Nursing Care of Clients with Immune Disorders Flashcards

1
Q

Normal immune system protects/defends
Disorders: lack of the ability of the body to protect itself against organism or actually attack itself

A

Immune disorders: concepts

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2
Q

Excesses or deficiencies of competent cells
Alterations in function of cells
Exaggerated responses to specific antigens
Immunologic attack on self

A

Disorders: lack of the ability of the body to protect itself against organism or actually attack itself

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3
Q

Gammopathies or Primary Immunodeficiency

A

Excesses or deficiencies of competent cells

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4
Q

Secondary Immune deficiencies

A

Alterations in function of cells

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5
Q

Hypersensitivity reactions

A

Exaggerated responses to specific antigens

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6
Q

Autoimmune disorders

A

Immunologic attack on self

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7
Q

Born with
Rare; genetic cause
(more common male to female 5-1)
More often recessive - often on X chromosome
Usually dx. in infants/toddlers
Some seen in adolescence/young adult
Often accompany autoimmune disorders
Common types
Clinical Manifestations:
Medical Treatment:

A

Immunodeficiency disorders: primary

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8
Q

Antibody deficiency
Phagocytic dysfunction
B cells or T cells, (or both) defects = not do job
Complement system deficiency

A

Common types - Immunodeficiency disorders: primary

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9
Q

Severe/recurrent infections, failure to thrive or positive family history

A

Clinical Manifestations: - Immunodeficiency disorders: primary

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10
Q

Antibiotics: infection/prophylactic - something that likely result in an infection (dental)
IVIG (IV immunoglobulin) or SQ IG
Hematopoietic stem cell transplant
No live vaccines - may get disease attempting to vaccinate against
Genetic counseling - highly recommended

A

Medical Treatment: - Immunodeficiency disorders: primary

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11
Q

Curative - give this - going to make new cells cont to make WBCs can cure

A

Hematopoietic stem cell transplant

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12
Q

Acquire
Etiology
Causes:
Diagnostics
Treatment
Assessment/Data Collection
N. Diagnosis
N. health promotion/pt teaching

A

Immunodeficiency disorders: secondary acquired immune deficiency

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13
Q

Due to malnutrition or HIV
Result of underlying disease processes or treatment
See Neutropenia = once become at high risk for sepsis
WBC <1,000/mm3 (5000-10000 mm3) - on neutropenic precautions

A

Etiology - Immunodeficiency disorders: secondary acquired immune deficiency

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14
Q

Autoimmune disorders
Immunotoxic medications
Alcoholism, drug abuse
Spleen removal
Malnutrition/stress
HIV

A

Causes: - Immunodeficiency disorders: secondary acquired immune deficiency

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15
Q

Corticosteroids = long-term; prolonged NSAID, Chemo - particular bllod cells; radiation
NADER - predive point where going to have low WBC count in response to med - highest risk for infection
Absolute neutrophil count - check before give chemo - status of WBCs before give chemo - not want bottom out numbers

A

Immunotoxic medications

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16
Q

WBC/diff: severe neutropenia - lab levels carefully - number segs and bands with pts
Segs - fully matured WBCs; should be high
Bands - immature WBCs; should have low; higher number - bandemia (band count greater than 10%) - consider what going on with pt - turning out immature WBCs increasing number immature ones
Bone marrow biopsy

A

Diagnostics - Immunodeficiency disorders: secondary acquired immune deficiency

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17
Q

Infections
Intravenous immunoglobulin (IVIG)
Hematopoietic stem cell transplant
Monoclonal antibody therapy
Growth factors (neupogen)

A

Treatment - Immunodeficiency disorders: secondary acquired immune deficiency

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18
Q

Provide to those lacking immunoglobulin

A

Intravenous immunoglobulin (IVIG)

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19
Q

Potential
Not curative
Can help reduce some comps

A

Hematopoietic stem cell transplant

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20
Q

Target antibodies to specific antigens
-mab

A

Monoclonal antibody therapy

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21
Q

Increase production of WBCs for pts

A

Growth factors (neupogen)

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22
Q

History-past infections, treatment response to various infections
Nutritional status, hygiene, use of alcohol/drugs/tobacco
Physical: monitor for Manifestations of infection
Pts do not have typical manifestations of infection - do more detailed assessment
Monitor: Manifestations infection

