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CMD Block 2 > Immunopathology (Word Doc) > Flashcards

Immunopathology (Word Doc) Flashcards

1
Q 
What type of hypersensitivity? 
Occurs rapidly (minutes)
A

I

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2
Q

What type of hypersensitivity?

Delayed reaction

A

IV

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3
Q

What type of hypersensitivity?

Ab react against cell-surface or extracellular antigens

A

II

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4
Q

What type of hypersensitivity?

Occurs in individuals previously sensitized to antigen

A

I

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5
Q

What type of hypersensitivity?

mediated by immuno reaction to Ab:Ag complexes

A

III

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6
Q

What type of hypersensitivity?

Affects the glomeruli

A

III

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7
Q

What type of hypersensitivity?

Caused by sensitized CD4 T cells

A

IV

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8
Q

What type of hypersensitivity?

May produce granulomas

A

IV

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9
Q

Primary associated disease?

Anti-Scl70 (an anti-DNA topoisomerase)

A

Systemic sclerosis, diffuse

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10
Q

Primary associated disease?
Anti-U1 RNP
(anti-RNP not otherwise specified)

A

Mixed connective tissue disease

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11
Q

Primary associated disease?

Anti-cyclic citrullinated peptide (anti-CCP)

A

Rheumatoid arthritis

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12
Q

Primary associated disease?

Anti-RNA polymerase (anti-U3 RNP)

A

Systemic sclerosis

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13
Q

Primary associated disease?

Anti-centromere

A

CREST syndrome

limited systemic sclerosis

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14
Q

Primary associated diseases (3)?

Anti-SSB (anti-La)

A

Sjogren syndrome
Neonatal lupus
Subcutaneous lupus

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15
Q

Primary associated diseases (2)?

Anti-Jo-1

A

Polymyositis

dermatomyositis

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16
Q

Primary associated disease?

Anti-nuclear (ANA)

A

Lupus

and many other rheumatic diseases

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17
Q

Primary associated disease?

Anti-Smith (anti-Sm)

A

Lupus

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18
Q

Primary associated diseases (3)?

Anti-SSA (anti-Ro)

A

Sjogren syndrome
Neonatal lupus
Subcutaneous lupus

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19
Q

Primary associated disease?

Anti-double-stranded DNA (anti-dsDNA)

A

Lupus

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20
Q

Primary associated disease?

Anti-myeloperoxidase

A
  1. Microscopic polyangiitis

2. Eosinophilic granulomatosis with polyangiitis (Churg Strauss)

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21
Q

Primary associated disease?

Anti-proteinase-3

A

Granulomatosis with polyangiitis (Wegener’s)

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22
Q

Common testing used in diagnosis of many rheumatological diseases?

A

Serology (antibody testing)

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23
Q

T/f: Finding the antibody in the patient’s serum is the main diagnostic goal–determining the Ab is determining the disease.

A

F: Finding these antibodies by no means makes the diagnosis of disease. That requires what is called “clinical-pathologic correlation”. This is because many normal people have these antibodies without these diseases.

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24
Q

T?F: It is common for people with one autoimmune disease to have other, overlapping diseases as well.

A

T
“many patients with autoimmune/rheumatological disease do not have clinical or pathologic manifestations limited to one single specific disease. Man have overlapping syndromes with features of more than one autoimmune disease.”

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25
Q

Patients with autoimmune diseases or transplantation are treated with:

A

immunosuppressive therapy

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26
Q

Common immunologic treatment that is also anti-inflammatory

A

corticosteroids

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27
Q

Two medications that treat immune diseases (and transplant rejection) via calcineurin inhibition:

A

Cyclosporine and tacrolimus

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28
Q

How does Calcineurin function in a normal lymphocyte?

A
  1. Calcineurin dephosphorylates “intracytoplasmic nuclear regulatory proteins”
  2. These regulatory proteins translocate into the nucleus, then become activated “intranuclear factors”
3. Once activated: promote T lymphocyte activation and secretion of: 
      TNF
      IFN-gamma
      IL-2 
      IL-4
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29
Q

Blocking calcineurin ultimately blocks:

A

T cell activation and secretion of signaling molecules (TNF, IFN-g. IL2, IL4)

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30
Q

Mycophenolate is used to treat what specific autoimmune disease?

