Brainscape's Knowledge GenomeTM

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


See full index

Year 5 Pathology > Immuno > Flashcards

Immuno Flashcards

1
Q

Allergic rhinitis

A

Loss smell, nasal itching and discharge, swollen and hyperemic nasal mucosa.
Tx with corticosteroid spray (fluticasone) +/- PO antihistamines

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

Hereditary angioedema

A

Laryngeal edema, abdo sxs (pain, D&V, constip, distension), ?swelling hands and feet.
Triggered by infections, stress, menstruation, ACEI

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

Acute urticaria

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

Urticarial vasculitis

A

Ecchymoses and hyperpigmentation may occur in healing process
Biopsy for dx

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

Classic urticaria reaction

A

Latex

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

Which Ig is a dimer?

A

IgA

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

Which Ig is most abundant?

A

IgG

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

Chemotactic agents

A

IL8, LTB4, C5a, bacterial products, kallikrein

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

Kostmann’s

A

Congenital neutropenia

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

Examples of Type II HSR

A 
Hemolytic anemias
Graves
Goodpastures
ITP
Myasthenia Gravis
Type I DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples Type III HSR

A 
SLE
HCV-associated MPGN
RA
Polyarteritis nodosa
Arthus reaction
Serum sickness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

c-ANCA

A

Wegener’s

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

p-ANCA

A

Polyarteritis nodosa

Microscopic polyangitis

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

Live vaccines

A 
MMR
BCG
Yellow fever
Oral polio (Sabin)
VZV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Killed vaccines

A

Rabies
Influenza (IM)
Polio (salk)
HAV

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

Subunit/congugate vaccine

A

Pneumococcal

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

Congugate vaccine

A

Hib

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

Recombinant vaccine

A

HBV

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

Detoxified vaccine

A

Tetanus

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

Inactivated bacterial preparation vaccine

A

Whole cell typhoid

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

Alum

A

Agent that produces predominantly Ab response through release IL-4 which primes naive B cells

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

Vaccination: active or passive immunity

A

Active

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

Immune globulin: active or passive immunity

A

Passive

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

Innate immunity composed of?

A

Epithelium
Mucus
Complement
Myeloid cells: granulocytes, macros, mast cells

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

TLRs

A

On cells of innate immune system.

Recognize PAMPs, e.g. CD14 (on macros) is a TLR that recognizes LPS on gram neg bacteria

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

TLR activation

A

Upregulates NF-KB

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

NF-KB

A

“On switch for acute inflamm response”

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

Which products of AA mediate vasodilation and increased vascular permeability?

A

PGI2, PGD2, PGE2

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

Mediate neutrophil chemotaxis

A

LTB4, IL8, C5a, bacterial products, kallikrein

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

Which AA products mediate vasoconstriction, bronchoconstriction, and increased vascular permeability?

A

LTC4, LTD4, LTE4

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

Activators or mast cells

A

Tissue trauma
C3a, C5a
Cross linking of IgE by antigen

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

Immediate response of mast cells

A

Histamine release:

  • arteriole vasodilation
  • increased vascular permeability at post-cap venule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Delayed response of mast cells

A

Production AA metabolites, esp LTs

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

Classical pathway complement

A

C1 bings IgG or IgM that is bound to an antigen

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

Alternative pathway complement

A

Microbial products directly activate

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

Mannose lectin binding pathway complement

A

MBL binds mannose on microorganisms

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

All complement pathways meet where

A

Production C3 convertase, C5 convertase

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

Complement proteins that trigger mast cell degranulation

A

C3a, C5a

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

Complement protein that acts as opsonin for phagocytosis

A

C3b

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

Hageman factor

A

Inactive pro-inflamm protein produced by liver.
Activated on exposure to subendothelial or tissue collagen
Activates coag and fibrinolytic systems, complement, kinin system

IMPORTANT IN DIC!!!

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

Bradykinin functions

A

Vasodilation
Increased vascular permeability
Pain

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

Pain mediators

A

Bradykinin, PGE2

Sensitize sensory nerve endings

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

Rubor and Calor

A

Due to vasodilation causing increased blood flow

HISTAMINE, PGs, bradykinin

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

Tumor

A

Leakage fluid at post-cap venule into interstitial space

Histamine, tissue damage

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

Fever mechanism

A

Pyrogens cause release IL1, TNF which increase COX activity in perivascular cells of hypothalamus. Increased COX=increased PGE2 which increases temp set point

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

Steps of neutrophil arrival

A
  1. Margination
  2. Rolling
  3. Adhesion
  4. Transmigration
  5. Phagocytosis
  6. Destruction phagocytosed material
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Rolling-mechanism

A

Selectin speed bumps.
P selectin from Weibel Palade bodies, histamine mediated.
E selectin induced by TNF, IL1

