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GENERAL PATHOLOGY > Diseases of the Immune System > Flashcards

Diseases of the Immune System Flashcards

1
Q

protection from infectious pathogens

A

immunity

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2
Q

Body’s first line of defense

A

innate immunity

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3
Q

mechanisms that are ready to react to infections even before they occur, and that have evolved to specifically recognize and combat microbes

A

innate immunity

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4
Q

mechanisms that are stimulated by (“adapt to”) microbes and are capable of recognizing microbial and nonmicrobial substances

A

adaptive immunity

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5
Q

what constitutes innate immunity?

A
  • recognition of microbes and damaged cells
  • activation of various mechanisms
  • elimination of the unwanted substances
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6
Q

components of innate immunity

A 
epithelia
monocytes and neutrophils
dendritic cells
natural killer cells
mast cells
innate lymphoid cells
soluble proteins
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7
Q

acts as mechanical barriers to the entry of microbes from the outside environment

A

EPITHELIA of the skin, gi, and respiratory tracts

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8
Q

are phagocytes in the blood that can be rapidly recruited in sites of infection

A

Monocytes and neutrophils

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9
Q

antigen presenting function; sense microbes

and cell damage and stimulate the secretion of cytokines

A

Dendritic cells

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10
Q

provide early protection against many viruses and intracellular bacteria

A

NK cells

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11
Q

produce mediators of inflammation

A

Mast cells

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12
Q

protects against extracellular microbes and their toxins

A

Humoral immunity

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13
Q

mediated by B lymphocytes

A

Humoral immunity

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14
Q

secreted products of humoral immunity

A

antibodies/ immunoglobulins

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15
Q

for defense against intracellular microbes

A

Cell-mediated (or cellular) immunity

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16
Q

mediated by T lymphocytes

A

Cell-mediated (or cellular) immunity

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17
Q

constitute 60-70% of lymphocytes in the blood

A

T lymphocytes

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18
Q

types of T lymphocytes

A

cytotoxic, helper and regulatory T cells

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19
Q

where do T lymphocytes develop

A

thymus

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20
Q

T lymphocytes are mainly seen where

A

in paracortex of lymph nodes, periarteriolar lymphoid sheaths of spleen

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21
Q

recognize a cell-bound antigen by means of an antigen-specific T-cell receptor (TCR)

A

T lymphocytes

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22
Q

co-receptors in T-cell

activation

A

CD4 and CD8

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23
Q

recognize antigens displayed by MHC molecules on the surfaces of antigen- presenting cells

A

αβ TCR

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24
Q

CD4 binds to

A

Class II Membrane Histocompatibility Complex

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25
Q

CD8 binds to

A

Class I MHC

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26
Q

constitute 10-20% of circulating lymphocytes

A

B lymphocytes

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27
Q

B lymphocytes are found

A

in peripheral lymphoid tissues (follicles of the cortex of lymph nodes and spleen, and mucosa-associated lymphoid tissues)

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28
Q

recognize antigen via the B-cell antigen receptor complex (Membrane-bound IgM and IgD)

A

B lymphocytes

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29
Q

develop into plasma cells that secrete antibodies

A

B lymphocytes

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30
Q

present antigens to T cells when recruited in T-cell zones of lymphoid organs

A

Dendritic cells (Interdigitating dendritic cells)

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31
Q

example of dendritic cells

A

Langerhans cells

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32
Q

present in the germinal centers of lymphoid follicles in the spleen and lymph nodes
- present antigens to B cells

A

Follicular dendritic cells

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33
Q

APC that are capable of phagocytosis

A

Macrophages

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34
Q

key effector cells in certain forms of cell- mediated immunity

A

Macrophages

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35
Q

participate in the effector phase of humoral immunity

A

Macrophages

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36
Q

destroy abnormal cells without prior exposure

A

Natural Killer Cells

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37
Q

aka large granular lymphocytes

A

Natural Killer Cells

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38
Q

enumerate cells of the immune system

A 
T lymphocytes
B lymphocytes
Dendritic cells
macrophage
NK cells
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39
Q

primary, or central lymphoid organs (thymus & bone marrow)