A

Assessment/Data Collection - Immunodeficiency disorders: secondary acquired immune deficiency

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23
Q

VS, lab values, C&S reports from wounds, lesions, sputum, urine, blood - determine infection
Pay attention to WBC - segs and bands
Trend imp

A

Monitor: Manifestations infection

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24
Q

Ineffective protection
Risk for Infection
Risk for impaired skin integrity
Ineffective health maintenance
Imbalanced nutrition: less
Social isolation
Fear r/t threat to well-being

A

N. Diagnosis - Immunodeficiency disorders: secondary acquired immune deficiency

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25
Q

Prevention of infection
Lifestyle mod. to reduce risk
Nutrition and diet
Neutropenic precautions
Manifestations of infection
Medication teaching
Prophylactic med regimen: Follow-up care with physicians/specialists

A

N. health promotion/pt teaching - Immunodeficiency disorders: secondary acquired immune deficiency

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26
Q

Frequent and quality Handwashing
Avoid crowds/infections
Good Hygiene and cleaning home
Daily bath, foot care, good dental hygiene
Scrub raw fruits and veg throroughly, food storage and preparation - heat to correct temp
Cleaning kitchen, bathroom surfaces

A

Prevention of infection

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27
Q

Acquired
Pathophysiology
Stage I: Category A
Stage 2: Category B
Stage 3: Category C
Risk factors HIV
Lab tests for diagnosing and tracking
Nurse role: HIV screening process
N. counseling
Gerontology considerations
Medical care
PrEP med
Medical treatment: probs with compliance:
Collaborative care
Opportunistic diseases
N. process: assessment/diagnosis
Diagnosis
AIDS N. process: planning/goals
AIDS N. interventions
N. health maintainence

A

Immunodeficiency disorders: secondary HIV/AIDS

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28
Q

Retrovirus: intracellular parasite - act as a parasite
HIV targets cells with CD4 receptors (special T cells)
Complex life cycle that turns the host cells into “factories” for HIV
Retrovirus hijac RNA - turn CD4 into factories that produce HIV to go throughout body

A

Pathophysiology

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29
Q

Contract infection
Primary infection: Rapid viral replication (1-3 weeks) Feel cold, flu like symptoms - broad symptoms then go Asymptomatic (can go for 10 yrs) - spread illness during time
CD4 - 500-1200 normally

A

Stage I: Category A

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30
Q

HIV symptomatic: CD4 <200 - now classified as AIDS
AIDS begins

A

Stage 2: Category B

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31
Q

Severe AIDS-CD4 <100
At risk for Opportunistic diseases - not typ see in gen pop

A

Stage 3: Category C

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32
Q

Sharing infected injection drug use equipment - share needles
Having sex with infected individuals (male and female)
Infants born to mothers with HIV infection and/or breast-fed by HIV-infected mothers
People who received organ transplants, HIV-infected blood, or blood products (esp between 1978-1985)
Reduce risk
Postexposure prophylaxis (PEP)

A

Risk factors HIV

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33
Q

Abstinence
Being faithful - limit partners
Always use condoms
Transmitted in body fluid = more blood and sexual transmission
Occupational exposures - needle stick

A

Reduce risk

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34
Q

Stuck self needle already injected in pt that HIV +
Reduce chance of seroconversion - reduce change starting make HIV virus and reduce chance become +; has start within 72 hrs of exposure

A

Postexposure prophylaxis (PEP)

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35
Q

EIA
Western blot
Viral load
CD4/CD8
OraQuick

A

Lab tests for diagnosing and tracking

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36
Q

Enzyme immunoassay
Antibodies are detected, resulting in + results and marking end of window period
Do serial testing with them
Not enough to confirm HIV - do Western blot

A

EIA

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37
Q

Definitive confirmation test
Able detect antibodies
Also detects HIV antibodies; confirms EIA

A

Western blot

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38
Q

Measures HIV RNA in the plasma
Low or high viral load - more likely transmit the virus with a higher viral load

A

Viral load

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39
Q

monitor CD4 and CD8 cells
These are markers found on lymphocytes
HIV kills CD4 cells which results in significantly impaired immune sys

