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NUR 612 Advanced Pathophysiology > Module 2.4 Immune disorders > Flashcards

Module 2.4 Immune disorders Flashcards

1
Q

Primary Immune disorders

A

Congenital or inherited

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2
Q

Why are primary disorders increasing in number over time

A

increased awareness and diagnosis. NOT increased incidence.

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3
Q

Humoral Immunity

A

B-cells, antibody immunity

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4
Q

Cell Mediated Immunity

A

T-Cell

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5
Q

4 Major Categories of Immune system

A

Humoral
Cell-Mediated
Compliment System
Phagocytosis (bridge between innate and acquired)

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6
Q

B-cell immunodeficiency is associated with

A 
Enteroviruses
Streptococcus
H. Influenzae
Giardia lamblia (protozoa)
NO FUNGALS
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7
Q

T-Cell Immunodeficiency is associated with

A

Herpes
Salmonella
Mycobacteria
Candida Albicans and many other fungal infections

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8
Q

Combined T-cell and B-cell immunodeficiency is associated with

A

All viruses
Neisseria Meningitis
Toxoplasmosis gondii

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9
Q

Allografts

A

from other people

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10
Q

Autografts

A

From self

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11
Q

Transient Hypogammaglobulinemia of infancy

A

transient deficiency in some infants. Causes recurrent pyrogenic illnesses

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12
Q

B-cell immunodeficiency is usually not associated viruses. Why? What’s the exception?

A

B-cells don’t engage with intracellular pathogens.

Exception: enteroviruses

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13
Q

What causes x-linked agammaglobulinemia

A

Pre-B Cells fail to migrate to lymphoid tissue resulting in no immunoglobulin production at all

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14
Q

DiGeorge Syndrome

A

Primary T-Cell Deficiency
Congenital heart disease
Hypocalcemia
Complete or partial failure of Thymus and parathyroid development.

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15
Q

Most common primary immunodeficiency

A

Primary Humoral (B-cell) deficiency. (70%)

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16
Q

Secondary Cell Mediated immunodeficiencies are caused by

A

Acute viral syndromes

some cancers

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17
Q

Severe Combined Immunodeficiency (SCIDs)

A

X-linked inheritance

Combined T cell and B cell deficiency

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18
Q

Ataxia–telangiectasia

A

Autosomal Recessive Inheritance

Combined T cell and B cell deficiency

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19
Q

Ataxia–telangiectasia S/S

A 
Occulocutaneous telangiectasis (big red vessels in eyes).
Ataxia (kid cant walk when it's time to learn).
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20
Q

Ataxia-telangiectasis immune effects

A

T-Cell function unchanged but decreased in number

Deficiency in IgA IgE and IgG

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21
Q

Wiskott-Aldrich Syndrome

A

X- Linked recessive (affects boys primarily)

Combined T cell and B cell deficiency

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22
Q

Wiskott-Aldrich Syndrome S/S

A

Thrombocytopenia
Recurrent Infections
Eczema

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23
Q

Wiskott-Aldrich Syndrome Prognosis

A

life expectancy 15 years

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24
Q

Wiskott-Aldrich Syndrome immune effects

A

Low IgM
High IgA and IgE
Limited T-cell function which improves with time

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25
Q

Wiskott-Aldrich Syndrome treatment

A

Stem Cell or Bone Marrow transplant

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26
Q

How are most primary compliment system disorders acquired

A

autosomal recessive

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27
Q

Hereditary angioneurotic edema is associated with

A

Primary compliment system disorders.

28
Q

Hereditary angioneurotic edema is caused by

A

Swollen mucous membranes (airway, lips, deep localized tissue swelling)

29
Q

What causes Secondary compliment system disorders

A

Rapid activation -> depletion

or reduced synthesis of compliment components

30
Q

Dysfunction of the phagocytic system would make one particularly susceptible to:

A

FUNGAL INFECTIONS!
Candida species
Filamentous fungi

May also result in chronic granulomatous disease (CGD)

31
Q

Hypersensitivity types and their associated systems

A

Type I - IgE mediated
Type II - Antibody mediated
Type III - Complement mediated
Type IV - T-Cell Mediated

32
Q

Type I hypersensitivity

A

Allergies! Causes release of histamines from MAST cells

33
Q

Management of Type I

A

Avoid offending agent
Nasal steroids
Cromolyn Sodium (Mast cell stabilizer)
Desensitization (allergy shots)

34
Q

What is the basic principle behind desensitization

A

Increase IgG antibodies to the antigen so that IgG binds rather than IgE which is what causes the reaction.