A

Generative Lymphoid organs

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40
Q

where T and B lymphocytes develop or mature

A

Generative Lymphoid organs-

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41
Q

secondary lymphoid organs where adaptive immune response are initiated

A

Peripheral lymphoid organs

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42
Q
  • concentrate antigens, APCs, and lymphocytes
A

Peripheral lymphoid organs

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43
Q

Peripheral lymphoid organs

A

lymph node
spleen
Cutaneous and mucosal lymphoid systems

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44
Q

concentrate antigens from lymph

A

lymph node

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45
Q

trap blood-borne antigens

A

spleen

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46
Q

(GI and respiratory tracts, pharyngeal tonsils, Peyer’s patches)

A

Cutaneous and mucosal lymphoid systems

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47
Q

excessive and harmful reaction to antigens

A

hypersensitivity

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48
Q

Elicited by exogenous environmental antigens or endogenous self antigens

A

hypersensitivity

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49
Q

Imbalance between the effector mechanisms and the control mechanisms

A

hypersensitivy

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50
Q

Associated with the inheritance of particular susceptibility genes

A

hypersensitivity

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51
Q

Mechanisms of tissue injury are the same as the effector mechanisms of defense

A

hypersensitivity

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52
Q

types of hypersensitivity diseases

A
  • Immediate Hypersensitivity (Type I Hypersensitivity)
  • Antibody-mediated Disorders (Type II Hypersensitivity)
  • Immune Complex–mediated Disorders (Type III Hypersensitivity)
  • Cell-mediated Immune Disorders (Type IV Hypersensitivity)
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53
Q

TH2 cells, igE antibodies, mast cells, other leukocytes

A

type 1

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54
Q

secreted antibodies igM and igG injure cells by promoting phagocytosis and injure tissue by inducing inflammation

A

type 2

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55
Q

igM and igG will form a antigen-antibody complex that will be deposited in the tissues and induce inflammation affecting many organs in the body

A

type 3

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56
Q

sensitized t lymphocytes ( th1, th17, cytotoxic t cells) cause of tissue injury

A

type 4

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57
Q

allergy

A

type 1

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58
Q

Rapid immunologic reaction occurring in a previously

sensitized individual

A

type 1

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59
Q

Triggered by the binding of an antigen to IgE antibody on the surface of mast cells

A

type 1

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60
Q

Systemic disorder (anaphylactic shock) or local reaction (localized cutaneous rash or blisters, hives, skin allergies, nasal and conjunctival discharge in allergic rhinitis and conjunctivitis, bronchial asthma, hay fever, allergic gastroenteritis in food allergies

A

type 1

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61
Q

characterized by vasodilation, vascular leakage, and smooth muscle spasm or glandular secretions

A

Immediate reaction

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62
Q

characterized by infiltration of tissues with eosinophils, neutrophils, basophils, monocytes, and CD4+ T cells, as well as tissue destruction

A

Late-phase reaction

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63
Q

Most immediate hypersensitivity disorders are caused by

A

excessive TH2 responses which stimulate IgE production and promote inflammation

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64
Q

first to be released mediator of hypersensitivity

A

Preformed Mediators

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65
Q

Preformed Mediators

A

Vasoactive amines (Histamine)
Enzymes
Proteoglycans

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66
Q

cause intense sm contraction, increase vascular permeability and increase mucus secretions

A

histamine

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67
Q

cause tissue damage leading to degeneration of kinins and activated components of complement

A

enzymes

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68
Q

heparin; package and store amines in the granules

A

proteoglycans

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69
Q

Lipid Mediators

A

Leukotriene B4, C4, D4
Prostaglandin D2
Platelet-activating factor

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70
Q

Cytokines

A

TNF, IL-1, chemokines, IL-4

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71
Q

most potent, vasoactive and spasmogenic agent known. they are more active than histamine in increasing vascular permeability and cause bronchial smooth muscle contraction