A

CD4/CD8

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40
Q

In-home HIV test
Get results of viral load and CD4 count

A

OraQuick

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41
Q

Pre and post test counseling - nervous
Sequence due to “Window Period” - virus not fully ramped up
Retesting essential at 3 wks, 6 wks, and 3 mo
3 weeks - 3 months between infection with HIV and seroconversion (production of antibodies against the virus) - body time to seroconvert; to take PEP need HIV test to start - not previously HIV + = come back again for further testing later
Serial testing imp
HIV screening may be negative if done early - early tests not always indicative

A

Nurse role: HIV screening process

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42
Q

Focus on client’s own unique circumstances/risks - pt situation
Acknowledge/support for positive steps already made - explain what happened and make no judgments
Enhance self-perception of risk - engage risky behaviors - educate them
Use explicit language - plain, straightforward language
Help client set goal to reduce chance of acquiring/ transmitting HIV - PEP if qualify; HIV+ steps take to avoid transmitting and not + avoid virus
Avoid providing unnecessary information
Use condoms, use protection during oral sex, don’t share sex toys - anything exposed to body fluid - not share

A

N. counseling

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43
Q

One quarter of people living with HIV: age > 50
Reasons
Unprotected intercourse - esp postmenopausal women
Do not consider themselves at risk
Social bias toward homosexuality - NOT TRUE
Current or past use IV drugs (share needles)
Received HIV-infected blood before 1985 - if received blood before 85 should get a HIV test
Reduction in immune system function

A

Gerontology considerations

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44
Q

Antiretroviral therapy (ART)
to suppress virus
Prevent or decrease complications
Monitor disease progression & immune function - CD4 counts and viral load
Manage symptoms
Prevent dev. of opportunistic disease
Detect and treat early
Prevent transmission of HIV to partners/others

A

Goals: - Medical care

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45
Q

Suppress HIV replication/prevents drug resistance
Reduce morbidity and prolong duration of life/quality of survival
Restore and preserve immunologic function
Suppress plasma HIV viral load - less risk spread or immunosuppression
Prevent HIV transmission
In U.S., ART is now recommended for all HIV-infected patients regardless of their viral load or CD4+ count

A

Goals of ART: - Medical care

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46
Q

Truvada (combo: emtricitabine and tenofovir)
Pre-Exposure Prophylaxis
High risk indivs
Reduces risk of transmission From known HIV+ people to HIV-
Need to use condoms
Need baseline HIV testing and other labs every 3 months - hard kidneys, liver
Does not protect from STD
Daily dose; Do not miss any doses - decrease effectiveness of med

A

PrEP med

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47
Q

Risk of damage to kidney/liver
Lactic acidosis
Osteopenia (bone softening) - higher risk for fractures
Headache
Abd. Pain - diarrhea
Weight loss

A

Adverse effects - PrEP med

48
Q

Do not miss any doses of TRUVADA. Missing doses may increase your risk of getting HIV-1infection.
To further help reduce your risk of getting HIV-1:
Know your HIV status and the HIV status of your partners. If your partner is living with HIV, your risk of getting HIV is lower if your partner consistently takes HIV treatment every day.
Get tested for other sexually transmitted infections. Other infections make it easier for HIV to infect you.
Practice safer sex by using latex or polyurethane condoms to lower the chance of sexual contact with body fluids.
Talk to your healthcare provider about all the ways to help reduce HIV risk.

A

Patient ed - PrEP med

49
Q

CNS: depression, neuropathies, fatigue
GI/Bili: N/V/D - subside after used to it but chronic use can wax and wane, Pancreatitis, Hepatotoxicity - monitor liver labs
Renal: stones, nephrotoxicity, renal failure - monitor labs
CV: HTN, MI, stroke, dysrhythmias
Pulmonary: bronchitis, dyspnea
MS/skin: Osteopenia; Fat redistribution syndrome (lipodystrophy)
Hematologic: anemia, neutropenia, thrombocytopenia - serial labs
Endocrine: Insulin resistance - longer on it so can turn into diabetes

A

AE - long-term antiretroviral therapy - PrEP med

50
Q

Compliance is huge issue with HIV patients
CDC estimates 36% of HIV pts use ART; only 76% have suppressed viral loads - follow-up how compliant with ART
Positive relationship between patient and health care provider is associated with better adherence - nonjudgemental; consistency with HCPs

A

Medical treatment: probs with compliance:

