Brs Chapter 5 Immune Dysfunction

Front 1

What are the 3 main types of lymphocytes and how are they identified?

Back 1

B cells, T cells, and Natural Killer cells (NK)
they are identified by cell-surface glycoproteins specific for both cell type and stage of differentiation

Front 2

Where do B cells originate?
Where do they differentiate?

Back 2

stem cells in the bone marrow
bone marrow and peripherally in germinal centers of lymph nodes and lymphoid follicles of the spleen

Front 3

What is a characteristic feature of B cells?
What percent of circulating peripheral blood lymphocytes are B cells?

Back 3

the presence of surface immunoglobulin
15%

Front 4

Where do T cells originate?
Where do they differentiate?
Where can mature T cells be found?
What percent of circulating peripheral blood lymphocytes are T cells?

Back 4

stem cells in the bone marrow
thymus
paracortical and deep medullary areas of lymph nodes and periarteriolar sheaths of the spleen
70%

Front 5

What are the two subclassifications of T cells and how abundant are they in circulating T cells?
What is the normal ratio of CD4+ to CD8+ T cells?
What is the ratio in AIDS patients?

Back 5

CD4+ T cells (60%) and CD8+ T cells (30%)
2:1
0.5:1 or less

Front 6

What is another name for NK cells and why?
What percentage of circulating lymphocytes are NK cells?

Back 6

large granular lymphocytes (LGLs)
large size, pale cytoplasm, and prominent granulation
15%

Front 7

What do NK cells kill?
Specific sensitization involved?
Antibody involved?
ADCC?

Back 7

tumor cells, fungi, and cells altered by viral infection
NO
NO
antibody-dependent cell-mediated cytotoxicity (ADCC) the method in which NK cells lyse other cells

Front 8

Macrophages are derivatives of peripheral blood ___ and are members of the ___ system of cells.

Back 8

monocytes
mononuclear phagocyte

Front 9

What are 3 things that macrophages do?

Back 9

1) secrete cytokines, acid hydrolases, neutral proteases, and prostaglandins
2) process and present antigens to CD4+ T cells (along with human leukocyte antigen (HLA) class II antigens)
3) participate in delayed hypersensitivity reactions (directly killing tumor cells)

Front 10

What characterizes dendritic cells? (2 things)
What is the main similarity between dendritic cells and macrophages?
What is the main difference between dendritic cells and macrophages?

Back 10

dendritic cytoplasmic processes and expression of large quantities of cell surface HLA class II antigens
they are both antigen-presenting cells (APC)
dendritic cells are poorly phagocytic

Front 11

What characterizes Langerhans cells of the skin?
How are they similar to dendritic cells of lymphoid tissue?

Back 11

presence of Birbeck granules (tennis racket-shaped cytoplasmic structures)
antigen-presenting cells and express HLA class II antigens

Front 12

Give 3 types of cells that express human leukocyte antigen (HLA) class II antigens?

Back 12

macrophages, dendritic cells, and langerhans cells

Front 13

Give 3 types of cells that secrete cytokines.
What is the role of cytokines?

Back 13

lymphocytes, monocytes-macrophages, and NK cells
act as effector molecules influencing the behavior of B, T and NK cells, monocytes, macrophages, hematopoietic cells, and others

Front 14

This system consists of 20 plasma proteins that form a membrane attack complex to lyse target cells.
How are the plasma proteins activated?

Back 14

Complement system
2 pathways: classic pathway and alternate pathway

Front 15

What initiates the classic pathway of complement activation?
The final lytic form of activated complement is the result of _____

Back 15

reaction with antigen-antibody complexes
a series of enzymatic cleavages and recombinations (cleavage products cause cell lysis)

Front 16

What initiates the alternate pathway of complement activation?
Like the classic pathway, what causes cell lysis?

Back 16

nonimmunologic stimuli such as invading microorganisms
cleavage products

Front 17

What is the name of the genes that code for HLA antigens?
Where are they located?
What is the HLA system used for?