A

leukotriene c4 and d4

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72
Q

highly chemotactic for neutophils, eosinophils and monocytes

A

leukotriene b4

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73
Q

most abundant mediators produced in mast cells by the cyclooxigenase pathway and causes intense bronchus spasm and increase mucus secretion

A

prostaglandin d2

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74
Q

produced by some mast cells population. causes platelet aggregation, release of histamine, bronchus spasm, increase vascular permeability and vasodilation

A

platelet-aggregating factor

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75
Q

promotes leukocyte recruitment

A

chemokines

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76
Q

amplify th2 response

A

IL4

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77
Q

characterized by fall in blood pressure (shock) caused by vascular dilation; airway obstruction due to laryngeal edema

A

anaphylaxis

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78
Q

characterized by airway obstruction caused by bronchial smooth muscle hyperactivity; inflammation and tissue injury caused by late phase reaction

A

bronchial asthma

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79
Q

characterized by increase mucus secretion; inflammation of upper airways, sinuses

A

allergic rhinitis, sinusitis (hay fever)

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80
Q

characterized by increased peristalsis due to contraction of intestinal muscles

A

food allergies

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81
Q

type II hypersensitivity

A

Antibody-Mediated (Type II) Hypersensitivity
Opsonization and Phagocytosis  Inflammation
Cellular Dysfunction

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82
Q

antigen combines with antibody in the circulation

A

type 3

83
Q

complexes may be formed at sites where antigen has been “planted” previously

A

type 3

84
Q

caused by inflammation resulting from cytokines produced by CD4+ T cells and cell killing by CD8+ T cells

A

type 4

85
Q

Affect the humoral and/or cellular arms of adaptive immunity

or the defense mechanisms of innate immunity

A

Primary immunodeficiency disorders

86
Q

Most are detected in infancy between 6 months and 2 years of life

A

Primary immunodeficiency disorders

87
Q

May arise as complications of cancers, infections, malnutrition, or side-effects of immunosuppression, irradiation, or chemotherapy for cancer and other diseases

A

Secondary immunodeficiency states

88
Q

AIDS

A

Secondary immunodeficiency states

89
Q

caused by Human immunodeficiency virus (HIV)

A

AIDS

90
Q

non transforming human retro virus, lenti virus family

A

HIV

91
Q

types of HIV

A

HIV-1 and HIV-2

92
Q

most common type of HIV associated with AIDS in US, EUROPE, CENTRAL AFRICA

A

HIV 1

93
Q

causes AIDS in WEST AFRICA and INDIA

A

HIV 2

94
Q

two major targets of AIDS

A

Immune system and the CNS

95
Q

hallmark of AIDS

A

Profound immune deficiency, primarily affecting cell- mediated immunity

96
Q

structures of HIV

A

virus core
p17
virion envelope
viral glycoproteins gp120 and gp141

97
Q

the most readily detected viral antigen and is the target for the antibodies that are used for the diagnosis of HIV infection

A

major capsid protein p24 ( virus core)

98
Q

3 viral enzymes

A

protease, reverse transcriptase, and integrase

99
Q

what are found in the virus core

A

major capsid protein p24
2 copies of genomic RNA
nucleocapsid protein p7/p9
3 viral enzymes

100
Q

matrix protein that surrounds viral core

A

p17

101
Q

critical for HIV infection of cells.