51
Q

Side effects of meds - fatigue, diarrhea, nausea
Psychological/mental illness/neurocognitive impairment
Low health literacy - not realize importance
Low social support - psych issue; afford meds
High alcohol consumptions/active substance abuse
Homelessness/poverty
Nondisclosure of HIV serostatus, denial stigma
Inconsistent access to medication

A

Barriers to adherence to treatment plan

52
Q

Opportunistic infections
Respiratory failure
Cachexia and wasting - before ART initiated
Medication side effects
Education and support
PT, OT, dietary, counseling (indiv and group)
Educate about self-care
Community support systems
Emotional and ethical concerns

A

Collaborative care

53
Q

Psoriasis
Kaposi’s sarcoma
Respiratory
Neurologic Manifestations
Gynecologic Manifestations
Integumentary Manifestations
GI Manifestations
Candidiasis-common
Patho where body can typ fight it off
HIV wasting syndrome -10% weight loss
Cancers:
Eyes: Cytomegalovirus Retinitis
Oral lesions from genital warts

A

Opportunistic diseases

54
Q

Worse in people with HIV+

A

Psoriasis

55
Q

most common opportunistic eye infection seen in patients who are immunosuppressed is cytomegalovirus (CMV)
Type cancer
Gen can fight off if not immunocompromised

A

Kaposi’s sarcoma

56
Q

Pneumocystis jiroveci pneumonia
Cytomegalovirus (CMV)
Legionella species
Frequently resides in venting and ducting
Mycobacterium avium complex
Tuberculosis

A

Respiratory

57
Q

HIV encephalopathy
Cryptococcus neoformans
Fungal meningitis

A

Neurologic Manifestations

58
Q

Candidiasis (thrush - seen often), genital warts, PID, cancer

A

Gynecologic Manifestations

59
Q

Herpes zoster and herpes simplex
Eczema or psoriasis

A

Integumentary Manifestations

60
Q

(oral to rectum)

A

GI Manifestations

61
Q

Diarrhea/weakness/fever >30 days

A

HIV wasting syndrome -10% weight loss

62
Q

Kaposi’s sarcoma (human herpesvirus-8)
Lymphoma

A

Cancers:

63
Q

Leading cause of blindness in AIDS

A

Eyes: Cytomegalovirus Retinitis

64
Q

More likely to have wart outbreaks

A

Oral lesions from genital warts

65
Q

Assess physical and psychosocial status
Identify risk factors: IV drug use, sexual practices
Immune system function
Nutritional status
Skin integrity - imp to prevent infections
Respiratory status and neurologic status
Fluid and electrolyte balance
Knowledge level of disease process - health literacy imp

A

N. process: assessment/diagnosis

66
Q

Impaired skin integrity
Diarrhea
Risk for infection
Activity intolerance
Disturbed thought processes
Ineffective airway clearance
Pain
Imbalanced nutrition
Social isolation
Anticipatory grieving
Deficient knowledge

A

Diagnosis

67
Q

Absence of infection
Expression of grief - expected and norm; need them to cope and not feel hopeless
Improved nutritional status
Increased socialization
Increased knowledge regarding disease prevention and self-care
Increased comfort
Improved airway clearance
Improved activity tolerance
Maintenance of skin integrity
Resumption of usual bowel patterns
Improved thought processes

A

AIDS N. process: planning/goals

68
Q

Interventions: Neuro Status
Interventions: Activity
Interventions: Skin
Interventions: Bowels
Interventions: Nutrition
Interventions: Isolation

A

AIDS N. interventions

69
Q

Assess mental/neurologic status
Use clear, simple language (mental status)
Establish and maintain a daily routine
Orientation techniques
Ensure patient safety and protect from injury
Strategies to maintain and improve functional ability
Instruct and involve family in communication and care
Ensure patient safety -protect

A

Interventions: Neuro Status

70
Q

Balance between activity and rest
Maintain balance between activity and rest
Fatigued easily
Instruction regarding energy conservation techniques
Relaxation measures
Collaboration with other members of the health care team