A

systemic lupus erythematosus

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31
Q

How does Mycophenolate mofetil inhibit lymphocyte proliferation?

A
  1. Inhibits purine biosynthesis, which:
  2. Inhibits DNA replication, thus:
  3. Preventing lymphocyte proliferation
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32
Q

Two drugs used to treat rheumatoid arthritis and systemic lupus erythematosus?

A

Azathioprine

Hydroxychloroquine

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33
Q

Purine analog; Screws up DNA replication.

A

Azathioprine

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34
Q

This low-toxicity antibiotic happens to be anti-inflammatory.

A

Hydroxychloroquine

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35
Q

3 drugs that block TNF-alpha

A

infliximab
etanercept (Enbrel)
adalimumab (Humira)
(do we actually need to memorize this? Grrrr I doubt I will remember it even if I try)

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36
Q

This drug is an antibody to CD20 on B lymphocytes

A

Rituximab

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37
Q

This drug is an antibody to B-cell activating factor

A

Belimumab

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38
Q

This drug is an antibody that blocks IL-6 receptors

A

Tocilizumab

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39
Q

This drug is an antibody to CD52

A

Alemtuzumab

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40
Q

This drug decreases the incidence of transplant rejection and increases the risk of opportunistic infection; creates a permanent AIDs-like effect.

A

Alemtuzumab

(help me understand why anyone would take this?? no idea, I guess if you kill CD4 cells you stop transplant rejection, but then you just gave yourself AIDS. Id like to hear that commercial… Do not take Alemtuzumab on an empty stomach. All patients experience AIDS after taking this medication….)

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41
Q

What cells express CD52?

A

high levels:
-normal and malignant B + T lymphocytes

lower levels:

  • monocytes
  • macrophages
  • eosinophils
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42
Q

6 gross pathological findings in Lupus (SLE)

A
  1. synovitis
  2. pleuritis
  3. pericarditis
  4. peritonitis
  5. endocarditis (with vegitations on either side of valve)
  6. moderate splenomegaly
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43
Q

Lupus is most common in what population?

A

Women, black, 15-45

will be more severe in black/asian

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44
Q

5 things that cause Lupus:

2 specific, 3 broad

A
  1. failure of self-tolerance
  2. antinuclear antibodies
  3. genetic factors
  4. environmental factors (UV)
  5. Immuno factors
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45
Q

What microscopic pathological feature implies active Lupus?

A

IgG:complement deposits in the glomerulus (this causes “wire-loop” lesions; most common in diffuse proliferative nephritis)

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46
Q

Microscopic Pathology of Lupus:

A
  1. acute necrotizing vasculitis of small arteries and arterioles
  2. nephritis (50%)
  3. cerebritis (50%)
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47
Q

5 patterns of glomerulonephritis seen in Lupus:

A
  1. minimal
  2. mesangial
  3. focal proliferative
  4. diffuse proliferative
  5. membranous
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48
Q

Major Lupus symptoms: (9 listed)

A 
Most common:
joint pain
fever (sometimes of unknown origin)
fatigue
weight loss
Also:
pleuritic CP
photosensitivity
nephrotic syndrome
angina
hair loss
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49
Q

What common symptom of Lupus may lead to edema?

A

Nephrotic syndrome

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50
Q

Signs of Lupus: (8)

A
  1. erythematous skin rash over bridge of nose and cheeks + other sites
  2. edema (first in feet)
  3. hematuria (usually only microscopic)
  4. neuropsychiatric (psychosis, seizures)
  5. oral ulcers
  6. interarticular skin rash on fingers
  7. peri-ungual erythema around fingernails
  8. alopecia
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51
Q

Diagnosis of Lupus: (6)

A
  1. ANA (present in 100%, also ~15% of normals)
  2. anti-double-stranded DNA or anti-Sm Ab
  3. hematologic abnormalities (anemia, thrombocytopenia, etc.)
  4. proteinuria
  5. urinary red cell casts
  6. kidney biopsy
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52
Q

Treatment for Lupus: (2)

A

corticosteroids and immunosuppressive medications

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53
Q

Sjogren syndrome

A

Autoimmune chronic inflammatory disease of lacrimal glands and salivary glands, causing dry eyes and dry mouth

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54
Q

What is the term for eye problems associated with Sjogren syndrome?