A

Viral glycoproteins gp120 and gp41

102
Q

epidemiology of AIDS

A
  • Homosexual or bisexual men
  • Intravenous drug abusers
  • Hemophiliacs
  • Recipients of blood and blood components
  • Heterosexual contacts of members of other high-risk groups
  • HIV infection of the newborn
103
Q

constitute the largest group of people affected with aids

A

Homosexual or bisexual men

104
Q

routes of transmission of aids

A

Sexual transmission
Parenteral transmission
Mother-to-infant transmission

105
Q

Enhanced by coexisting sexually transmitted diseases

A

Sexual transmission

106
Q

2 ways,of sexual transmission

A
  1. Direct inoculation into the blood vessels breached by
    trauma
  2. Infection of dendritic cells or CD4+ cells within the mucosa
107
Q

intravenous drug abusers, hemophiliacs, recipients of blood transfusion

A

Parenteral transmission

108
Q

most common cause of pediatric aids

A

Mother-to-infant transmission

109
Q

in utero ( transplacental spread), during delivery ( infected birth canal), after birth ( ingestion of breast milk)

A

Mother-to-infant transmission

110
Q

most common mode in US

A

transmission during birth ( intrapartum), immediate period thereafter ( peripartum)

111
Q

co receptors of hiv

A

CCR5 and CXCR4

112
Q

CD4 binding

A

gp120

113
Q

penetration

A

gp41

114
Q

Defective macrophage and dendritic cell

functions

A

Loss of CD4+ T cells

115
Q

Destruction of architecture of lymphoid tissues

A

Loss of CD4+ T cells

116
Q

self-limited acute illness with nonspecific symptoms, including sore throat, myalgias, fever, weight loss, and fatigue, resembling a flulike syndrome

A

Acute retroviral syndrome

117
Q

few or no clinical manifestations of the HIV infection are present.

A

Chronic infection: Phase of clinical latency

118
Q

Patients are either asymptomatic or develop minor opportunistic infections, such as oral candidiasis (thrush), vaginal candidiasis, and perhaps mycobacterial tuberculosis

A

Chronic infection: Phase of clinical latency

119
Q

characterized by a breakdown of host defense, and severe, life-threatening clinical disease

A

AIDS

120
Q

serious opportunistic infections, secondary neoplasms, or clinical neurologic disease emerge

A

AIDS

121
Q

clinical features or common manifestations of AIDS

A 
Fever
Weight loss
Diarrhea
Generalized lymphadenopathy
Multiple opportunistic infections 
Neurologic disease
Secondary neoplasms
122
Q

account for the majority of deaths for untreated patients with AIDS

A

Multiple opportunistic infections

123
Q

treatment for aids

A

HAART Highly Active Antiretoviral therapy

124
Q

lack of responsiveness to an individual’s own antigens

A

Self-tolerance

125
Q

Unresponsiveness to an antigen induced by exposure of lymphocytes to that antigen

A

Immunologic Tolerance

126
Q

Immature self-reactive T and B lymphocyte clones that recognize self antigens during their maturation in the central lymphoid organs are killed or rendered harmless

A

Central Tolerance

127
Q

Negative selection or deletion

A

T cells

128
Q

Receptor editing

A

B cells

129
Q

Anergy
Suppression by regulatory T cells
Deletion by apoptosis

A

Peripheral Tolerance

130
Q

when lymphocytes that recognizes self antigens may be rendered functionally unresponsive

A

anergy

131
Q

prevent immune reaction against self antigens

A

Suppression by regulatory T cells

132
Q

t cells that recognizes self antigens may receive signals that promote their death by apoptosis

A

Deletion by apoptosis

133
Q

general principles

A

Defective tolerance or regulation
Abnormal display of self antigens
Inflammation or an initial innate immune response

134
Q

General Features of Autoimmune Diseases

A

Chronic, with relapses and remissions, and the damage is often progressive

Clinical and pathologic manifestations are determined by the nature of the underlying immune response

135
Q

an immune response against one self antigen causes tissue damage releasing other antigens resulting in the activation of lymphocytes by newly encountered epitope

A

epitope spreading

136
Q

Injury is caused by deposition of immune complexes and binding of antibodies to various cells and tissues

A

Systemic Lupus Erythematosus (SLE)