A

Interventions: Activity

71
Q

Assess / reposition every 2 hr
Pressure reduction devices
Skin care

A

Interventions: Skin

72
Q

Eliminate food irritants
Meds as prescribed
Frequent routine assessment of skin and mucosa
Encourage patient to maintain balance between rest and activity
Reposition at least every 2 hours and as needed
Pressure reduction devices
Instruct patient to avoid scratching
Use gentle, nondrying soaps or cleansers
Avoid adhesive tape
Perianal skin care
Assess bowel pattern; factors that exacerbate diarrhea
Avoid foods that act as bowel irritants, such as raw fruits and vegetables, carbonated beverages, spicy foods, and foods of extreme temperatures
Small, frequent meals
Administer medications as prescribed
Assess and promote self-care strategies to control diarrhea

A

Interventions: Bowels

73
Q

Control N/V/oral discomfort
Weigh daily
Relieve thrush as best as possible
High calorie/protein food
Fluid 2-3L day
Monitor weight, I&O, dietary intake
Dietary consult:high calorie, high protein, low fat
Control of nausea with anti-emetics
Oral hygiene
Treatment of oral discomfort
Dietary supplements
Enteral feedings or parenteral nutrition
Fluid intake 2-3 L day
Advise no alcohol
Fluid intake 2-3 L/day
Promotion of nutrition
Monitor weight
Provide high calorie, high protein, low fat
May become lactose intolerance
Destruction of intestinal villa
Can not absorb diet high in fat
Persons develop high metabolic rate as disease progresses and have an ↑ loss of body protein

A

Interventions: Nutrition

74
Q

Acceptance and understanding
Promote an atmosphere of acceptance and understanding
Assess social interactions and monitor behaviors
Allow patient to express feelings
Address psychosocial issues
Provide information R/T spread of infection
Educate ancillary personnel, family, and partners

A

Interventions: Isolation

75
Q

Encourage exercise
Don’t stop medications - prolong quality and length of life
Stress reduction - avoid excessive
Maintain vaccinations
Monitor labs
Assess for infections
Know When to call HCP for s/s of infection
Discuss risky behaviors and how to adjust these

A

N. health maintainence

76
Q

Rejection
Graft vs host disease
Hyperacute
Acute
Chronic rejection
N. implications
N. diagnosis

A

Transplant

77
Q

Graft versus Host
Graft - organ transplanted into the patient
Host - pt receiving transplant
Hyperacute
Acute
Chronic
Medications to prevent rejection
Prednisone
Tacrolimus (Prograf)
Cyclosporine (Neoral)
Mycophenolate Mofetil (CellCept)
Imuran (Azathioprine)
Rapamune (Rapamycin, Sirolimus)
Azathioprine (Imuran)
Sirolimus (Rapamune)
Everolimus (Zortress)
Specific types of transplants located in diff body systems - rejection process can be very complication - organ not self and try to destroy anything not self - suppress immune sys

A

Rejection

78
Q

Graft = Transplant
Host = Receptacle
Natural killer and cytotoxic cells
Attack transplant
Immune system reacts to non-self and destroys transplant
Must suppress the immune system

A

Graft vs host disease

79
Q

Occurs immediately
Antibodies react to antigens
Activates Complement cascade
Activates Blood clots throughout new organ - lead to necrosis - and various enzymes
Huge Inflammation
Massive cellular destruction
Kidneys most at risk
Once starts, cannot be stopped
s/s:
Physiologic distress
Low BP
High HR
Elevated Cr
Protein in urine
Mass rejection
Inflammatory response

A

Hyperacute

80
Q

1 week to 3 months
2 diff mechanisms
1.Antibody mediated vasculitis leads to vessel necrosis - destroys vessels
2.Cytotoxic and NK cells start inflammatory process and cellular lysis - kills cells - lyse cells so organ cannot func
Organ death may occur or may be medically managed.
Recognized quick enough may be able to save the organ with med changes

A

Acute

81
Q

Result of Inflammation and scarring - scar tissue develops from inflammation
Vessel occlusion
Chronic ischemia because of blood vessel injury
Specific to type of transplanted organ
From of graft versus hosts - foreign organ
In all pts - rate which occurs or controlled varies
Cure: retransplantation - delay as much as possible, preserving the integrity of the transplanted organ

A

Chronic rejection

82
Q

Be aware of rejection in conjunction with specific transplanted material (ie renal failure in kidney transplant
Give scheduled anti-rejection medication as scheduled - imp of regimen
Know anti-rejection medication and side effects
Know the anti-rejection medication lab values for therapeutic readings
Watch for manifestations of infection (Elevated temperature and heart rate)

