alert bracelet
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Hypersensitivities
Prevention:
1. Identification of high-risk persons
2. Patient education
3. desensitization
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Hypersensitivities
II. Urticaria and Angioedema
A. Urticaria: may occur as an IgE-mediated local
anaphylactic response
B. Angioedema: form of urticaria but involves SQ
tissue rather than the skin
Both are self-limiting (Rest)
Mgt:
1. Epinephrine
2. Antihistamines
3. Corticosteroids
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Hypersensitivities
III. Atopic Allergy
It is a less severe form of Type I
s/sx depends whether inhalation,
ingestion, skin contact is themode/means
Common forms: Hay fever, Allergic
Asthma, Atopic Dermatitis
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Hypersensitivities
B. Cytotoxic Hypersensitivity
Involves direct binding of IgG or IgM to an
Ag on a cells , surface
This AB then triggers the destruction of thecell by phagocytic attack, non-specific
lymphocytic attack or cell lysis
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Hypersensitivities
I. BT Reactions
Most common form of Type II
Dangerous
Nsg. Responsibilities:1. Warm blood at room Temp.
2. Countercheck with another RN (date, Blood
Serial #)
3. Transfuse4. Be at bedside for the first 15 to 30 minutes
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Hypersensitivities
C. Type III
Immune complex Hypersensitivity
Rare type
Serum Sickness
D. Type IV
Most rare of all
Cell-mediated (T cells) Tissue transplant rejection
S
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SLE
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