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

Adhesion-mechanism

A

Cellular adhesion molecules (CAMS) (on endothelium) and integrins (on neutrophils) bind

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

Upregulators CAMS

A

TNF

IL-1

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

Upregulators integrins

A

C5a, LTB4

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

Leukocyte adhesion deficiency

A

AR defect in CD18 subunit of integrin
Thus no adhesion
Sxs/signs: delayed separation umbilical cord, neutrophilia, recurrent bacterial infections without pus

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

Chediak Higashi disease

A 
Protein trafficking defect (microtubules)-phagosome can't bind with lysosome
Sxs:
Pyogenic infections
Neutropenia (can't divide)
Giant granules by Golgi
Defective primary hemostasis
Albinism
Peripheral neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

O2 dependent killing

A 
Most effective
Generates HOCl (O2 -> superoxide ->H2O2 ->HOCl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

O2 independent killing

A

Less effective

Via enzymes in leukocyte: lysozyme, major basic protein

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

CGD

A

NADPH oxidase defect
Infections and granulomas with catalase positive organisms
Nitro-blue tetrazolium test (NBT) remains colorless

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

Catalase positive organisms

A 
S aureus
Pseudomonas cepacia
S marcescens
Nocardia
Aspergillus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

MPO deficiency

A

MPO converts H2O2 to HOCl.

In theory similar to CGD but reality: only increased risk Candida

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

When in inflamm do macros peak

A

2-3 days after start inflamm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

When in inflamm do neutrophils peak

A

24 hrs after start inflamm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How do macros get from blood into periphery

A

Same way neutrophils do (margination, rolling, adhesion, transmigration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Method by which macrophages kill

A

O2 INdepedent, esp lysozyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Outcomes acute inflamm

A

Resolution and healing (IL10, TGF-B)
Continued acute inflamm (macros call in more neuts via IL-8)
Abscess formation
Chronic inflamm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Chronic inflamm cells

A

Lymphos and plasma cels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Stimuli for chronic inflamm

A 
Persistent infection (MCC)
Viruses, mycobacteria, parasites, fungi
AI
Foreign material
Some cancers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

T cell activation requirements

A
  1. Binding antigen/MHC complex

2. Secondary signal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Types CD4+ cells

A

TH1, TH2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

TH1 products

A

IL2, IFN-gamma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

IL2

A

T cell growth factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

IFN-gamma

A

Macrophage activator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

TH2 products

A

IL4
IL5
IL10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

IL4

A

IgE

72
Q

IL5

A

IgA

73
Q

IL10

A

Inhibits TH1

74
Q

CD8+ cells

A

Perforins, granzyme

Express FasL which binds Fas on target cell

75
Q

First Igs on B cell

A

IgD, IgM

76
Q

Granuloma-key feature

A

Epitheliod histiocyte

77
Q

Ddx-non-caseating granuloma

A 
Foreign material, e.g. leaking breast implant
Sarcoidosis
Berylliosis
Crohns
Cat scratch (stellate shaped)
78
Q

Ddx-caseating granuloma

A

TB

Fungus

79
Q

DiGeorge syndrome

A

Developmental failure 3rd and 4th pharyngeal pouch
22q11 microdeletion
T cell deficiency, hypocalcemia, abnormalities great vessels, heart, and face

80
Q

T cell deficiency symptoms

A

Viral and fungal infections

81
Q

B cell deficiency symptoms

A

Bacterial, protozoal infections

82
Q

3rd pharyngeal pouch

A

Inferior parathyroids, thymus

83
Q

4th pharyngeal pouch

A

Superior parathyroids

84
Q

SCID

A 
Defective cell-mediated and humoral immunity.  All the infections, including opportunistic.
Etiologies:
1. Cytokine receptor defects
2. Adenosine deaminase deficiency
3. MHC class II deficiency

Tx-sterile isolation, stem cell transplant

85
Q

Cell-mediated immunity

A

T cells

86
Q

Humoral immunity

A

B cells

87
Q

X linked agammaglobulinemia

A

Complete lack Igs due to disordered B cell maturation
Bruton tyrosine kinase (BTK) mutation
Infections with bacteria, enterovirus, Giardia
Avoid live vaccines

88
Q

Common variable deficiency

A

Low Ig due to B cell or TH cell defects
(Exams: mutation MHC III)
Bacteria, enterovirus, Giardia infections
Increased risk AI disorders, lymphoma

89
Q

Which two immunodeficiencies result in bacterial, enterovirus, and Giardia infections?

A 
Common variable
X linked (Bruton) agammaglobulinemia
90
Q

Most common Ig deficiency

A

IgA

91
Q

IgA deficiency

A

Mucosal infections, esp viral.