A

N. implications

83
Q

Some of the most common side-effects of anti-rejection medicines can include higher blood pressure, higher blood sugar, weight gain, an increased chance of having infections, and increased risk of some forms of cancer.
is an increased risk of infection. Other, less serious side effects can include loss of appetite, nausea, vomiting, increased hair growth, and hand trembling. These effects typically subside as the body adjusts to the immunosuppressant drugs
stomach upset

A

Know anti-rejection medication and side effects

84
Q

Prednisone is available in liquid as Prelone (15 mg/5 ml) or in 1 mg, 2.5 mg, 5 mg, 10 mg, 20 mg, or 50 mg tablets. The tablets can be cut in half if necessary.
Prograf is available as liquid or in 0.5 mg, 1 mg, and 5 mg capsules.
Neoral is available in liquid form or in 25 mg and 100 mg capsules.
CellCept is available in liquid or in 250 mg capsules or 500 mg tablets.
Imuran comes as a 50 mg tablet that can be broken up. Some pharmacies, including the outpatient pharmacy at Cincinnati Children’s, can also prepare a liquid version of Imuran for patients who have trouble taking the tablet.
Rapamune comes in 1 mg and 2 mg tablets or as solution containing 1 mg/1 ml
5-20 ng/mL

A

Know the anti-rejection medication lab values for therapeutic readings

85
Q

Ineffective Protection r/t immunotherapy suppression

A

N. diagnosis

86
Q

Types
Type I -IgE mediated (allergy, angioedema, anaphylactic) - most severe and most rapid intervention
Type II -Cell specific (hemolytic reactions with blood transfusion)
Type III-Immune complex mediated (autoimmune disorders - RA)
Type IV-Cell-mediated (TB test and is +; Poison Ivy, Transplant rejection)
Types May occur simultaneously and/or sequentially (one can turn into another type)

A

Altered immune response: hypersensitivity disorders

87
Q

IgE
Hypersensitive reaction to an allergen
Involves blood vessels, all layers of skin, mucous membranes, and subcutaneous tissues
Depth of swelling can result in airway issue
Most common area:
Lips, face, tongue, larynx, and neck
Cause: ingested meds
Most common ACEIs and NSAID; food allergies
Greatest risk within the first 24 hours after taking the first dose, reaction can occur after days, months, and even years of therapy
Collaborative care and interventions

A

Angioedema (Type 1)

88
Q

Potential for airway obstruction due to mucosal swelling
Anxiety due to cerebral hypoxia and threat of death
Interventions focus
Stop reaction and ensuring an adequate airway
Reverse angioedema before laryngeal edema forms and intubation is needed - edema not reversed may do emergent tracheostomy if the pt does have airway that blocks off
Maintain gas exchange
Apply O2
Decrease swelling
Epinephrine
Corticosteroids
Diphenhydramine - Benadryl
Laryngeal edema forms
If intubation is not possible emergency tracheostomy if cannot stop swelling before airway blocked off
Antigen drug still in system – continue dose of meds to fight off drug
Go to ICU

A

Collaborative care and interventions - Angioedema (Type 1)

89
Q

Most severe
Unanticipated severe allergic reaction with rapid onset
Response = amount of allergen, amount of mediator released, sensitivity of target organ and person, route of entry
Clinical Manifestation:
Causative agents
Mild to severe; local or systemic
N. - prevention
Collaborative management
pt/fam edu: care and use of automatic epinephrine injections

A

Anaphylaxis (type 1)

90
Q

Overall edema, laryngeal edema, hypotension, bronchospasm, cardiovascular collapse, shock (anaphylactic shock because decrease in fluid from intravascular space)

A

Clinical Manifestation: - Anaphylaxis (type 1)

91
Q

Medications -Antibiotics and radiocontrast agents (most serious)
Foods, antitoxins, insect stings, latex

A

Causative agents - Anaphylaxis (type 1)

92
Q

Avoidance of potential Allergens
ALWAYS check for allergies/assess risk
Stay with patient when receiving new drugs especially IV antibiotics
Teach patient use of EpiPen, wear Medical ID bracelet or necklace
Desensitization therapy
Body exposure to small injection of allergen, gradually increasing doses to build up immunity (under medical supervision)