Back 17

histocompatibility genes
short arm of chromosome 6, the major histocompatibility complex
organ transplantation- HLA typing and matching of donor recipient for tissue compatibility

Front 18

What are the class I HLA antigens?
Where are they found?
Class I antigens are the main antigens involved in ____.

Back 18

HLA-A, HLA-B, and HLA-C antigens
on almost all human cells
tissue graft rejection (serologic testing for HLA-A and HLA-B antigens is used to predict the likelihood of long term graft survival)

Front 19

What are the class II HLA antigens?
Where are they found?

Back 19

HLA-D, HLA-DP, HLA-DQ, and HLA-DR
immunocompetent cells (macrophages, dendritic cells, langerhans cells, B cells, and some T cells)

Front 20

How are HLA-D antigens identified?
How are HLA-DP, HLA-DQ, and HLA-DR antigens identified?

Back 20

mixed lymphocyte reactions
standard serologic techniques or by mixed lymphocyte reactions

Front 21

How are HLA antigens linked with disease?
What is an example?

Back 21

there is a significant associated of certain HLA antigens with a number of specific diseases
HLA-B27 antigen is associated with 90% of cases of ankylosing spondylitis

Front 22

What mediates adaptive immunity?
What are the drawbacks?

Back 22

B and T lymphocytes and specific antigens
not immediate; take time for optimal reactivity

Front 23

What are some examples of innate immunity?
What is innate immunity associated with?

Back 23

phagocytosis and activation of complement
toll-like receptors

Front 24

What are hypersensitivity reactions?
Which types require the active production of antibody by plasma cells?
Which type is mediated by the interaction of T cells and macrophages?

Back 24

adverse reactions caused by immune mechanisms
Types I, II, and III
Type IV

Front 25

What is type I hypersensitivity?
Steps:
1) ____ antibody is produced by ____ and is stimulated by ____. The antibody is then bound to the ___ receptors of ___ and ___ cells.
2) On subsequent exposure, ___ reacts with the bound ____, resulting in ____ and degranulation of ____ and ____ cells. Step 2 requires ____ of antibody on the surface of the ___ cell.
3) Degranulation results in ___ release, which causes what?
4) Chemotactic substances recruit ____, resulting in ____.

Back 25

immediate or anaphylactic hypersensitivity
1) IgE; IgE B cells; antigen; Fc; basophils; mast cells
2) antigen; IgE antibody; cytolysis; basophils; mast cells; cross-linking; mast
3) histamine; increased vascular permeability
4) eosinophils; tissue and peripheral blood eosinophilia

Front 26

What are 3 examples of type I hypersensitivity?

Back 26

allergic reactions, systemic anaphylaxis (anaphylactic shock), and angioedema

Front 27

What is type II hypersensitivity?
3 pathways?

Back 27

antibody-mediated or cytotoxic hypersensitivity
complement-fixing antibodies, antibody-dependent cell-mediated cytotoxicity (ADCC), and reaction of anti-receptor antibodies with cell-surface receptor protein

Front 28

In Type II hypersensitivity reactions, the complement-fixing antibodies react directly with antigens that are ____.
The interaction of ____ with the cell surface results in ____ and ____.
Where are the antigens involved usually located?
4 examples?

Back 28

integral components of the target cell
complement; cell lysis; destruction
They are usually localized to tissue basement membranes or blood cell membranes.
warm antibody autoimmune hemolytic anemia, hemolytic transfusion reactions, hemolytic disease of the newborn, and Goodpasture syndrome

Front 29

In Type II hypersensitivity reactions, the ADCC pathway begins with the antibody reacting with ____.
The ____ portion of the antibody molecule reacts with the ____ receptors of many cytotoxic leukocytes, most importantly ____.
How are the target cells killed?
Is complement involved?

