Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology 1 > Ch. 6 Disorders Of The Immune System > Flashcards

Ch. 6 Disorders Of The Immune System Flashcards

0
Q

Two forms of immune response?

A

Natural and acquired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
0
Q

Where is IgA found?

A

Mainly in mucosal secretions (tears, nasal, resp. tract), breast milk, intestinal tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What does “immunity” mean?

A

From Latin term - exemption from duty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is natural immunity?

A

Mechanical and cellular defense mechanism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Function of IgA?

A

Protective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is acquired immunity?

A

Concept of self vs non self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is IgE found?

A

Trace amts in serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

3 protective proteins in natural immunity?

A

Complement, properdin, lysozyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What secretes IgE?

A

sensitized plasma cells in tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is properdin ?

A

Plasma protein that activates alternative complement pway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are IgEs attached to?

A

Locally attached to mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are lysozymes?

A

Low molecular weight proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Function of IgE?

A

Mediates allergic rxns in tissues (hay fever, asthma) and protects against parasites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where are lysozymes found?

A

Tears, nasal secretions, intestinal secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where is IgD found?

A

Exclusively on B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is immunocompetence?

A

Ability to mount a response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Function of IgD?

A

Participates in antigenic activation of B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the body’s first line of defense?

A

Skin - mechanical and chemical barriers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Is IgD released into serum of body fluids?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the body’s second line I defense?

A

Skin - inflammatory response, phagocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is MHC?

A

Major histocompatibility complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the body’s third line of defense?

A

Skin - specific immune responses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why is MHC essential?

A

For presentation of antigens to T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the cells of the immune system?

A

Lymphocytes, plasma cells, macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is MHC aka?

A

human leukocyte antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Types of lymphocytes?

A

T and B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Two groups of MCH , and what are they receptors for?

A

Type 1 - R/Cs for CD8 Type 2 - r/cs for CD4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Types of t lymphocytes?

A 
T helper (CD4+)
T suppressor/cytotoxic (CD8+)
Natural killer (NK) cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Role of MHC in immune response?

A

antigen presenting cell (macrophage or B cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Major lymphoid organs?

A

Thymus, bone marrow, lymph nodes, tonsils, spleen, Peyer’s patches

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Function of MHC?

A

presentation of antigen to T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is Waldeyer’s ring?

A

Lymph nodes, tonsils, adenoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why are antigen presenting cells important?

A

T cells can only react to membrane bound antigens. W/O APCs there is NO T CELL RXN to antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What does a basophil become in tissue?

A

Mast cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where are MHC type 1 found?

A

On ALL NUCLEATED CELLS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does a monocytes become in tissue?

A

Macrophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What do MCH type 1 link APCs to?

A

suppressor and/or cytotoxic T lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does a b lymphocyte become in tissue?

A

Plasma cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What do MCH type 2 mediate?

A

attachment of APC to helper T lymphocyte

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Microscopic Difference between b lymphocyte and plasma cell?

A

Lymphocyte = scant cytoplasm, few organelles

Plasma cell = well developed cytoplasm and prominent rough ER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Function of MHC type 2?

A

presentation of EXOGENOUS ANTIGENS that are first internalized and processed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is RER responsible for in plasma cells?

A

Production of immunoglobulins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are HLA subtypes used for?

A

Used diagnostically to identify pathologies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Five classes of immunoglobulins?

A

IgG, IgM, IgA, IgE, IgD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is HLA type B27 used to identify?

A

Psoriasis, ANKYLOSING SPONDYLITIS, Inflammatory bowel disease, Reiter’s syndrome (PAIR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are all immunoglobulins composed of?

A

Light and heavy chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is an epitope?

A

Antigenic site - can be many on an antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which chains are the same in all immunoglobulins and which are specific to each?

A

Light chains the same

Heavy chains specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What to antibodies to SOLUBLE antigens form?

A

Soluble complexes that can be found in circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the two regions on each chain of immunoglobulins?

A

Constant (Fc) and variable (Fab)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What to antibodies to NON-SOLUBLE antigens form?

A

Bind to fixed antigens on cells - coat the cell surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the two light chains?

A

Kappa and lambda

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What do antigen-antibody complexes do?

A

Bind and activate complement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What links immunoglobulin chains together?

A

Disulfide bonds between CYSTEINES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is complement?

