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Pathopharmacology > NUR 228 Exam 1 > Flashcards

NUR 228 Exam 1 Flashcards

1
Q

Hypersensitivity

A

a NORMAL immune response that is inappropriately triggered OR excessive OR produces undesirable effects on the body.

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2
Q

What are two basic triggers?

A

antigen-antibody reaction
antigen-lymphocyte interaction

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3
Q

What is in common between types I, II, III hypersensitivity reactions?

A

they are all mediated by antibodies produced by B cells
-specifically PLASMA cells

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4
Q

What causes type IV hypersensitivity

A

mediated by T cells

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5
Q

What kind of hypersensitivity reactions does meds typically cause?

A

type I and IV

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6
Q

What type of hypersensitivity reaction does PCN cause

A

all four types

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7
Q

What kind of mediated reaction is type I

A

IgE mediated reaction

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8
Q

Type I hypersensitivity reaction

A

caused by B cells
Immediate reaction
occurs after being sensitized to an antigen

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9
Q

what antigens cause type I hypersensitivity?

A

environmental(pet dander, bee stings)
Foods (nuts, seafood, eggs)
Medications (penicillin, contrast dye)

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10
Q

What are key immune cells involved in Type 1 reaction?

A

B lymphocytes
IgE (antibody)
Mast cells (granulocyte)

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11
Q

Etiology of Type 1

A

Genetic link
1 parent allergic=30%
2 parents allergic= 50%

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12
Q

What is the pathogenesis of type 1?

A

-person exposed
-IgE antibody made
-IgE antibody attaches to mast cell
-person exposed again
-allergen binds to the IgE antibodies that are attached to the mast cells
-triggers the release of chemical mediators from the mast cell

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13
Q

Potent vasodilation causes

A

stuffy nose
lower blood pressure
wheals on skin

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14
Q

Increased vascular permeability causes

A

edema
runny nose

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15
Q

Bronchial smooth muscle constriction causes

A

breathing difficulties
wheezing

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16
Q

Stimulates irritant receptors causes

A

itching

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17
Q

Atopic reactions

A

local
inherited tendency to become sensitive to allergens
Ex: allergic rhinitis, asthma, urticaria(hives)

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18
Q

Anaphylactic reaction

A

systemic
life threatening because of bronchial constriction, airway obstruction, vascular collapse.
treat quickly

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19
Q

Most common triggers of atopic and anaphylactic reactions?

A

Atopic: pollen, dust, mold, animal dander
Anaphylactic: meds, bee stings, foods

20
Q

What causes the symptoms from a type 1 hypersensitivity reaction?

A

release of chemical mediators

21
Q

What is type II caused by?

A

b-cells

22
Q

Etiology of Type II reactions

A

exposure to antigen or foreign tissue/cells
antigens are located on cell surface

23
Q

What are the key characteristics of a type II reaction

A

-antigens stimulate antibody production
-antibodies recognize and attach to cell surface antigens
-direct destruction of targeted cells that contain the antigen
——-cell lysis
——-phagocytosis

24
Q

what immune cells are involved with a type II reaction?

A

antibodies (IgG and IgM)
complement
WBCs (phagocytes)

25
Q

what are the examples of antigens of type II

A

blood
some of your body’s own cells (autoimmune)
erythroblastosis fetalis

26
Q

What are some example disorders from type II

A

blood transfusion reaction
newborn/mother Rh incompatibility
autoimmune disorders
certain drug reactions

27
Q

What are some examples of type II manifestations of a transfusion rx?

A

Fever
Chills
angina
N/V
restlessness and anxiety
headache

28
Q

What kind of reaction is type III?

A

Immune complex reaction

29
Q

Key characteristics of type III hypersensitivity

A

antigen-antibody COMPLEXES (attach to each other) form
deposit into tissues
inflammatory response causes tissue damage

30
Q

Etiology of Type III HSRx?

A

autoimmune
low grade infection
inhaled antigens from molds or contaminated plants

31
Q

What are possible offending antigens for type III?

A

bodys own tissues/dna
Inhaled antigens from mold or contaminated plants
bacteria or viruses

32
Q

What are key immune cells involved in type III sensitivity?

A

IgG and IgM antibodies that clump with antigens
complement
neutrophils and mast cells

33
Q

Type III Pathogenesis?

A

antigen-antibody complex formed in blood
deposits in tissue
activation of complement + chemoattraction of neutrophils
Fc Receptor
Release of enzymes and free radicals
Tissue distruction

34
Q

What are clinical manifestations of Type III?

A

depends on where the complexes are deposited in the tissue
Rheumatoid arthritis: joints
Glomerulonephritis: kidney failure
Systemic lupus erythematosus: skin and organs

35
Q

What are the primary differences between type II and type III?

A

type II- reactions occur on the cell surface and result in direct cell death or malfunction

type III- immune complexes are deposited into tissues and the resulting INFLAMMATION destroys the tissue

36
Q

What is type IV hypersensitivity?

A

Delayed hypersensitivity

37
Q

What are key characteristics of Type IV hypersensitivity

A

delayed hypersensitivity response
NO antibody involvement

38
Q

What are key immune cells for type IV

A

T cells
Cytokines
Mast cells and macrophages

39
Q

Etiology of type IV

A

delayed cellular reaction to an antigen

40
Q

What are some antigens for type IV

A

plant oils
cosmetics
nickel
tuberculin
organ transplant
skin graft

41
Q

Type IV pathogenesis

A

small incomplete antigen (hapten) penetrates the skin
Hapten combines with human protein to form the complete antigen
T cells become aware of antigen
T cells attack the antigen via:
-direct attack of t cell
-release of cytokines
-macrophages

42
Q

what are clinical manifestations of type IV

A

generally peak 48-72 hours
contact dermatitis
tuberculin hypersensitivity

43
Q

Autoimmunity

A

the immune system recognizes “self” cells as foreign
an immune responses is initiated
your bodies own tissues are injured

44
Q

Etiology of autoimmunity

A

genetic factors
environmental triggers

45
Q

antigenic mimicry

A

some viruses/bacteria look like “self”
self cells similar to these foreign cells are attacked

46
Q

Risk factors of autoimmunity

A

over age 50
genetics
female
African american, hispanic, asian, native american
viral bacterial infections

47
Q
A

Pathopharmacology (3 decks)

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