A

N. - prevention - Anaphylaxis (type 1)

93
Q

Stop drug/Change IV tubing/fluid bolus - fluid support - stablize BP - support kidneys to help clean it out
Call Rapid Response/Code cart
Patent Airway/Oxygen
Apply O2 100% NRB (non rebreather), place pt. in High Fowler’s position
Suction prn/ABGs prn
Monitor VS/pulse oximetry - tele
Medication
Subcutaneous epinephrine 1:1000 (0.3 to 0.5 ml) followed by continuous IV
Diphenhydramine (Benadryl)–block histamine; can give H2 blockers - pepsid type medications - reduce inflammation
Corticosteroids: second line drug
ICU- monitor for rebound (delayed reaction - still in their body) 4-8 hours after initial reaction

A

Collaborative management - Anaphylaxis (type 1)

94
Q

Practice assembly of injection device training device
Keep the device with you at all times.
Use device when any symptom of anaphylaxis is present and call 911
When needed, inject drug into top of high on outside of thigh high, with needle entering straight down.
Inject drug right through pants; avoid seams/pockets (fabric thicker)
After use go to nearest hospital for monitoring (next 4 to 6 hours)
Keep two drug-filled devices in case more than one dose is needed
Protect device from light and avoid temperature extremes

A

pt/fam edu: care and use of automatic epinephrine injections - Anaphylaxis (type 1)

95
Q

Autoantibodies directed against self cells that have foreign protein or other antigen
Autoantibodies bind with self cell creating immune complex
Self cell destroyed with attached protein
Examples
Hemolytic transfusion reactions (patient receives wrong blood type during a transfusion)
Clinical Manifestations
Collaborative management

A

Cytotoxic reactions (Type 2): EX: Hemolytic

96
Q

Pallor
Fatigue
Lightheadedness
Weakness
Dark urine
Jaundice
Heart murmur tachycardia
Enlarged liver/spleen

A

Clinical Manifestations - Cytotoxic reactions (Type 2): EX: Hemolytic

97
Q

Stop offending drug or blood product
Plasmapheresis
Filtration of blood to remove antibodies)
Treat symptoms
Complication
Hemolytic crisis and kidney failure
Hemolytic crisis
Large numbers of red blood cells are destroyed over a short time
Body cannot make enough RBCs to replace destroyed RBC-severe anemia leads to kidney damage
Precipitated by nonspecific factors
infection, surgery and transfusion
Kidney damage occurs due to the large deposits of debris and clotting

A

Collaborative management - Cytotoxic reactions (Type 2): EX: Hemolytic

98
Q

Antigen-antibody complexes formed in circulation and deposited later in vessel walls or other tissue (kidney, vessels, skin, joints)
IgG and IgM antibody-antigen immune complexes in circulation
Harmful effects caused by complement cascade activation
Attracts neutrophils
Unsuccessful phagocytosis
Release of lysosomal enzymes into inflammatory site
Many immune disorders are type 3
Ex: S. lupus, Rheumatoid arthritis
Autoimmune diseases

A

Immune complex rxns (type III)

99
Q

Production of antibodies against the body’s own cells; destructive process
Both antibody- and cell-mediated responses and products are directed against normal body cells
Incidence in general population around 5%
Over 200 diseases
Autoimmune disorders overlap
more than one disorder tend to occur
Women most commonly affected
Can affect all ages and gender
Autoimmune CT disorders
Primary target two major structural protein molecules
Elastin: major component of ligaments and skin
Collagen: component of tissues and blood vessels
Classic Diseases
Rheumatoid Arthritis
Systemic Lupus Erythematosus
Scleroderma
Many others

A

Autoimmune diseases - Immune complex rxns (type III)

100
Q

Damage to joints bilaterally & symmetrically
Women child bearing years
Exacerbations/remission
Triggers (physical and emotional stress)
Clinical Manifestations
Diagnosis criteria: American Rheumatism Association

A

RA

101
Q

Difficult to rise AM (pain, stiffness)
Joint pain/deformities
Rheumatoid nodules
Systemic

A

Clinical Manifestations - RA

102
Q

Four of Seven Criteria for diagnosis
Morning stiffness > 1 hour 6 wk duration
Soft tissue swelling of wrist, metacarpophalangeal or proximal interphalangeal joints for 6 wk duration
Symmetric soft tissue swelling
Rheumatoid nodules
Positive serum rheumatoid factor test
Radiographic changes in hands or wrist joints