Back 29

the antibody reacts directly with integral surface antigens of targeted cells
Fc; Fc receptors; NK cells
Fc receptor-bound cytotoxic leukocytes
no

Front 30

In Type II hypersensitivity reactions, which variant is sometimes classisfied as type V hypersensitivity?
What occurs here?
What disease is this?
What is the result of this reaction?

Back 30

reaction of anti-receptor antibodies with cell-surface receptor protein
the reaction of thyroid-stimulating immunoglobulin with the TSH receptor of thyroid follicular cells
Graves disease
antigen-antibody reaction mimics the effect of TSH on the follicular cells and results in glandular hyperplasia and hyperproduction of thyroid hormone with clinical hyperthryroidism

Front 31

Type III hypersensitivity is also called the ____.
Steps
1) ____ produced in response to antigen, results in circulating ____.
2) What usually happens to immune complexes? How can this step go wrong?
3) The immune system complexes bind ____, which is chemotactic for neutrophils. The neutrophils release ____, resulting in ____.
4) _____ is activated with promotes coagulation, causing ____ of small vessels and activation of ____ causing vasodilation and edema.
5) Finally, ___ causes microthrombus formation and leads to the release of ____ from platelet dense granules.

Back 31

immune complex
1) exogenous antibody; antigen-antibody complexes
2) usually removed by cells of the mononuclear phagocyte system; insoluble aggregates of immune complex are deposited in vessel walls and are smaller and less easily removed by phagocytes
3) complement; lysosomal enzymes; tissue damage
4) Hageman factor (XII); thrombosis; kinin
5) platelet aggregation; vasoactive amines

Front 32

5 examples of the anti-receptor antibody reaction with cell-surface receptor proteins (Type II hypersensitivity)?

Back 32

serum sickness, systemic lupus erythematosus, arthus reaction, polyarteritis nodosa, and immune complex-mediated glomerular diseases

Front 33

Type IV hypersensitivity is also called ___.
What are the two pathways?

Back 33

cell-mediated hypersensitivity
delayed hypersensitivity and cytotoxic T lymphocyte-mediated cytotoxicity

Front 34

In Type IV hypersensitivity, delayed hypersensitivity begins when _____ reacts with the antigen, which was presented by ____. It also reacts with ____ on the macrophages, cuasing stimulation of ____.
What happens on subsequent contact with antigen?
What do the secretions stimulate?
2 examples?

Back 34

T-cell receptor of CD4+ lymphocytes; macrophages; HLA class II antigens; antigen-specific CD4+ memory T cells
CD4+ memory T cells proliferate and secrete cytokines
phagocytic activity of macrophages
tuberculin reaction and contact dermatitis

Front 35

In type IV hypersensitivity, what is cytotoxic T lymphocyte-mediated cytotoxicity?
What cells are usually targeted?
How are they recognized?
Target cell ____ recognized as self-antigens.

Back 35

direct CD8+ T cell-mediated killing of target cells.
tumor cells or virus infected cells
the specific target cell antigen is recognized by the T-cell receptor of CD8+ lymphocytes
HLA class I antigens

Front 36

what mediates hyperacute transplant rejection?
when does rejection occur?
what kind of rejection is present?

Back 36

antibody-mediated
within minutes of transplant
Arthur reaction marked by acute inflammation, fibrinoid necrosis, and extensive thrombosis

Front 37

what mediates acute transplant rejection?
when does rejection occur?
what kind of rejection is present?

Back 37

t-cell mediated
days or weeks after transplant
infiltration of lymphocytes and macrophages

Front 38

what mediates chronic transplant rejection?
when does rejection occur?
what kind of rejection is present?

Back 38

antibody-mediated
months to years after transplant
vascular damage

Front 39

X-linked agammaglobulinemia of Bruton?
Absence of plasma cells in tissues results in ____.
Absent ____ in lymphoid tissue.
Effects?