NB: celiacs tend to have this a lot

92
Q

Hyper-IgM syndrome

A 
Mutation in CD40L or CD40R...problem with class switching-no 2nd signal.
Decreased IgA, IgG, IgE causes recurrent infections, esp mucosal
93
Q

Wiskott Aldrich syndrome

A

Defect in WASP (Wiskott-Aldrich Syndrome Protein)
Thromboytopenia, eczema, recurrent infections (humoral and cell mediated)
X linked

94
Q

C5-C9 deficiency

A

Neisseria infections

95
Q

C1 inhibitor deficiency

A 
Hereditary angioedema (esp periorbital edema).
Excess activation complement (therefore vasodilation and increased vascular permeability)
96
Q

Primary mech for autoimmunity

A

Loss of self tolerance: many self-reactive lymphos regularly generated but undergo TOLERANCE (central and peripheral). E.g. negative selection in thymus causes self-reactive lymphos to undergo apoptosis

97
Q

AIRE mutation

A

AI polyendocrine syndrome (APECED): hypoparathyroidism, adrenal failure gonadal failure, alopecia, vitiligo, candida.
Failure of negative selection: no AIRE to express “self”.
AIRE is also called “autoimmune regulator”

98
Q

Central tolerance in bone marrow

A

Negative selection: if bind “self” too strongly, either undergo receptor editing or apoptosis

99
Q

Peripheral tolerance

A

In blood. Anergy (no second signal) or apoptosis via Fas death receptor

100
Q

ALPS

A

Autoimmune Lymphoproliferative Syndrome
Mutation in Fas apoptotic pathway
Cytopenias, LAD, HSM (LAD and HSM due to proliferation lymphos….can lead to lymphoma)

101
Q

FOXP3 mutation

A

IPEX syndrome

102
Q

IPEX syndrome

A

Immune dysfn Polyendocrinopathy Enteropathy X linked
Polyendo–thyroiditis, diabetes
Enteropathy–diarrhea

103
Q

CD25 polymorphisms

A

Associated with autoimmunity, e.g. MS, Type I diabetes

104
Q

HLA B27

A

Ankylosing spondylitis

105
Q

Environmental triggers for autoimmunity

A 
Infection (self reactive activated)
Molecular mimicry (antigen resembles self-antigen)
106
Q

Reason for female bias in autoimmunity

A

Esrogen decreases tolerance, therefore more self-reactive lymphocytes

107
Q

SLE

A

Type III HSR
Decreased levels CH50, C3, C4
ANA, anti-dsDNA, anti-Sm

108
Q

Drug induced lupus

A

Hydralazine, procainamide, isoniazid
Anti-histone Abs
CNS, renal involvement rare

109
Q

Antiphospholipid syndrome

A

Abs + hypercoagulable state
Lifeling anticoagulation–arterial and venous thromboses
Can occur with SLE but more commonly is primary disorder

110
Q

Sjogrens

A

AI destruction lacrimal, slaivary glands
Type IV HSR
Anti-SSA, SSB, ANA, RF
Increased risk B cell lymphoma (U/L enlargement parotid)

111
Q

Systemic sclerosis

A 
Fibroblast activation causing collagen deposition.  Massive amounts fibrosis
Limited type (CREST) and diffuse type
112
Q

CREST syndrome antibody

A

anti-centromere

113
Q

Diffuse systemic sclerosis Ab

A

anti-topoisomerase I

114
Q

Mixed connective tissue disease–Antibodies

A

Anti U1 RNP antibodies

115
Q

Labile tissues

A

Continuously cycle to regenerate tissue.
Small and large bowel
Skin
Bone marrow

116
Q

Stable tissues

A

Quiescent but can re-enter cell cycle.

LIVER

117
Q

Permanent tissues

A

Heal by repair; no regenerative capacity
Myocardium
Skeletal muscle
Neurons

118
Q

Initial phase repair

A

Formation of granulation tissue

119
Q

Granulation tissue mediators

A

Fibroblasts, capillaries, myofibroblasts

120
Q

Scar formation

A

Result of repair

Type III collagen replaced by Type I

121
Q

Causes delayed wound healing

A

Infection (MCC)
Vit C, Cu, Zn deficiency
Foreign body/continued inflamm, diabetes, ischemia, malnutrition

122
Q

Hypertrophic scars

A

Excess production of Type I collagen

123
Q

Keloid scars

A

Excess production scar tissue out of proportion to wound
Type III collagen
*Earlobe

124
Q

Bare lymphocyte syndrome

A

Deficiency in MHC I or MCH II
Low IgA, IgG
Associated with sclerosing cholangitis (hepatomegaly, jaundice)

125
Q

IFN-gamma deficiency

A

Can’t form granulomas
TB
And salmonella, for some reason

126
Q

OKT3

A

Aka muromonab.
Monoclonal antibody (mAb) against CD3.
Treats rejection episodes in transplant pts, by clearing T cells from circulation.
Use when acute steroid-resistant rejection of heart, liver, kidney transplants