A

Diagnosis criteria: American Rheumatism Association - RA

103
Q

Red = erythematosis
Lupus = wolf
Red wolf
Immune complexes invade organs
Characterized by variability
Mild to severe
Women in childbearing years
Exacerbation/remissions
Triggers:
Clinical manifestations
Criteria for diagnosis (American college of rheumatology)

A

Systemic Lupus Erythematosus

104
Q

Hormones
Menses/pregnancy exacerbate disease
Sun exposure
Infections
Drugs

A

Triggers: - Systemic Lupus Erythematosus

105
Q

Fever/fatigue/weak
Polyarthritis (non-deforming)
Myalgias
Raynaud’s/rashes
Peripheral neuropathies
Nephritis
leading cause of death
May affect many organs

A

Clinical manifestations - Systemic Lupus Erythematosus

106
Q

Four or more serially or simultaneously
Malar rash
Discoid rash
Photosensitivity
Oral ulcers
Arthritis (usually non-deforming)
ANA titer abnormal (>20)
Serositis (Pleuritis/Pericarditis)
Other organ involvement

A

Criteria for diagnosis (American college of rheumatology) - Systemic Lupus Erythematosus

107
Q

“Disease turns pt to stone”
Inflammation and progressive tissue fibrosis and occlusion of microvasculature by collagen
Two types
CM
Diagnostics tests and med treatment (autoimmune CT diseases)

A

Scleroderma (systemic sclerosis)

108
Q

African-American
Women middle age
Exacerbation/remissions

A

Inflammation and progressive tissue fibrosis and occlusion of microvasculature by collagen - Scleroderma (systemic sclerosis)

109
Q

Limited cutaneous disease-most common
Symmetric skin thickening limited to distal extremities and face.
Diffuse cutaneous disease
Organ involvement

A

Two types - Scleroderma (systemic sclerosis)

110
Q

Raynaud’s (early sign 90%)
Skin hardening
Sclerodactyly (Stiff fingers)
Telangiectasias
Dilated superficial blood vessels
Heartburn/dysphagia
Joint pain
Pulmonary fibrosis
Anti-centromere antibody
SCL-70

A

CM - Scleroderma (systemic sclerosis)

111
Q

Specialized blood tests
(RA factor, ANA, LE prep, complement levels)
CBC/Chemistry
Liver/renal function
X-ray joints
Chest X-ray
ECG
NO Cure
Pain control
Meds: Immunosuppressive
Physical therapy
Diet high in calories /vitamins
Joint support
Surgery
Correct deformity, restore function

A

Diagnostics tests and med treatment (autoimmune CT diseases) - Scleroderma (systemic sclerosis)

112
Q

Anxiety
Fatigue
Pain
Impaired mobility
Ineffective coping
Potential for Infection
Body Image
Knowledge deficit
Readiness for enhanced self-care
Assess for organ involvement
Prevent infection
Joint protection
Pain management
Skin Protection
Manage fatigue/Energy conservation
Enhance body image
Compliance with therapeutic regimen
Manage medications and side effects
Maintain optimal role function and self image

A

Autoimmune CT diseases: n. Diagnosis and intervetnions

113
Q

Assist with coping
Hereditary concerns
Pregnancy and sexual counseling
Ability to work
Physical changes may cause problems for body image and social isolation

A

Psychological Issues - Autoimmune CT disease: n. Counseling and edu

114
Q

Coping with chronic illness
Avoidance of stress
Protection from infections
Establish exercise program
Diet and nutrition counseling
Sun restriction/physical limits
Pregnancy

A

Patient / Family Education - Autoimmune CT disease: n. Counseling and edu

115
Q

Mediated by T cell lymphocytes – do not involve antibody
Delayed: 12-72 hours after exposure to antigen
Example: TB test, poison ivy, Graft vs Host
Graft-versus-host disease (GVHD)
Immune cells present in donor tissue (the graft) attack host’s own tissues
Clinical manifestations
Skin rash, jaundice, GI
Immunosuppressive medications (prednisone; cellcept)are primary therapy

A

Delayed hypersensitivity (Type IV)