Back 39

occurs in male infants, is characterized by failure of antibody synthesis due to a mutation in the B cell tyrosine kinase (Btk) gene (cannot turn pre-B cells into B cells)
absence of serum immunoglobulin
germinal centers
recurrent bacterial infections (steptococci, staphylococci, pneumococci)

Front 40

What is the most common inherited B cell defect?
What causes this?
effects?

Back 40

isolated IgA deficiency
inability of IgA B cells to mature to plasma cells
usually asymptomatic but may have occasional anaphylactic reactions or infections

Front 41

What is common variable immunodeficiency?
Results in ____
Manifest clinically by ___

Back 41

group of disorders caused by failure of terminal B-cell maturation
hypogammaglobulinemia
recurrent bacterial infections

Front 42

DiGeorge syndrome?
How does this occur?
Results in ___
Mainfest clinically by ___

Back 42

congenital T-cell deficiency
hypoplasia of the thymus and parathyroid glands during embryonic development
failure of T-cell maturation resulting in lymphopenia
recurrent viral and fungal infections and tetany

Front 43

CATCH 22?

Back 43

DiGeorge syndrome
C ardiac defects
A bnormal facies
T hymic hypoplasia
C left palate
H ypocalcemia
microdeletion of chromosome 22

Front 44

Severe combined immunodeficiency disease (SCID) is also known as ___
deficiency of ___, which manifests as profound ____ and severed defects in ___ and ___ immunity.

Back 44

swiss type agammaglobulinemia
T and B cells; lymphopenia; humoral and cell-mediated

Front 45

what causes SCID?
approximately 50% of autosomal recessive cases are caused by ____ which causes ____

Back 45

can be autosomal recessive or X-linked
adenosine deaminase (ADA) deficiency; accumulation of substances that are toxic to lymphocytes

Front 46

clinical manifestations of SCID?
anatomic manifestations of SCID?

Back 46

infections, malignancy, failure to thrive, and graft-versus-host disease
thymic hypoplasia and hypoplasia of lymph nodes and tonsils

Front 47

What is Wiskott-Aldrich syndrome?
It is a ___ disorder

Back 47

immunodeficiency with thrombocytopenia and eczema
x-linked

Front 48

What is hyper-IgM syndrome?
It is a ___ disorder
results in increased propensity to ___

Back 48

normal of elevated levels of IgM, but failure of isotype switching to IgG, IgA, or IgE
x-linked and autosomal recessive
pyogenic infections

Front 49

what causes AIDS?
Mechanisms of HIV infection:
1) The HIV virion expresses a cell surface protein, ___, with binding sites for ___.
2) Two recognition sites on gp120 for ____ and ____ are involved in entry of HIV into the cell.

Back 49

human immunodeficiency virus (HIV)
gp120; CD molecule on the surface of the CD4+ T cell
coreceptors CCR5 and CXCR4

Front 50

Individuals that are____ are said to be highly resistant to some strains of HIV.

Back 50

homozygous for mutated CCR5 receptor

Front 51

What CD4+ cell types are targets for HIV infection?
How are monocytes and macrophages involved in HIV infection?
How does HIV affect neural cells?

Back 51

monocytes, macrophages, dendritic cells, langerhans cells, and microglial cells of the CNS
they may function as reservoirs for HIV and vehicles for entry into the CNS
directly by way of CD4 receptors or compete through the gp120 protein for neural receptor sites for neuroleukin

Front 52

What happens after gp120 is bound to CD4 and HIV is internalized into the cell?
___ is integrated into the host genome
HIV may remain in its ___ form for some time until activated by ____ or ____.

Back 52

DNA is synthesized by reverse transcription from genomic viral RNA
proviral DNA
proviral; cytomegalovirus or Epstein-Barr virus (EBV)

Front 53

What occurs during the latent period of HIV?
Where can the HIV virus be found?