A

Effector system -> lysis of cells, agglutination, recruitment of inflammatory cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the largest immunoglobulin?

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is hypersensitivity rxn Type I?

A

Anaphylactic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the function of IgM?

A

Neutralize microorganisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is hypersensitivity rxn Type II?

A

cytotoxic antibody mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How many complement binding sites does IgM have?

A

5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is hypersensitivity rxn Type III?

A

immune complex mediated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the first immunoglobulin to appear on immunization or initial immune response?

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is hypersensitivity rxn Type IV?

A

cell mediated - DELAYED

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is a natural antibody against ABO blood group antigen?

A

IgM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Which hypersensitivity rxns are ANTIBODY mediated?

A

Types I, II, and III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the smallest immunoglobulin?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Which hypersensitivity rxns are CELL mediated?

A

Type IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What is the most copious immunoglobulin?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Mnemonic to remember hypersensitivity rxns?

A

ACID

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

How much IgG is produced on initial immunization?

A

Small amounts- elevated with time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which Ig is Type I hypersensitivity mediated by?

A

IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How are IgG amounts boosted?

A

Re-exposure to antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What cell type mediates hypersensitivity rxn type I?

A

Mast cells or basophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Where can you find Fc receptors for IgG?

A

Macrophages, PMNs, lymphocytes, eosinophils, placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which hypersensitivity rxn has a “late-phase” response?

A

Type I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What does IgG act as?

A

Opsonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How long does type I hypersensitivity rxn take and why?

A

After 4-6 hrs. Slow reacting substances of anaphylaxis (SRS-As)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is the only type of immunoglobulin to pass through placenta?

A

IgG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Diseases caused by type I hypersensitivity rxns?

A

Hay fever (allergic rhinitis), asthma, atopic dermatitis, anaphylactic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is hay fever?

A

Allergic rhinitis. Typically seasonal allergy to pollen, can be due to other foreign substance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Signs/symptoms of hay fever?

A

nasal itching, sneezing, nasal/conjunctival inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Tx for hay fever?

A

anti-histamines, vit. C, desensitization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is asthma?

A

Rxn affecting bronchi. Hypersensitivity to inhaled antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Are all forms of asthma immunologically mediated?

A

NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What is asthma mediated by?

A

SRS-As

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Who is usually affected by asthma?

A

children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

signs/symptoms of asthma?

A

coughing and wheezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What mineral is indicated to relax airway muscles?

A

Magnesium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is atopic dermatitis?

A

Eczema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

When does atopic dermatitis usually occur?

A

childhood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What percentage of all children are affected by atopic dermatitis?

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What percentages of children affected w/ atopic dermatitis have family Hx?

A

50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What is genetic predisposition to atopic dermatitis associated with?

A

hyperproduction of IgE in response to environmental allergens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the allergen that causes atopic dermatitis?

A

Can be anything. Inhaled, ingested in food, or direct skin contact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What does topical corticosteroid suppression of atopic dermatitis tend to lead to?

A

Asthma/hay fever developing later in childhood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is anaphylactic shock?

A

Severe, systemic response to allergen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Common causes of anaphylactic shock?

A

Bee sting, anesthetics (hospital), radiographic contrast (hospital)

58
Q

What is the mechanism of anaphylactic shock?

A

Massive release of histamine and other vasoactive substances

59
Q

Signs/symptoms of anaphylactic shock?

A

Choking secondary to laryngeal edema, wheezing/SOB secondary to bronchial spasm, pulmonary edema, systemic circulatory collapse d/t hypotension

60
Q

Tx for anaphylactic shock?

A

Epinephrine STAT, high flow O2 non-rebreather

61
Q

What causes type II hypersensitivity?

A

Cytotoxic antibody that reacts to antigen in cells or tissue components

62
Q

Which Ig mediates Type II hypersensitivity?

A

IgG or IgM

63
Q

What does activation of complement in type II hypersensitivity lead to?

A

Cell lysis

64
Q

Pathogenesis of type II hypersensitivity?

A

binding of antibody to antigen on cell surface -> complement activation -> cell lysis

65
Q

Diseases caused by type II hypersensitivity rxn?

A

Hemolytic anemia, goodpasture syndrome, graves disease, myasthenia gravis, idiopathic thrombocytopenic purpura, erythroblastosis fetalis, rheumatic fever, bullous pemphigoid

66
Q

What is hemolytic anemia?

