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MedSurg 1 > Immune Disorders > Flashcards

Immune Disorders Flashcards

1
Q

Types of Immune Responses:

A

Altered Immune Responses:
Type I: IgE-mediated Anaphylactic reactions
-anaphylaxis, angioedema, atopic reactions (allergic rhinitis, eczema, asthma), urticaria

Type II: Cytolytic/toxic reactions
-hemolytic blood transfusion reaction

Type III: Immune Complex reactions
-autoimmune diseases (SLE)

Delayed Hypersensitivity Reactions:
Type IV: Cell-mediated response (contact dermatitis)

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2
Q

Immunocompetence

A

the body is able to identify, inactivate and destroy foreign substances

appropriate way to respond

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3
Q

Altered Immune Response:

A

Incompetent/under-responsive: severe infection, immunodeficiency disease, malignancy may occur

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4
Q

Overresponsive:

A

hypersensitivity, allergies, autoimmune diseases

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5
Q

Type I: Overview

A

occurs in pts who are highly susceptible to certain allergens

first exposure: IgE antibodies form and attach to mast cells and basophils

second and subsequent exposure: allergens attach to IgE causing cells to release chemicals-histamine, ECF-A, leukotrienes, serotonin, kinin, bradykinin which target organs/tissues and cause sx

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6
Q

Type I: Sx

A 
Smooth muscle contraction
increased vascular permeability
Vasodilation
Hypotension
Pruritis
increased mucus production
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7
Q

Type 1: Anaphylactic Reactions

A

Anaphylaxis:
usually occurs w/in minutes
life threatening d/t bronchial constriction and vascular collapse
if d/t injection or insect bite initially will see itching, edema, erythema at site

Shock (vascular collapse):
rapid weak pulse
decrease BP
dilated pupils
dyspnea
possible cyanosis

Bronchial and angioedema

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8
Q

Type 1: Tx

A 
ABC's
O2
Epinephrine (0.5ml every 5-10min)
Antihistamine
IV steroid

*these vasoconstrict and increase BP

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9
Q

Type 1: Angioedema

A

swelling in deeper layers of skin (eyelids, lips, tongue, larynx, hands, feet, GI tract, genitalia)
progression
skin may appear normal or have reddish hue
if lesions may be itchy
several hours to days

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10
Q

Type 1: Atopic Reaction

A

occurs in 20% of population

form of allergy which is hypersensitive and occurs in part of the body that is not in contact with the allergen

inherited tendency to be sensitive to environmental allergies includes: allergic rhinitis, asthma, atopic dermatitis/eczema, urticaria

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11
Q

Type 1: Asthma

A

bronchial action d/t ECF -A (slow reacting substance of anaphylaxis) & histamine

bronchial smooth muscle contraction

excessive mucus

edema of bronchial mucosa

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12
Q

Type 1: Atopic Dermatitis

A 
Eczema:
chronic inherited skin disorder
caused by environmental allergens
an "itch that rashes"
skin reaction is more generalized or can be patchy-redness, swelling, cracking, weeping of clear fluid, scaling and crusting

Tx: hydrocortison, moisturizer, hydration

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13
Q

Type 1: Urticaria

A

acute skin reaction to systemic allergen occurring in atopic person

sx: transient wheals varying in size and shape with flaring caused by histamine

rapid development post-exposure

lasting minutes to hours

itching

tx: antihistamines, epinephrine if sever and no response to antihistamine

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14
Q

Type II: Cytotoxic and Cytolytic Reactions Overview

A

Reaction d/t activated complement system which mediates the reaction - involves IgG and IgM

causes cell destruction-erythrocytes, leukocytes, platelets

seen in:

  • ABO and Rh incompatibility blood transfusion reactions
  • autoimmune and drug related hemolytic anemias, leukopenia, thrombocytopenia
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15
Q

Type II: Acute Hemolytic Transfusion Reaction Overview

A

90% d/t mislabeled blood product or wrong pt

develop in first 15 min of starting blood product transfusion

agglutination of RBC obstructs capillaries which blocks clotting factors and can allow bleeding

RBC destruction releases Hgb which is filtered by kidney

Kidney tubules blocked can lead to Acute Renal Injury (ARI)