Back 53

low-level virion production with infectivity
blood, semen, vaginal secretions, breast milk, and saliva

Front 54

infection with HIV virus results in depletion of ___ cells.
___ ratio is also greatly reduced
What does the loss of CD4+ helper T cells cause?
Despite the ability to produce specific antibodies, patients will demonstrate ____ due to ____.

Back 54

CD4+ T cells
CD4+: CD8+ T cell ratio (often to less than 1)
failure in humoral and cell-mediated hypersensitivity reactions
hypergammaglobulinemia

Front 55

What is Wiskott-Aldrich syndrome?
It is a ___ disorder

Back 55

immunodeficiency with thrombocytopenia and eczema
x-linked

Front 56

What is hyper-IgM syndrome?
It is a ___ disorder
results in increased propensity to ___

Back 56

normal of elevated levels of IgM, but failure of isotype switching to IgG, IgA, or IgE
x-linked and autosomal recessive
pyogenic infections

Front 57

what causes AIDS?
Mechanisms of HIV infection:
1) The HIV virion expresses a cell surface protein, ___, with binding sites for ___.
2) Two recognition sites on gp120 for ____ and ____ are involved in entry of HIV into the cell.

Back 57

human immunodeficiency virus (HIV)
gp120; CD molecule on the surface of the CD4+ T cell
coreceptors CCR5 and CXCR4

Front 58

Individuals that are____ are said to be highly resistant to some strains of HIV.

Back 58

homozygous for mutated CCR5 receptor

Front 59

What CD4+ cell types are targets for HIV infection?
How are monocytes and macrophages involved in HIV infection?
How does HIV affect neural cells?

Back 59

monocytes, macrophages, dendritic cells, langerhans cells, and microglial cells of the CNS
they may function as reservoirs for HIV and vehicles for entry into the CNS
directly by way of CD4 receptors or compete through the gp120 protein for neural receptor sites for neuroleukin

Front 60

What happens after gp120 is bound to CD4 and HIV is internalized into the cell?
___ is integrated into the host genome
HIV may remain in its ___ form for some time until activated by ____ or ____.

Back 60

DNA is synthesized by reverse transcription from genomic viral RNA
proviral DNA
proviral; cytomegalovirus or Epstein-Barr virus (EBV)

Front 61

What occurs during the latent period of HIV?
Where can the HIV virus be found?

Back 61

low-level virion production with infectivity
blood, semen, vaginal secretions, breast milk, and saliva

Front 62

infection with HIV virus results in depletion of ___ cells.
___ ratio is also greatly reduced
What does the loss of CD4+ helper T cells cause?
Despite the ability to produce specific antibodies, patients will demonstrate ____ due to ____.

Back 62

CD4+ T cells
CD4+: CD8+ T cell ratio (often to less than 1)
failure in humoral and cell-mediated hypersensitivity reactions
hypergammaglobulinemia; polyclonal B cell activation

Front 63

AIDS is characterized by severe immunodeficiency manifested by ___, ____, ____, and ____.

Back 63

opportunistic infection, kaposi sarcoma, B-cell non-Hodgkin lymphoma, and central and peripheral nervous system manifestations

Front 64

What is Kaposi sarcoma?

Back 64

rare neoplasm associated with human herpesvirus 8 which is also called Kaposi sarcoma herpesvirus (KSHV)

Front 65

What is HIV seropositivity?



What is AIDS marked by?

Back 65

begins soon after initial HIV infection, antibodies to the proteins coded by the genes of retroviral gag, env, and pol can be demonstrated, especially antibodies to gp120 and p24 proteins
HIV infection complicated by specified secondary opportunistic infection or malignant neoplasms

Front 66

Autoimmunity is the apparent inability to ____
4 examples of autoimmune diseases?

Back 66

distinguish self from nonself
autoimmunue hemolytic anemia, Hashimoto thyroiditis, idiopathic adrenal atrophy, and connective tissue diseases

Front 67

What are the 4 associations that are usually present in autoimmity?