A

kerato-conjunctivitis sicca

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55
Q

What is the term for oral problems associated with Sjogren syndrome?

A

xerostomia

56
Q

Primary form of Sjogren syndrome.

A

limited to eyes and mouth, also called sicca syndrome

57
Q

Secondary form of Sjogren syndrome.

A

Associated with other autoimmune diseases

  • rheumatoid arthritis (most common)
  • lupus
  • polymyositis
  • systemic sclerosis
  • vasculitis
  • thyroiditis
58
Q

Sjogren syndrome is most common in what population?

A

35-45 year-old women

59
Q

Causes of Sjogren’s Syndrome (2)

A
  1. T cell attacks self antigen in the ductal epithelial cells
  2. T cells attack an antigen in glands that are virally-infected (by virus that is specific for the epithelial cells in the lacrimal/salivary glands)
60
Q

Gross pathology of Sjogren’s Syndrome:

A
  • dry ocular and oral mucosa

- enlarged salivary and lacrimal glands.

61
Q

Microscopic pathology of Sjogren’s Syndrome:

A

intense infiltration of CD4 T lymphocytes

destruction of gland architecture

+/- plasma cells, +/- germinal centers
(what does this mean?)

Renal involvement: interstitial nephritis

62
Q

Signs of Sjogren’s Syndrome:

A
  • dry mucous membranes of eyes/mouth
  • conjunctival/oral ulcers
  • enlarged salivary/lacrimal glands
63
Q

Diagnosis of Sjogren’s Syndrome:

A

anti-SSA or anti-SSB Ab

64
Q

Treatment of Sjogren’s Syndrome:

A
  • -Topical therapy: eyes, mouth and other dry mucosal surfaces
  • -Systemic cholinergic agents to stimulate secretions
  • -Hydroxychloroquine
  • -Sometimes rituximab for extraglandular disease
65
Q

What condition do people with Sjogren’s Syndrome often develop?

A

lymphoma

66
Q

Systemic sclerosis

A

Chronic disease with abnormal accumulation of fibrous tissue in skin and other organs

67
Q

Early visceral involvement is characteristic of ____ systemic sclerosis.

A

diffuse

68
Q

Late visceral involvement is characteristic of ____ systemic sclerosis.

A

limited

69
Q

Involvement of the skin of fingers, forearms and face is characteristic of ____ systemic sclerosis.

A

Limited

70
Q

Widespread skin involvement is characteristic of ____ systemic sclerosis.

A

diffuse

71
Q

What causes the increased growth factors characteristic of Systemic sclerosis?

A

increased growth factors (leading to fibrosis) are caused by:

  1. abnormal immune response
  2. vascular damage
72
Q

Genes (2) involved in systemic sclerosis.

A

HLA-II and fibrillin-1

73
Q

T/F: Cytokines produced by CD4 T cells stimulate fibroblasts.

A

T (the fibroblasts then secrete collagen)

74
Q

What is involved in the microvascular disease associated with systemic sclerosis?

A
  1. Intimal proliferation
  2. capillary dilatation
  3. endothelial injury (increased vWF) + platelet activation leads to fibrosis
75
Q

In systemic sclerosis, skin is initially _____ and ultimately ______.

A

edematous; fibrotic

76
Q

In systemic sclerosis, what is the characteristic gross skin pathology?

A

Decreased mobility = mask-like face and clawlike hands

77
Q

In systemic sclerosis, what is the characteristic gross GI pathology?

A
  • -Fibrous replacement of muscular wall (often in esophagus)
  • -Lower esophageal sphincter dysfunction
  • -Decreased peristalsis (causing GERD and Barrett metaplasia)
78
Q

In systemic sclerosis, what is the characteristic microscopic skin pathology?