A

Prototype type II rxn - several forms

67
Q

Forms of hemolytic anemia?

A

systemic autoimmune disorder (eg. SLE), foreign chemicals (drugs rxn, attachment to RBCs as haptens)

68
Q

What are the “two good pastures” affected in goodpasture syndrome?

A

Kidneys and lungs

69
Q

Cause of goodpasture syndrome?

A

Autoimmunity to component of collagen TYPE IV that has become autoallergenic

70
Q

signs/symptoms of goodpasture syndrome?

A

HEMOPTYSIS = most prominent. Dyspnea, cough, fatigue, fever, weight loss are common. 40% of pts have HEMATURIA

71
Q

What is seen on x-ray of pt with goodpasture syndrome?

A

Bilateral alveolar opacities (d/t alveolar hemorrhage)

72
Q

What causes Graves disease?

A

Autoantibody against thyroid r/c for TSH. Stimulatory => continuous synthesis of T3/T4 (hyperthyroid)

73
Q

Signs/symptoms of Graves disease?

A

EXOPHTHALMOS, goiter, muscle wasting, fine hair, sweating, tachycardia, wt. loss, oligomenorrhea, tremor

74
Q

What causes exophthalmos in Graves disease?

A

Igs directed to specific R/Cs in orbital fibroblasts and fat - results in release of proinflammatory cytokines, inflammation, and accumulation of glycosaminoglycans

75
Q

What is Myasthenia Gravis?

A

hypersensitivity type II disorder. Caused by autoantibody and Cell-mediated DESTRUCTION OF ACH RECEPTORS

76
Q

Who is most commonly affected by myasthenia gravis?

A

young women

77
Q

What makes symptoms of myasthenia gravis better/worse?

A

Worsen with muscle activity, improve with rest

78
Q

How is myasthenia gravis diagnosed?

A

antibody testing to Ach r/c, electromyography, IV edrophonium challenge

79
Q

Signs/symptoms of myasthenia gravis?

A

Most common = ptosis, diplopia, muscle weakness after using affected muscle, proximal limb weakness

80
Q

What percentage of myasthenia gravis pts have affected ocular muscles?

A

Initially 40%, eventually 85%

81
Q

What happens to hand grip in myasthenia gravis?

A

Alternates between weak and normal (milkmaid’s grip)

82
Q

What happens to neck muscles in myasthenia gravis?

A

may become weak

83
Q

When does generalized myasthenia develop in MG pts?

A

Usually w/in first 3 yrs

84
Q

What happens to sensation and DTRs in MG pts?

A

NORMAL

85
Q

What is a type III hypersensitivity rxn due to?

A

acute inflammation in response to circulating antigen-antibody immune complexes deposited in vessels or tissues

86
Q

What do ag-ab complexes do in type III hypersensitivity rxns?

A

Can activate complement system OR bind to/activate certain immune cells => release of inflammatory mediators

87
Q

What do the consequences of immune complex formation depend on in type III rxns?

A

Relative proportions of antigen and antibody in immune complex

88
Q

Progression of type III hypersensitivity rxns?

A

Early - excess antigen, small ag-ab complexes which DO NOT activate complement. Later (antigen/antibody more balanced) - larger immune complexes, deposited in various tissues causing systemic rxns

89
Q

Diseases cause by type III hypersensitivity rxns?

A

Serum sickness, poststreptococcal glomerulonephritis, arthus rxn, polyarteritis nodosa, systemic lupus erythematosus, rheumatoid arthritis, hypersensitivity pneumonitis

90
Q

What is poststreptococcal glomerulonephritis?

A

Type III rxn, usually follows upper respiratory tract infection by nephritogenic streptococcal strain

91
Q

Pathogenesis of poststreptococcal glomerulonephritis?

A

Antigen “planted” onto glomerular basement membrane during filtration -> complement inflammation evoked

92
Q

What is the Arthus rxn?

A

immune-complex mediated rxn, involves deposition of ag-ab complexes mainly in the vascular walls, serosa, and glomeruli

93
Q

According to CDC, how often are Arthus rxns reported after vaccinations?

A

RARELY

94
Q

Which vaccines can cause Arthus rxns?

A

TETANUS toxoid-containing or DIPHTHERIA toxoid-containing

95
Q

What is the antigen for polyarteritis nodosa in Arthus rxn?