137
Q

Systemic Lupus Erythematosus (SLE) hypersensitivity reaction

A

type 3

138
Q

characterized by vast array of autoantibodies ( ANAs Anti Nuclear Antibodies)

A

Systemic Lupus Erythematosus (SLE)

139
Q

Injury to the skin, joints, kidney, and serosal

membranes is prominent

A

Systemic Lupus Erythematosus (SLE)

140
Q

Predominantly affects women of childbearing age

A

Systemic Lupus Erythematosus (SLE)

141
Q

may be acute or insidious in its onset typically chronic remitting and relapsing and often febrile illness

A

Systemic Lupus Erythematosus (SLE)

142
Q

SLE manifestations

A

Discoid rash
Oral Ulcers
Photosensitivity
Arthritis
Malar rash
Iimmunologic disorders
Neurologic disorder (seizure or psychosis)
Renal Disorder (Nephritic manefestations)
ANA
Serocitis (Pleuritis, pericarditis)
Hematologic disorders ( anemia, leukopenia, thrombocytopenia)

143
Q

Hallmark of SLE

A

production of ANA

144
Q

positive in 95-100% of cases but are also positive for a lot of autoimmune diseases

A

generic ANA

145
Q

more specific antibodies for SLE

A

DS DNA

SMITH antibodies

146
Q

factors that contribute in the development of SLE

A

Genetic Factors
Immunologic Factors
Environmental Factors- ultraviolet (UV) light, gender bias, drugs

147
Q

fundamental defect of SLE

A

failure of the mechanisms that maintain self-tolerance

148
Q

SLE is not only a hypersensitivity disease, but also an autoimmune disease

A

true

149
Q

organ mainly affected by SLE

A

kidney

150
Q

least common lupus nephritis

A

class 1

151
Q

most common lupus nephritis

A

class 4

152
Q

classes of nephritis

A 
class 1 Minimal mesangial LN
class 2 Mesangial proliferative LN
class 3 Focal LN
class 4 Diffused LN
class 5 Membranous LN
class 6 Advance Sclerosing LN
153
Q

end stage renal disease

A

class 6

154
Q

most patients of SLE are diagnosed with

A

class 4

155
Q

other organ affected by SLE

A

skin

156
Q

SLE Clinical Features

A

Young woman with butterfly rash over the face
Fever, photosensitivity
Characterized by flare-ups and remissions for years or decades

157
Q

treatment for SLE

A

Steroids, immunosuppressive drugs

158
Q

cause of death in SLE

A

Renal failure and infections

159
Q

Chronic disease characterized by dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) resulting from immunologically mediated destruction of the lacrimal and salivary glands

A

Sjögren Syndrome

160
Q

dry mouth

A

xerostomia

161
Q

dry eyes

A

keratoconjunctivitis sicca

162
Q

ANAs are detected in 50% to 80% of patients

A

Sjögren Syndrome

163
Q

more specific antibodies that can be detected in 90% of patients

A

SS-A (Ro) and SS-B (La)

164
Q

diagnosis of Sjögren Syndrome

A

Biopsy of the lip (to examine minor salivary glands)

165
Q

diagnosis of Sjögren Syndrome on microscopic examination

A

intense lymphocytic and plasma cell infiltration with ductal epithelial hyperplasia in the salivary gland

166
Q

Chronic inflammation thought to be the result of autoimmunity

A

Systemic Sclerosis (Scleroderma)

167
Q

Widespread damage to small blood vessels

A

Systemic Sclerosis (Scleroderma)

168
Q

Progressive interstitial and perivascular fibrosis

in the skin and multiple organs

A

Systemic Sclerosis (Scleroderma)

169
Q

Characterized by excessive fibrosis throughout the body

A

Systemic Sclerosis (Scleroderma)

170
Q

most commonly affected organ in Systemic Sclerosis (Scleroderma)

A

skin

171
Q

frequently involved organs in Systemic Sclerosis (Scleroderma)

A 
GIT
Kidney
Heart
Muscles
Lungs
172
Q

cause of death in Systemic Sclerosis (Scleroderma)