A
  • Dense collagen deposition in dermis with decreased appendages
  • Thinning of epidermis
  • Loss of rete pegs
  • Perivascular infiltrates of CD4 T-cells
  • Thickening of capillary/arterial basal lamina
79
Q

In systemic sclerosis, what is the characteristic microscopic lung pathology?

A

Vascular changes promote:

  • pulmonary hypertension
  • interstitial fibrosis
80
Q

In systemic sclerosis, what is the characteristic microscopic kidney pathology?

A

Vascular changes promote:

  • hypertension
  • renal failure

Intimal thickening of interlobular arteries leads to:

  • ischemia
  • infarction
81
Q

Symptoms of systemic sclerosis:

A

Raynaud’s phenomenon (Numbness, tingling, cyanosis of peripheral skin)

Joint pain and / or stiffness.

Digestive problems secondary to decreased gut motility

82
Q

Signs of systemic sclerosis:

A

Early: edema of the hands and feet (most prominent in the morning)

Later: thickened, hard and / or shiny skin

83
Q

In the serology of patients with systemic sclerosis (diffuse vs limited?):

A

Diffuse:
Anti-DNA topoisomerase I aka Anti-Scl70
Anti-U3 RNP

Limited:
Anti-centromere
Anti-U3 RNP

84
Q

Diagnosis of systemic sclerosis suggested by:

A 
generalized cutaneous sclerosis
hypertension
renal failure
pulmonary hypertension 
fibrosis
85
Q

Non-pharmacologic treatment of systemic sclerosis:

A

Exercise, splinting, avoiding cold

86
Q

Pharmacologic treatment and procedures of systemic sclerosis: (6)

A 
Immunomodulators
antifibrotics
cyclophosphamide
methotrexate
glucocorticoids
Hematopoietic stem cell transplantation
87
Q

Puffy fingers are a sign of what disease?

A

systemic sclerosis

88
Q

Hyperacute rejection is characterized by …

A

high titers of preformed Abs

89
Q

Histologically, how does a transplanted kidney damaged by immunosuppressant drugs differ from a transplanted kidney damaged by host rejection?

A

Drug: vacuolization, calcification, and giant mitochondria

rejection: lymphocytes

90
Q

What is polyomavirus nephropathy?

A

caused by BK virus and causes formation of inclusion bodies and epithelial cell injury and lysis

91
Q

T or F: Transplant pts can have simultaneous infection and rejection

A

T

92
Q

What is PLTD?

A

post-transplant lymphoproliferative disorder: proliferation of lymphocytes to full blown malignant lymphoma

93
Q

The proliferative cells in PLTD have normally been infected with _____ which is “awaken” by _____

A

Epstein-Barr virus and is awaken by immunosuppressants

94
Q

Bc cells from a transplanted organs leave the transplanted organ and take up residence elsewhere in the body, every transplant recipient is considered to be a ______. What type of cell most commonly leaves the transplant?

A

chimera; T lymphocyte –> GVHD

95
Q

What 2 organs are especially attacked during GVHD?

A

skin and GI tract

96
Q

GVHD in the skin causes _____

A

generalized erythematous rash which goes on to cause fibrosis

97
Q

GVHD in the GI tract usually clinically manifests as _______

A

bloody diarrhea

98
Q

All cells that are attacked in GVHD die via …

A

apoptosis

99
Q

Congenital immunodeficiency with B cells unable to make Abs and is not evident until 6 mos of age

A

XLA from Btk deficiency

100
Q

What is a common feature of common variable immunodeficiency?

A

hypogammaglobulinemia

  • diff than XLA bc it affects men and women equally and has a much later onset (20s-30s)
  • not a SCID bc T cell # are fine
101
Q

What does isolated IgA deficiency leave an individual susceptible to?

A

susceptible to anaphylaxis with blood transfusion

Why?????? Nichols be cray

102
Q

Deficiency in both cellular AND humoral immunity

A

SCID

103
Q

What is a congenital X linked disorder with immunodeficiency, eczema, and thrombocytopenia?

A

Wiskott-Aldrich syndrome

104
Q

What is AIDS?