A

UNKNOWN

96
Q

Early stages of Arthus rxn?

A

focal fibrinoid necrosis, acute inflammation

97
Q

Chronic stages of Arthus rxn?

A

wall destruction, microaneurysms, thrombosis, occlusion/infarct

98
Q

Why is “nodosa” part of the name in Arthus rxn (polyarteritis nodosa)?

A

Because of fibrous nodules along medium size arteries that are affected (nodosa = knotty)

99
Q

What is seen histologically in glomerulonephritis associated with SLE?

A

deposition of complement-activating immune complexes - IgG, and consequent infiltration by inflammatory cells

100
Q

What are type IV hypersensitivity rxn?

A

DELAYED hypersensitivity - T cell mediated

101
Q

Four subtypes of type IV hypersensitivity rxn, and cells involved?

A

Iva = Type 1 helper T cells, IVb = type 2 helper T cells, IVc = cytotoxic T cells, IVd = IL-8-secreting T cells

102
Q

How are T cells activated (type IV hypersensitivity)?

A

sensitized after contact w/ a specific antigen, activated by REEXPOSURE to same antigen

103
Q

How do T cells damage tissue (type IV hypersensitivity)?

A

by direct toxic effects OR through release of cytokines

104
Q

Diseases caused by type IV hypersensitivity rxns?

A

Contact dermatitis (NO GRANULOMA), chronic transplant rejection, graft-vs-host dz, tuberculosis, leprosi, fungal infections, rxn to tumors, sarcoidosis, Type I DM, MS, Guillain-Barre syndrome, Hashimotos thyroiditis, PPD

105
Q

What is type I DM theorized to be?

A

virally triggered autoimmune response (immune system attacks virus infected cells as well as Beta cells in pancreas)

106
Q

What virus is implicated in type I DM?

A

Coxsackie virus family (German measles)

107
Q

Types of transplantation? (4)

A
  1. autograft (self) 2. isograft/synergeneic graft (identical twin or clone) 3. homograft/allograft (w/in species) 4. xenograft
108
Q

What should be tested for before allografting?

A

histocompatibility using HLA antigens

109
Q

Types of transplant rejection? (3)

A
  1. hyperacute reaction 2. acute reaction 3. chronic rejection
110
Q

What happens in chronic transplant rejection?

A

obliteration of arterial lumen

111
Q

What determines the outcome of transfusion?

A

Major blood types (ABO system)

112
Q

What agglutinin does Type A blood have?

A

B agglutinin

113
Q

What agglutinin does type B blood have?

A

A agglutinin

114
Q

What agglutinin does type AB blood have?

A

NONE

115
Q

What agglutinin does type O blood have?

A

BOTH A and B agglutinin

116
Q

Which blood types can type A GIVE to?

A

A, AB

117
Q

Which blood types can type A RECEIVE from?

A

A, O

118
Q

Which blood types can type B GIVE to?

A

B, AB

119
Q

Which blood types can type B RECEIVE from?

A

B, O

120
Q

Which blood types can type AB GIVE to?

A

AB

121
Q

Which blood types can type AB RECEIVE from?

A

AB, A, B, O UNIVERSAL ACCEPTOR

122
Q

Which blood types can type O GIVE to?

A

O, AB, A, B UNIVERSAL DONOR

123
Q

Which blood types can type O RECEIVE from?

A

O

124
Q

What happens if type A is given to a person who is type B?

A

HEMOLYSIS

125
Q

What happens if type B is given to a person who is type A?

A

HEMOLYSIS

126
Q

What happens if type A is given to a person who is type AB?

A

NO REACTION - Acid and water rxn rule

127
Q

What happens if type AB is given to a person who is type A?

A

HEMOLYSIS

128
Q

What happens if type A is given to a person who is type O?

A

HEMOLYSIS

129
Q

What happens if type O is given to a person who is type A?

A

NO REACTION

130
Q

What is Rh factor?

A

(+) or (-) charge on blood cells

131
Q

What happens if Rh- mother has Rh+ fetus? (first pregnancy)

A

Nothing

132
Q

What happens if Rh- mother has Rh+ fetus? (SECOND pregnancy)

A

Mother is sensitized to Rh+, => anti-Rh cells cause erythroblastosis fetalis in fetus

133
Q

What should be given to an Rh- w/in 12 hrs postpartum?