35
Q

Primary/initial phase of Type 1 response

A

IgE stimulates Mast cells, basophils and eosinophils.

Vasodilation
Vascular Leakage (swelling)
Smooth muscle contraction

36
Q

Secondary/late phase of Type 1 response

A

More intense infiltration of tissue with eosinophils

Endothelial cell damage

37
Q

What causes the secondary/late phase response of type 1 hypersensitivities

A

T-cell recruitment of eosinophils
+
Degranulation of mast cells causing release of membrane phospholipids (arachidonic acid, prostaglandins, leukotriens).

38
Q

What determines the severity of type 1 reactions

A

Degree of Sensitization (# of IgE receptors on mast cells or number of mast cells).
NOT the quantity of exposure.

39
Q

Grades of Type reactions

A

I: Cutaneous and Muscle Erythema, Urticaria.
II: Multisystem S/S Hypotens. Tachycardia, dyspnea, N/V, Diarrhea
III: Bronchospasm, dysrhythmias
IV. Cardiac Arrest

40
Q

ABC priority

A

BAC now

41
Q

Type II (cytotoxic) reactions are mediated by

A

IgG and IgM

42
Q

Most common Type II reaction example

A

Blood transfusion reactions and Hemolytic disease of the newborn

43
Q

Which antibody causes hemolytic disease of the newborn

A

IgG - only one that can cross placenta

44
Q

SEE PAGE 319 IN BOOK FOR TYPE 2 REACTION TABLE

A

SEE PAGE 319 IN BOOK FOR TYPE 2 REACTION TABLE

45
Q

Serum Sickness

A

Systemic Type 3 (immune complex) reaction

Takes 1-2 weeks to manifest

46
Q

Arthus Reaction

A

Localized Type 3 (immune complex) reaction

47
Q

What causes type 3 reaction

A

Antibody-Antigen complex forms, binds to cell membrane causing compliment system activation which attracts inflammatory cells

48
Q

Type IV hypersensitivity

A

T-cell mediated.

Can be Direct cell-mediated or Delayed Type

49
Q

Delayed Type IV reaction

A

CD4 T cells release cell damaging cytokines

Contact dermatitis, farmer’s lung,

50
Q

Direct Cell Mediated Type IV reaction

A

CD8 T Cells kill antigen bearing target cells

51
Q

Latex reactions are what type of reactions

A

Can be type I or IV

Symptoms determine the type

52
Q

Transplanted tissue categories and definitions

A

Allogeneic - Similar HLA types between donor and recipient (may or may not be related)

Syngeneic - Identical twins

Autologous - Same person

53
Q

Central tolerance

A

Elimination of self reactive T-cells (in thymus) and B-cells (in bone marrow)

54
Q

Peripheral tolerance

A

Deletion of auto-reactive cells that escaped central tolerance elimination

55
Q

Hyperacute Transplant Rejection

A

occurs almost immediately.

Type II reaction, arthus reaction.

56
Q

Acute Transplant Rejection

A

Occurs in first few months

T-Lymphocytes respond to antigens in graft tissue.

57
Q

Chronic Host-Versus-Graft Rejection

A

Occurs over years

Fibrosis of blood vessels in transplanted organ. unknown mechanism

58
Q

Graft Versus Host Disease

A

Grafted organ attacks host body. takes 10-14 days

59
Q

GVHD requirements

A

must be an organ with functional immune component

Host immune system must be compromised to the point of being unable to destroy the transplanted organ.

60
Q

GVHD Clinical manifestations

A

Palm and feet rashes

61
Q

Systemic Lupus Erythematosus

A

Autoimmune disease
Butterfly rash
Causes systemic issues with most organs/systems

62
Q

Autoimmune Hemolytic Anemia

A

Antibodies attack host blood cells

63
Q

Pemphigus Vulgaris

A

Blistering of skin and Epithelial linings.

64
Q

Hashimoto Thyroid

A

first ever autoimmune disease discovered

Causes hypothyroid

65
Q

Diagnostic criteria for autoimmune disorders

A

Evidence of autoimmune reaction
Determination that it’s not secondary to another condition
Lack of other identified causes
Lab tests

66
Q

Lab tests to demonstrate autoimmune reactions

A

Indirect Fluorescent Antibody Assay (IFA)
Particle agglutination assay
Enzyme Linked Immunosorbent assay (ELISA)

NUR 612 Advanced Pathophysiology (21 decks)

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