IMMUNO NURSING

8/7/2019 IMMUNO NURSING

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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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Portal of exit

-Respiratory tract

-GI tract -GU tract

-Open lesions

-from bloodstream


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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 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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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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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


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


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


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


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


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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IMMUNO NURSING