Back 67

1) presence of autoantibodies
2) comorbidity with other autoimmune diseases
3) morphologic changes such as lymphoid follicle formation (Hashimoto thyroiditis)
4) association with specific HLA haplotypes

Front 68

Autoimmunity
host antigens may recognize as ___ if modified by infection, inflammation, or complexing with a drug
what happens when antigens that are usually isolated from the immune system are exposed to trauma or inflammation? example?

Back 68

non-self
they are recognized as foreign; thyroglobulin,, lens protein, and spermatozoa

Front 69

what are specific autoantibodies?

Back 69

antibodies directed against host tissue, present in many autoimmune diseases

Front 70

What are three immunoregulation problems with autoimmunity?

Back 70

1) increase in helper T-cell function or decrease in suppressor T-cell function
2) nonspecific B-cell activation
3) thymic defects of B-cell defects

Front 71

What are some examples of some autoimmune disorders that may be caused by genetics?

Back 71

Hashimoto thyroiditis, pernicious anemia, type 1 diabetes mellitus, and Sjorgen syndrome (all associated with other autoimmune disorders)

Front 72

What are the HLA antigen associations of Hashimoto thyroiditis and type 2 diabetes?

Back 72

Hashimoto- HLA-DR5 and HLA-B5
Type 2 diabetes- HLA-DR3 and HLA-DR4

Front 73

List the 6 connective tissue disorders that are autoimmune in origin.

Back 73

Systemic Lupus Erythematosus (SLE)
Progressive systemic sclerosis (PSS or scleroderma)
Sjogren syndrome
Polymyositis
Mixed connective tissue disease (MCTD)
Polyarteritis nodosa

Front 74

SLE most often affects who?
What distinguishing things mark SLE?
Which organ systems are usually affected?

Back 74

women (80%) of childbearing age
extensive immune complex-mediated inflammatory lesions involving multiple organ systems
*kidney*, joints, skin, serous membranes, and lungs

Front 75

SLE clinical manifestations
in joints?
skin?
Raynaud phenomenon?
Serosa?
endocarditis?
spleen?
kidney?
eye?

Back 75

joints- arthralgia and arthritis
skin- characteristic butterfly rash over nose
raynaud- vasospasm of fingers
serosal inflammation (pericarditis and pleuritis)
endocarditis- vegetation on mitral valve leaflet (Libman-Sacks)
spleen- onion-skin appearance from fibrosis around splenic arterioles
kidney- glomerular changes
eye- cytoid bodies (yellow cotton wool-like lesions)

Front 76

___ antibodies are found in almost all pts with SLE
best tests in SLE are for ____ DNA and ____.

Back 76

antinucleosome-specific autoantibody (ANA)
double stranded DNA and Sm (Smith) antigen

Front 77

SLE tests give a biologic false positive for ___ due to ___.

What combination of antibodies is almost diagnostic of SLE?

Back 77

syphilis; anticardiolipins

antibodies specific for lupus:
anti-ds-DNA and anti-Sm antigen

Front 78

Progressive Systemic sclerosis (PSS) involves widespread _____ and ____ changes.
What does it affect?
Who does it affect?

Back 78

fibrosis; degenerative
skin, GI tract (especially esophagus), heart, muscle, lung, and kidney
yound women

Front 79

PSS is marked by the presence of ___ in 1/3 of patients.

Back 79

ANA anti-Scl-70

Front 80

CREST syndrome?

CREST is ANA marked with ___ activity.

Back 80

C alcinosis
R aynaud phenomenon
E sophageal dysfunction
S clerodactyly
T elangiectasia

anticentromere

Front 81

PSS characteristics of
face?
hand?
raynaud?
visceral organs?