A

renal failure
cardiac failure
pulmonary insufficiency
intestinal malabsorption

173
Q

types of scleroderma

A

Diffuse scleroderma

Limited scleroderma

174
Q

widespread skin involvement at onset, with rapid progression and early visceral involvement

A

Diffuse scleroderma

175
Q

skin involvement is often confined to fingers, forearms, and face. limited in the skin

A

Limited scleroderma

176
Q

CREST syndrome

A

Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly, and Telangiectasia

177
Q

more common in female with 3:1 ratio. and on 50-60yo

A

scleroderma

178
Q

manifestations of scleroderma

A 
Raynaud phenomenon
Dysphagia
Respiratory difficulties
Malignant hypertension
Renal failure
179
Q

episodic vasoconstriction of the arteries and arterioles of the extermities

A

raynau phenomenon

180
Q

attributed to esophageal fibrosis and its resultant hypomotility abdominal pain, intestinal obstruction or malabsorption syndrome with weightloss and anemia reflect involvement of small intestine

A

dysphagia

181
Q

pulmonary fibrosis, and may result in right sided cardiac dysfunction
myocardial fibrosis may cause arrhythmias or cardiac failure

A

Respiratory difficulties

182
Q

majority of patients of scleroderma would have

A

diffused sclerotic atrophy of the skin which usually begins in the fingers and the distal regions of the upper extremities and extends proximally to involve the upper arms, shoulder, neck and face

183
Q

histologic manifestations of scleroderma

A

edema and peri vascular infiltrates together with swelling and degeneration of collagen fibers

184
Q

progressive atrophy and collagenous fibrous replacement of the muscularis

A

Alimentary tract

185
Q

affected in 90% of patients with scleroderma

A

Alimentary tract

186
Q

inflammation of the synovium, with hypertrophy and hyperplasia of the synovial soft tissues; fibrosis later ensues

A

Musculoskeletal system

187
Q

prominent vascular lesions

A

kidneys

188
Q

pulmonary hypertension and interstitial

fibrosis

A

lungs

189
Q

pericarditis with effusion, myocardial fibrosis, and thickening of intramyocardial arterioles

A

heart

190
Q

extracellular deposits of fibrillar proteins are responsible for tissue damage and functional compromise

A

Amyloidosis

191
Q

abnormal folding of proteins which becomes insoluble aggregates

A

Amyloidosis

192
Q

a pathologic proteinaceous substance, deposited in the extracellular space in various tissues and organs of the body

A

Amyloidosis

193
Q

appears as an amorphous, eosinophilic, hyaline, extracellular substance that, with progressive accumulation, encroaches on and produces pressure atrophy of adjacent cells

A

Amyloidosis

194
Q

made up largely of continuous, nonbranching fibrils

A

amyloid

195
Q

stain for amyloids which under ordinary light impart a pink or red color to the tissue deposits

A

congo red stain

196
Q

more striking and specific stain of amyloids when observed by polarizing microscopy

A

green bifringens

197
Q

most common forms of amyloid

A

AL (amyloid light chain)
AA (amyloid-associated)
β amyloid (Aβ)

198
Q

derived from Ig light chains produced in

plasma cells

A

AL (amyloid light chain)

199
Q

seen in multiple myeloma

A

AL (amyloid light chain)

200
Q

non-Ig protein synthesized by the liver

- associated with chronic inflammation, and is often called secondary amyloidosis

A

AA (amyloid-associated)

201
Q

core of cerebral plaques found in Alzheimer disease

A

β amyloid (Aβ)

202
Q

Other biochemical distinct proteins found in amyloid deposits:

A

Transthyretin/TTR)

 β2-microglobulin

203
Q

Senile systemic amyloidosis

A

Transthyretin/TTR

204
Q

Hemodialysis-Associated Amyloidosis

A

β2-microglobulin

GENERAL PATHOLOGY (5 decks)

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