127
Q

Cyclosporin

  • MOA
  • SE
A 
Inhibits calcineurin (therefore T cells)
SE: gum hypertrophy
128
Q

Azathioprine

-Mech

A

Metabolized to 6MP. Prevents DNA synthesis, esp lymphocytes

129
Q

Sirolimus

A

Aka rapamycin

Inhibits T cell prolif by binding FK-binding protein 1A (FKBP-1a)

130
Q

Anti-Jo1

A

Dermatomyositis

131
Q

Anti-smooth muscle

A

AI hepatitis

132
Q

Anti-centromere

A

CREST syndrome

133
Q

Anti-topoisomerase I

A

Diffuse scleroderma

134
Q

Antimitochondrial

A

PBC

135
Q

Anti-glutamic acid decarboxylase

A

T1DM

136
Q

Anti-endomysial

A

Celiac

137
Q

Anti-cardiolipin

A

Antiphospholipid
SLE
Syphilis

138
Q

Goodpastures

A

Against Type IV collagen.
Pulm, renal sxs (bleeding)
Immunofluoresence

139
Q

Myelin basic protein, proteolipid protein

A

Implicated in MS

140
Q

Stony fruits

A

Associated with oral allergy syndrome

141
Q

SLE treatment when steroids fail

A

Cyclophosphamide

142
Q

Abatacept

A

CTLA4-Ig fusion protein

Used in RA

143
Q

Mycophenolate

A

Inhibits IMP DH (guanine synthesis).
Transplant alternative to cyclophosphamide
Also used in AI diseases, vasculitides

144
Q

Denosumab

A

Anti-rank L

used in osteoporosis

145
Q

Basiliximab

A

mAb against IL-2alpha

146
Q

Rituximab

A

Anti-CD20

147
Q

Efalizumab

A

mAb against CD11a

148
Q

Ustekinumab

A

mAb to p40 subunit IL-12, IL-23.

Psoriatic arthritis

149
Q

Kveim test

A

Tests for sarcoidosis.
Not used in UK due to infection risk (involves placing sample of sarcoid pt’s spleen intradermally into pt and biopsying in 4-6 weeks to see if caseating granulomas)

150
Q

Latex fixation test

A

Used for rheumatoid factor

151
Q

Increased CD50

A

Acute or chronic inflamm

152
Q

HLA-DQ2

A

Celiac

153
Q

HLA-B27

A

Ank spon

154
Q

HLA-DR2

A

Goodpasture’s

155
Q

HLA-DR3

A

Graves, MG, SLE

156
Q

HLA-DR4

A

T1DM

RA

157
Q

Serum tryptase levels

A

Useful in diagnosing anaphylaxis

158
Q

Anti-desmoglein 1,3

A

Pemphigus vulgaris

159
Q

Isograft

A

Between twins

160
Q

Hyperacute rejection

A

Minutes to hours.

Preformed Abs

161
Q

Acute rejection

A

~1 week

Type IV HSR

162
Q

Chronic rejection

A

Months-years

163
Q

gp120

A

Envelope
Binds CXCR4 on surface CD4+ cell to gain entry

Initial step in HIV infection

164
Q

gp41

A

Penetrates CD4+ wall

165
Q

Tx for myasthenic crisis

A

Plasmapheresis

166
Q

Natalizumab

A

mAb against alpha4 integrin (T cell migration)

167
Q

Tocilizumab

A

mAb against IL-6

Castleman’s, RA

168
Q

Adalimumab

A

Fully humanized mAb to TNF-a

169
Q

Speckled immunofluroescence pattern

A

Anti-Jo1
Anti-Sm
Anti-RNP
Anti-Ro

170
Q

Nucleolar immunofluorescence pattern

A

anti-RNA polym (systemic sclerosis)

171
Q

Peripheral immunofluorescence pattern

A

anti-dsDNA

172
Q

Seronegative spondylarthropathies

A

Ank spon
Enteropathic arthritis
Psoriatic arthritis
Reactive arthritis

173
Q

anti-1A-2 and anti-phogrin antibodies

A

Diabetes

Against tyrosine phosphatase

174
Q

Hashimoto’s antibodies

A

anti-thyroid peroxidase

anti-thyroglobulin

175
Q

Kearns-Sayre syndrome

A

Initially eye stuff (ptosis, difficulties with eye movement, pigmentation retina), then prox muscle weakness, cardiac conduction defects, hearing loss, cerebellar ataxia
Hypoparathyroidism, primary gonadal failure, DM, hypopituitarism

176
Q

Hirata’s disease

A

Auto-Abs to serum insulin
Fasting hypoglycemia
JAPAN

Year 5 Pathology (6 decks)

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