Back 81

hypertrophy of collagen fibers of the subcutaneous tissue, leading to tightening of facial skin and fixed facial appearance
hand- sclerodactyly- claw like appearance
raynaud 75% pts, vasospasm in hand
the main organ affected is esophagus with dysphagia and interstitial pulmonary fibrosis

Front 82

Who does sjogren syndrome affect?
clinical manifestations...Triad of:
eyes?
mouth?
always associated with a ___

Back 82

women in their late middle age
keratoconjunctivitis sicca- dry eyes
xerostomia- dry mouth
CT disorder usually rheumatoid arthritis

Front 83

what is Sicca syndrome

PSS affects which glands?

what antibodies are present?

Back 83

xerostomia and keratoconjunctivitis alone

parotid and lacrimal

ANAs including anti-SS-B and anti-SS-A

Front 84

Polymyositis?

dermatomyositis?

Who does it affect?
What are they at at high risk for?

Back 84

chronic inflammatory process involving the proximal muscles of extremities (no cutaneous)

when the skin is involved with a reddish-purple rash on face and neck (heliotrope eyelids
women
malignancy

Front 85

In Mixed CT disease (MCTD), ___ involvement is uncommon.
MCTD is characterized by ____.

Back 85

renal
specific ANAs- high-titer anti-nRNP and immunofluorescent speckled nuclear appearance

Front 86

What characterizes Polyarteritis nodosa?
Occurs mainly in ___.
What antigen is present?
What is another name for this?

Back 86

segmental fibrinoid necrosis in the walls of small and medium arteries in any organ
men (in contrast to other CT diseases)
Hep B antigen (30%)
immune complex vasculitis

Front 87

Amyloidosis is a group of disorders characterized by ___.
What is amyloid?
It is characterized by abnormal ____.
Amyloidosis always has a ___ configuration.

Back 87

deposition of amyloid
group of substances that share a common physical feature that can be formed by a number of different proteins)
protein folding
beta-pleated sheet configuration

Front 88

Where can amyloid be found?
what does it look like and how does it stain with H&E?
It is characteristically stained with the ___ dye, demonstrating ___ when viewed under polarized light.

Back 88

extracellular, proximal to basement membranes
amorphous eosinophilic appearance
Congo red; apple green birefringence

Front 89

What is another name for primary amyloidosis?
What is the cause?
Where is amyloid deposition common?
primary amyloidosis is is frequently associated with ____

Back 89

immunocytic dyscrasia amyloidosis
deposition of amyloid fibrils derived from immunoglobulin light chains, referred to as AL (amyloid light chain) protein
tissues of mesodermal origin (heart, muscle, tongue, kidney)
plasma cell disorders

Front 90

What is another name for secondary amyloidosis?
What is the cause? precursor?
What is affected?
sago spleen?
secondary amyloidosis is a complication of ___

Back 90

reactive systemic amyloidosis
deposition of the amyloid protein AA; precursor is SAA (serum amyloid associated protein)
parenchymatous organs (kidney, liver, adrenals, pancreas, lymph nodes, and spleen)
tapioca-like granules (perifollicular involvement)
chronic inflammatory disease

Front 91

beta 2-microglobulin derived amyloid is seen in patients on ____
transthyretin derived amyloid is found in _____
calcitonin-derived amyloid is found in ____
AL amyloid is found in ____ and
is associated with ____ and ____.

Back 91

on long-term dialysis
senile amyloidosis and in a number of
hereditary disorders
medulary carcinoma of the thyroid
primary amyloidosis ; multiple myeloma and other plasma cell disorders.

Front 92

Goodpasture syndrome is marked by ______ due to antiglomerular basement membrane antibodies.
Also, Goodpasture syndrome is
an example of a _________ reaction.

Back 92

linear immunofluoresence
type II complement dependent hypersensitivity

Front 93

These antinuclear antibodies are indicative of what disorder?
1) Anti-Ro (or SS-A)?
2) anti-ribonucleoprotein (or RNP)?
3) anti-Jo-1?
4) anti-Scl-70?

Back 93

1) Sjögren syndrome
2) mixed connective tissue disease
3) polymyositis
4) scleroderma