A

syndrome of opportunistic infections, neoplasms, and dementia due to deficient cellular immunity (from HIV infection)

105
Q

What is amyloidosis?

A

progressive organ disfunction due to deposition of insoluble proteins in blood vessels and interstitium

106
Q

What are the 4 categories of systemic amyloidosis?

A

primary
secondary
induced
hereditary

107
Q

What is the epidemiology of amyloidosis?

A
  • late middle aged and elderly
  • primary or secondary tp another disease
  • 3200 new cases a year
108
Q

What is the common characteristic of proteins involved in the pathogenesis of amyloidosis?

A

they are beta pleated sheets

109
Q

What are Bence-Jones proteins?

A

aggregates of light chain Ig

110
Q

Amyloidosis with amyloid A is often secondary to ______

A

RA or chronic infalmmation

111
Q

What organs does primary amyloidosis most often involve?

A

heart, gut, skin, nerves, and tongue

112
Q

What is the protein that is deposited during primary amyloidosis?

A

AL (amyloid light chains… 1/3 kappa and 2/3 lambda)

113
Q

Some pts with amyloidosis have multiple myeloma but only __% with multiple myeloma have amyloidosis?

A

10

114
Q

Where is AL protein found?

A

urine and/or serum

115
Q

What organs does secondary amyloidosis tend to involve?

A

kidneys, liver, spleen, lymph nodes, adrenals, and thyroid

116
Q

With what syndromes is secondary amyloidosis assoc with?

A

RA, IBS, IV drug abuse, renal cell carcinoma, and Hodgkin’s disease

117
Q

What protein is deposited with secondary amyloidosis?

A

AA

118
Q

What is AA thought to be derived from ?

A

SAA (acute phase reactant) which circulates in HDL

119
Q

What organs does induced amyloidosis tend to involve?

A

nerves, joints, bone, gut, tongue

120
Q

What protein is deposited in induced amyloidosis?

A

AB2M (Beta-2-microglobin) (= light chain of MHC I)

121
Q

What is the cause of induced amyloidosis?

A

dialysis treatment is not able to filter out AB2M

122
Q

What is hereditary amyloidosis?

A

a variety of mediterranean fever

123
Q

What signs and symptoms are assc with hereditary amyloidosis?

A

fever, peritonitits, pleuritis, synovitis

124
Q

What protein is deposited in hereditary amyloidosis? And Where?

A

AA –> liver, spleen, kidney and adrenal

ATTR (amyloid transthyretin) –> affects peripheral and autonomic nerves

125
Q

Localized cardiac amyloidosis involves the deposition of ….

A

ATTR in ventricles or AANF in atria

126
Q

Localized cerebral amyloidosis involves the deposition of ….

A

AB (degradation product of APP in Alzheimer’s and Down Syndrome

127
Q

Localized thyroid amyloidosis involves the deposition of ….

A

calcitonin (medullary carcinoma)

128
Q

Localized pancreatic amyloidosis involves the deposition of ….

A

amyloid in islets (type II DM)

129
Q

What is the minor protein deposited in all of these amyloid disorders (except Alzheimer’s)?

A

AP (amyloid P)

130
Q

What is the gross pathology of amyloidosis of an organ?

A

enlarged and waxy

131
Q

Describe the microscopic morphology of amyloidosis.

A
  • hyaline eosinophillic materian in blood vessels, glomeruli , then interstitium
  • stains red with “Congo red” and apple green bifringence under polarized light
132
Q

What are the symptoms of amyloidosis?

A

nonspecific –> dyspnea –> light-headedness –> syncope (heart) –> edema (kidneys)

heart failure, renal failure, dementia, liver failure, neuropathy

133
Q

What are the signs of amyloidosis?

A

macroglossia (enlarged tongue)

134
Q

How is amyloidosis diagnosed?

A

biopsy showing extracellular deposit of hyaline that stains red with Congo red stain and shows apple green bifringence under polarized light

135
Q

What is the treatment for amyloidosis?

A

transplant

136
Q

What is the prognosis of amyloidosis?

A

poor without transplantation

CMD Block 2 (38 decks)

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