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16
Q

Type II: Acute Hemolytic Transfusion Reaction Sx

A 
fever, chills
low back pain
flushing
tachycardia
tachypnea
hypotension
vascular collapse
dark urine
watch for shock
*can lead to cardiac arrest, ARI, death
17
Q

Type II: Acute Hemolytic Transfusion Reaction Nursing Interventions

A

Stop transfusion and keep vein open (kvo) with NS
remain w/ pt, VS and focused assessment
notify HCP
frequent monitoring for Sx of complications, monitor I&O
collect necessary blood and urine samples
blood and tubing returned to lab for sampling/testing

18
Q

Febrile Reaction (Other type of blood product transfusion reaction):

A

caused by leukocyte incompatibility

commonly caused by multiple blood transfusions

Sx: sudden fever, chills, HA, flushing, muscle pain

Interventions: Stop transfusion, kvo, notify MD, antipyretics

Prevention: additional filter on tubing, use of leukocyte-poor blood products

19
Q

Allergic Reaction (other type of blood product transfusion reaction - type I immune response)

A

sensitive to plasma proteins

increases in pts with allergies
may be mild or anaphylactic

sx: hives, itching, flushing, wheezing, cyanosis, shock, cardiac arrest

Interventions: stop transfusions, kvo, notify MD

  • antihistamine
  • restart if sx transient and mild
  • do not restart if fever or resp sx
  • epinephrine

Prevention: admin antihistamine prior to transfusion if known hx allergies per order

20
Q

Circulatory Overload (other type of blood product transfusion reaction)

A

infusion rate too fast and/or pt with decreased cardiac or renal function

elderly at increased risk

Sx: dyspnea, cough, lungs-crackles, tachycardia, increased BP, distended neck veins

Interventions:

  • decrease infusion rate
  • raise HOB with feet dependent
  • notify MD
  • O2
  • diuretics

Prevention: adjust rate per pt size and tolerance

21
Q

Septicemia Reaction (other type of blood product transfusion reaction)

A

transfusion of contaminated blood products

Sx: rapid onset of chills, high fever, V, D, decrease BP, shock

Interventions:

  • stop transfusion, kvo, notify MD, VS
  • blood cultures, return blood and tubing to lab for testing
  • O2, IVF, antibiotics, vasopressors, volume expanders

Prevention: infuse within 4 hours
*general rule: blood products should never infuse longer than 4 hours (2-4 hours is good range)

22
Q

Type III: Immune Complex Reactions Overview

A

Complexes form (antigens and immunoglobulins) are deposited in tissues and capillaries, become fixed and release chemotactic factors leading to inflammation and destruction of involved tissue

Local or systemic, immediate or delayed

common sites: kidneys, skin, joints, blood vessels, lungs, heart

Autoimmune: ex) RA, SLE, Myesthenia Gravis, Type 1 DM

23
Q

Autoimmunity

A

immune system no longer differentiates self from non-self

cause is unknown: age, gender, hormones play part

principle factors include:

  • inheritance of susceptibility gene
  • initiation of autoreactivity by triggers (usually viral infection)
24
Q

Type III: SLE Overview

A

chronic progressive multi-system inflammatory disease, extremely variable, difficult to predict progression

periods of exacerbations and remissions

more common in women of child bearing age

African Americans, Asians, Native Americans

Cause is unknown, probably has genetic component

25
Q

Type III: SLE Precipitating Factors/ Triggers

A

menarche or pregnancy (esp the immediate postpartum period) due to hormonal fluctuations

sun exposure (can be from tanning beds due to UV light)

Meds

Stress (can cause flair up)

26
Q

Type III: SLE Sx (Early Symptoms, Skin, Musculoskeletal, Cardiopulmonary, PV, Renal, Nervous)

A

onset or exacerbation after menarche

Prodrome (early symptoms): excessive fatigue, fever, weight loss, arthralgia (joint pain)
*classic Sx when they all occur together

Skin: dry, scaly rash on sun exposed areas

  • butterfly rash on cheeks and nose (50% SLE pts have this)
  • ulcers of mouth and nose
  • alopecia w or w/o lesions (hair regrows except where lesions were)

Musculoskeletal: polyarthralgia w/ AM stiffness, arthritis (90%) non erosive but may have deformities

Cardiopulmonary: tachypnea, cough-restrictive lung disease)

  • arrhythmias d/t fibrosis of SA and AV node
  • HTN, CAD accelerates and need aggressive therapy
  • Pericarditis, endocarditis

Peripheral Vascular: Raynauds phenomenon - arterial vasospasm in response to cold/stress

Kidneys: Lupus nephritis (40% w/in 5 years of dx

  • starts with mild proteinuria and progresses rapidly to glomerulonephritis
  • goal of tx: to slow progression and preserve function by managing disease

Nervous system: seizures, peripheral neuropathy
-organic brain syndrome: disordered thought process, memory prob, depression, psychosis, probable recovery but with some residual impairment

27
Q

Type III: SLE Hematologic Sx

A

anemia, antibody formation against blood cells, bleeding and clotting problems

  • leukopenia-infection: increases susceptibility, pneumonina
  • common cause of death, fever needs to be taken super seriously, no live vaccines

thrombocytopenia: bleeding OR
hypercoagulability: excessive clotting and requires treatment with coumadin

28
Q

Type III: SLE Diagnostic Tests

A

ANA (antinuclear titer antibody) titer: positive 97% of time
Antismith antibodies (Anti-Sm): positive 30-40% of time and are considered diagnostic
ESR and CRP: used to monitor disease activity and response to treatment
Complement system: C3 and C4 are diagnostic for SLE - become depleted due to exaggerated inflammatory response
-CBC, BUN and creatinine, UA

29
Q

Type III: SLE Interventions

A

manage active phase of disease (exacerbations) while preventing long-term tissue damage

  • better prognosis associated with early dx
  • monitor for complications of disease (infection, bleeding/clotting, heart and lung, renal, neuro, and perform necessary interventions to address these problems)
30
Q

Type III: SLE Medications

A

corticosteroid: acute phase for inflammation and immunosuppression

NSAIDS: pain and inflammation

Plaquenil (antimalarial): decrease inflammatory response in joints, fever and fatigue (takes 2-3 months to take effect, not for acute, used for chronic)

Immunosuppressive Drug: methotrexate, imuran - chronic tx of inflammation and disease progression

MVI, Folic Acid, and Fe supplement

31
Q

Type III: SLE Tx

A

Plasmapheresis: done through IV access

  • removal of plasma containing antibodies, complexes, and inflammatory mediators (complements) that are causing tissue destruction
  • used in exacerbation phase when pt is not responding to corticosteroid tx
  • plasma volume is replaced with NS or LV

Acute phase: documentation of therapy, fever pattern, joint inflammation, fatigue

  • monitor respiratory and cardiac function (daily weight, I&Os d/t corticosteroid use, watch for sx of FVE)
  • monitor kidney function and watch for signs of renal failure
  • watch for s/sx of bleeding or clotting
  • neuro status, peripheral neuropathy
32
Q

Type III: SLE Education

A

Educate on disease process, therapy, risk for infertility

Avoid/ eliminate exposure to precipitating factors - fatigue, sun exposure, stress, infection

33
Q

Type III: SLE Psychological Considerations

A

vague onset - undiagnosed
hereditary considerations - genetic counseling
self-esteem issues as well as fatigue and pain interfering with quality of life
family/friend education re disease process
young adults have difficulty with decreased sun exposure and physical limitations

34
Q

Type IV: Delayed Hypersensitivity Overview

A

Sensitized T-lymphs attack antigens or release cytokines which attract macrophages, releasing enzymes causing tissue destruction

takes 24-48 hours for reaction to occur after exposure

ex) contact dermatitis, microbial hypersensitivities (TB), transplant rejections, some drug sensitivities

35
Q

Type IV: Contact Dermatitis

A

skin is first introduced to substance and epidermal proteins become antigenic. Memory cells form 7-14 days later)

subsequent exposure: person develops eczematous rash in 48 hours
-metals (nickle, mercury), catechols (poison ivy, oak, sumac), cosmetics, rubber compounds (latex)

acute sx: skin edematous, red, papules, vesicles, itchy, burning, stinging

latex allergies can be type I or type IV

36
Q

Type IV: Latex delayed hypersensitivity

A

caused by chemicals in manufacturing process of gloves

6-48 hours post-exposure

Sx: dryness, itching, fissures, redness, swelling, crusting (24-48 hours)

chronic exposure: leads to lichenification (thickening of skin), scaling, and hyperpigmentation

MedSurg 1 (18 decks)

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