A

RhoGAM - binds blood from fetus before immune system sensitized

134
Q

Clinical features of Rh factor incompatibility?

A
  1. Hydrops fetalis 2. Erythoroblastosis fetalis 3. Icterus gravis neonatorum
135
Q

If mother is Rh- and fetus is Rh+, what must father be?

A

Rh+

136
Q

What is icterus gravis neonatorum?

A

jaundice of basal ganglia of brain

137
Q

What is autoimmune disease?

A

abnormal response to self-antigens

138
Q

How do you make diagnosis of autoimmune disease?

A

look for: 1. autoantibodies 2. immune mechanisms 3. indirect evidence (ex. If steroids help)

139
Q

What causes autoimmune diseases?

A

Familial - genetic predisposition. Certain HLA-haplotypes more often linked to autoimmune diseases

140
Q

Which sex is more commonly affected by autoimmune diseases?

A

Women

141
Q

Types of autoimmune diseases? (2)

A
  1. systemic 2. single organ
142
Q

Examples of systemic autoimmune diseases?

A

SLE, rheumatic fever, rheumatoid arthritis, systemic sclerosis, polyarteritis nodosa

143
Q

Examples of single organ autoimmune diseases?

A

MS (CNS), Hashimotos thyroiditis/Graves disease (thyroid), autoimmune hemolytic anemia (blood), pemphigus vulgaris (skin), myasthenia gravis (muscle)

144
Q

What percentage of SLE pts have ANA?

A

Virtually all

145
Q

What percentage of SLE pts have kidney involvement?

A

75%

146
Q

Characteristic sign of SLE?

A

Butterfly rash

147
Q

When does first episode of acute rheumatic fever (ARF) most often occur?

A

Between 5 and 15 yrs - UNCOMMON before 3 or after 21

148
Q

How do you test for rheumatic fever prevention?

A

test for group A streptococcal (GAS) infection in pt with pharyngitis

149
Q

What is the incidence of rheumatic fever in the US?

A

<1/100,000

150
Q

When do higher attack rates of ARF occur?

A

with certain streptococcal M protein serotypes and STRONGER HOST IMMUNE RESPONSE

151
Q

Etiology of ARF?

A

GAS infection (host and environmental factors also important)

152
Q

What do GAS M proteins share epitopes with?

A

Proteins in synovium, heart muscle, and heart valve

153
Q

What is most often affected in rheumatic fever?

A

joints, heart, skin, CNS

154
Q

What is rheumatoid arthritis (RA)?

A

SYMMETRICALLY inflamed peripheral joints

155
Q

Which sex is more commonly affected by RA?

A

Women 2-3x more likely to be affected

156
Q

Pathophysiology of RA?

A

immunologic abnormalities (type III hypersensitivity). Plasma cells produce RHEUMATOID FACTOR antibodies

157
Q

Signs/symptoms of RA?

A

begins w/ systemic and joint systems - early morning stiffness, fatigue, malaise, anorexia, generalized weakness. Joints painful, swollen, stiff

158
Q

How do you differentiate RA from osteoarthritis?

A

RA is characteristically SYMMETRIC

159
Q

How long does morning stiffness typically last in RA pts?

A

> 60 min

160
Q

Types of immunodeficiency diseases? (2)

A

Primary (congenital) and Secondary (acquired)

161
Q

Primary immunodeficiency diseases? (3)

A
  1. Severe combined immunodeficiency 2. Isolated deficiency of IgA 3. DiGeorge’s syndrome
162
Q

What is severe combined immunodeficiency?

A

defect of lymphoid stem cells - Pre-B, pre-T cells

163
Q

What is the most common PRIMARY immunodeficiency disease?

A

Isolated deficiency of IgA (1:700)

164
Q

Which primary immunodeficiency disease is often asymptomatic?

A

Isolated deficiency of IgA

165
Q

What is DiGeorge’s syndrome?

A

T cell deficiency related to aplasia of thymus

166
Q

What is AIDS?

A

Acquired Immunodeficiency Syndrome

167
Q

What causes AIDS?

A

Human immunodeficiency virus (HIV) - RNA retrovirus

168
Q

What does HIV do?

A

infects T HELPER CELLS (CD4)

169
Q

Where is HIV stored in the body?

A

In macrophages and related phagocytic cells

170
Q

Clinical presentation of HIV/AIDS?

