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PATHO > Hypersensitivites > Flashcards

Hypersensitivites Flashcards

1
Q

What are immunosuppressants for?

A

Dec immune response—Transplant pt, autoimmune conditions; suppress cell-mediated immunity, anti inflammatory

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2
Q

Antihistamines

A

Dec sx of inflammatory immune response; suppress histamine mediator activity

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3
Q

Epinephrine Class

A

Vasopressor, bronchodilator, anti asthmatic, vasoconstrictor

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4
Q

Epinephrine indications

A

Severe allergic rxn, cardiac arrest, severe asthmatic attack

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5
Q

Epinephrine MOA

A

Inhibits release of mediators from mast cells; works on alpha receptors (arteries) and beta receptors (heart, lungs and skeletal muscles)

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6
Q

Epinephrine Side Effects

A

CV: angina, arrhythmia, HTN, tachycardia
CNS: nervousness, restless, tremor

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7
Q

Giving EPI

A

All routes but PO, SQ preferred, start with lowest dose possible (wt based in peds), be careful with the dose bc they can vary a lot

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8
Q

Epinephrine NC

A

Monitor VS closely and watch for reversal sx; overdose can be FATAL bc vasoconstriction—have coworker check dose if drawing it up; use TB syringe for SQ use; for home use, teach to take as directed and contact HCP and go to ED/clinic after taking; teach epipen has expiration date

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9
Q

Hypersensitivity

A

normal immune response that is excessive or inappropriately triggered or produces undesirable effects on the body

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10
Q

Hypersensitivities I, II, and III

A

mediated antibodies produced by plasma B cells

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11
Q

Hypersensitivity type IV MOA

A

Mediated by T cells (no B cell involvement)

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12
Q

Triggers for hypersensitivities

A

specific antigen-antibody reaction or specific antigen-lymphocyte interaction; occurs on second exposure with specific antigen

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13
Q

Type I

A

IgE mediated rxn; in response to someone developing an allergy after being sensitized to an antigen (rxn is 15-20 minutes after the second exposure to antigen); often pet dandruff and and pollen, foods (eggs, nuts), meds; genetic basis

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14
Q

Cells involved in Type 1

A

B lymphocyte, IgE antibodies, mast cells (granulocytes)

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15
Q

Type 1 pathogenesis

A

allergen attaches immature B cell w/ first exposure and B cell matures, B cell turned on and matures to plasma cell that makes IgE antibodies, IgE attach to mast cells which release chemical mediators at the second exposure, causing an allergic rxn rxn

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16
Q

What do chemical mediators cause in Type 1?

A

vasodilation—dec BP, stuffy nose, wheals on skin, bronchial constriction–throat swells, wheeze, stimulates irritant receptors—itchy, inc vasc permeability–edema and nose run

17
Q

What do allergy shots do?

A

dec sensitivity of B cells so they don’t release IgE antibodies

18
Q

Atopic rxn to Type 1

A

Acute and localized; asthma, allergies, rhinitis, runny nose, hives; pollen, dust, dandruff

19
Q

Anaphylactic rxn

A

systemic release of chemical mediators that cause life-threatening sx like swelling, airway obstruction, vascular collapse–shock

20
Q

Most common triggers for anaphylaxis

A

meds, bee stings, food; only need a small amount

21
Q

tx for anaphylaxis

A

GCC, anti-histamines; pt wear medical alert bracelets, carry EPI pen

22
Q

Type II hypersensitivity

A

Cytotoxic rxn mediated by immunoglobulins after exposure to antigens or foreign tissue/cells located on cell surface

23
Q

Type II Pathogenesis

A

Antigens stimulate an antibody response and form an antibody-antigen complex that attacks cells and destroys–cell lysis and phagocytes

24
Q

Cell involved in Type II hypersensitivity

A

IgG and IgM cells, complement cells (kill foreign antigens), phagocytes

25
Q

Examples of Cytotoxic antigens

A

blood transfusion, autoimmune disorders like DM, erythroblastosis fetalis–difference in Rh btwn mom and child, drug rxn

26
Q

How does cytotoxic rxn occur with different blood types?

A

Donor A and recipient B trigger anti-A and anti-B which all clump together and donor cells burst–blocks small vessels and debris in veins

27
Q

sx of Cytotoxic rxn

A

blood transfusion rxn–fever, chills, flush from chemical mediators, chest and back pain from clogged vessels, N/V, HA, anxiety, restless

28
Q

What should you do before and after a blood transfuion?

A

Take temperature before and after

29
Q

Type III hypersensitivity

A

Immune complex rxn; local or systemic antigen-antibody complex that attaches to tissue, causing INFLAMMATION which can cause tissue damage

30
Q

rheumatoid arthritis

A

antigen-antibody complex that attaches to joints

31
Q

Type III cause

A

autoimmune or low grade infx (body gets confused and attacks) or inhaled antigens from mold or contaminated plants

32
Q

Cells involved in Type 3 immune complex rxn

A

IgG and IgM (clump with antigens), complement (destroy tissues with mast cells), neutrophils (release chemical mediators and mast cells)

33
Q

Glomerulonephritis

A

Kidney failure from complex binding to kidneys

34
Q

systemic lupus erythematosus

A

complexes bind to skin and many organs, causing inflammation

35
Q

Type IV hypersensitivities and examples

A

Delayed hypersensitivity without antibody involvement; poison ivy, TB test, jellyfish sting, jewelry rxn, Crohn’s disease

36
Q

Immune cells involved in type IV

A

T cells (no B cells), cytokines, mast cells, macrophages

37
Q

Type IV etiology

A

delayed cell rxn to antigen from plant oils, cosmetics, nickel alloy, TB antigen, gluten, organ transplant/graft, contact dermatitis, tuberculin

38
Q

Type IV pathogenesis

A

small particles/incomplete proteins called “Hapten” penetrate the skin and combine with human proteins to form complete antigens; antigen processing cells (T cells) recognize and attach the antigen via direct attack and release cytokines and macrophages

39
Q

When does a delayed hypersensitivity peak?

A

48-72 hours

PATHO (32 decks)

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