A

Acute illness, asymptomatic infection, persistent generalized lympadenopathy

171
Q

What is the terminal phase of HIV?

A

AIDS

172
Q

Pathologic findings of CNS in AIDS?

A

meningitis, encephalitis, dementia

173
Q

Pathologic findings of Mouth in AIDS?

A

Herpes labialis, THRUSH

174
Q

Pathologic findings of lung in AIDS?

A

pneumonia

175
Q

Pathologic findings of small intestine in AIDS?

A

malabsorption

176
Q

Pathologic findings of large intestine in AIDS?

A

colitis, proctitis

177
Q

Pathologic findings of skin in AIDS?

A

KAPOSI’S SARCOMA, dermatitis, folliculitis, impetigo

178
Q

Pathologic findings of lymph nodes in AIDS?

A

lymphadenopathy

179
Q

Pathologic findings of tumors in AIDS?

A

lymphoma

180
Q

Opportunistic infections in lung in AIDS?

A

pneumocystitis carinii, aspergillus fumigatus, Candida albicans pneumonia

181
Q

Opportunistic infections in GI in AIDS?

A

Candida albicans, herpes or CMV, stomatitis, esophagitis, mycobacterium avium-intracellulare, cryptosporidium enteritis, fungal or bacterial proctitis

182
Q

Opportunistic infections in CNS in AIDS?

A

toxoplasma gondii encephalitis, cryptococcus neoformatns meningitis

183
Q

Tumors that develop in AIDS? (3)

A

Lymphoma of lymph nodes or GI tract, lymphoma of CNS, Kaposi’s Sarcoma

184
Q

4 types of immune deficiencies?

A
  1. decreased production 2. decreased activation 3. phagocytic cell deficiency 4. idiopathic dysfunction
185
Q

3 types of decreased production that cause immune deficiency?

A
  1. B cells 2. T cells 3. B AND T cells
186
Q

What does decreased production of B cells cause?

A

Brutons agammaglobulinemia

187
Q

What is brutons agammaglobulinemia associated with?

A

Recurrent bacterial infections

188
Q

Which sex is affected by Brutons agammaglobulinemia?

A

Boys (X LINKED)

189
Q

What is caused by decreased production of T cells?

A

Thymic aplasia - DiGeorge syndrome

190
Q

What does DiGeorge syndrome present with?

A

Tetany owing to hypocalcemia

191
Q

What is caused by deficiency of B AND T cells?

A

severe combined immunodeficiency (SCID)

192
Q

4 types of decreased activation that cause immune deficiencies?

A
  1. T Cells - IL12 r/c deficiency 2. B cells - hyper-IgM syndrome 3. B cells - Wiskott-Aldrich syndrome 4. Macrophages - Job’s syndrome
193
Q

What is Wiskott-Aldrich syndrome?

A

X linked defect in ability to mount IgM response to bacteria

194
Q

What is Wiskott-Aldrich syndrome associated with?

A

elevated IgA levels

195
Q

Triad of symptoms of Wiskott-Aldrich syndrome?

A

recurrent pyogenic infections, thrombocytopenic purpura, eczema

196
Q

What is Job’s syndrome?

A

failure of IFN-gamma production by helper T cells

197
Q

3 types of phagocytic cell deficiencies that cause immune deficiencies?

A
  1. Leukocyte adhesion deficiency syndrome (type 1) 2. Chediak-Higashi disease 3. Chronic granulmoatous disease
198
Q

4 idiopathic dysfunction that cause immune deficiencies?

A
  1. T cells - chronic mucocutaneous candidiasis 2. B cells - selective immunoglobulin deficiency 3. B cells - ataxia-telangiectasia 4. B cells - common variable immunodeficiency
199
Q

What is amyloid?

A

Inert extracellular material defined in terms of its PHYSICAL properties (NOT biochemical)

200
Q

Physical properties of amyloid?

A

Fibers 7.5 nm thick (electron microscopy), stains with Congo red (appears green under polarized light), Beta-pleated sheet (radiographic crstallography)

201
Q

Biochemical types of amyloid?

A

AA amyloid, AL amyloid, many other forms

202
Q

Clinical presentation of amyloid deposition? (2)

A
  1. systemic amyloidosis (deposition of amyloid in various organs) 2. localized organ-specific amyloid deposits (ex. Alzheimers dz in brain)

Pathology 1 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions