Chapter 4 Flashcards

(99 cards)

1
Q

Hypersensitivity reactions

A

injurious immune reactions
inappropriate targeting or inadequate control
causes secondary tissue injury

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

Hypersensitivity reactions are caused by what 3 factors?

A

Autoimmunity, microbial reactions, environmental reactions

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

4 Types of Hypersensitivity reactions

A
ACID
Type I: Allergies
Type II: Cytotoxic
Type III: Immune complex
Type IV: Delayed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Reactions to Harmless environmental antigens

A

Type I Hypersensitivity

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

Reaction categorized by:

  1. activation of Helper T cells
  2. Increased IgE antibody productions
  3. Mast cell deregulation (histamine)
A

Type I hypersensitivity

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

Deregulation of mast cells releases what?

A

Histamine

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

Release of histamine causes

A

vasodilation (edema), increase in mucous secretion, brochoconstriction

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

True or False. Type I hypersensitivity produces a local reaction

A

False, it can produce both a local reaction or a severe anaphylaxis

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

Type I hypersensitivity reactions take how long to manifest?

A

Minutes

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

Examples of Type I Hypersensitivity

A

Hay fever, hives, eczema, asthma, anaphylaxis

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

Type II Hypersensitivities cause…

A

opsonization (phagocytosis), inflammation, various non-injurious forms of dysfunction

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

Examples of Type II Hypersensitivities

A

ABO incompatibility, Acute Rheumatic Fever, Goodpasture Syndrome, Grave’s Disease

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

How do you diagnose Type II hypersensitivities?

A

Coombs’ test

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

Hypersensitivity reaction characterized by immune complex formation

A

Type III Hypersensitivity

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

Characterized by:

  1. Antigen exposure (IgG production)
  2. Antigen-antibody complexes go into tissues
  3. Complement activation causes inflammation
A

Type III Hypersensitivity

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

Inflammation of vessel walls, kidneys, and joints

A

Local complement activation from Type III Hypersensitivity

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

Fever, Arthritis, Vasculitis, Proteinuria, Lymphadenopathy

A

Systemic complement activation from type III Hypersensitivity

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

Examples of Type III Hypersensitivities

A

Lupus (SLE), Polyarteritis Nodosa (PAN), Reactive Arthritis (Reiter Syndrome), Serum Sickness

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

Immune complexes

A

deposited into vessel walls

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

Immune complexes cause tissue damage including ___

A

Fibrinoid Necrosis

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

Amount of time after exposure that Antigen-antibody complexes deposit into tissues?

A

5-10 days

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

T-Cell mediated inflammation

AKA “delayed” antibody independent

A

Type IV Hypersensitivity

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

Two types of Type IV hypersensitivity

A

Cytokine-mediated

Direct Cytotoxicity

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

Cytokine mediated type IV hypersensitivity

A

Involves CD4+ T cells
activates neutrophils and macrophages
can commonly progress into chronicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Direct cytotoxicity type IV hypersensitivity
CD8+ T cells attack antigenic cells Protease --> damage or apoptosis delayed reaction, possible granuloma formation e.g. poison ivy, TB, MS, Type 1 diabetes
26
Failed self-tolerance = self-reactive T & B cells
Autoimmune disorder
27
Central tolerance
apoptosis in thymus or marrow
28
Peripheral tolerance
inactivation or apoptosis of T & B cells
29
Prime targets of autoimmune tissue damage
connective tissue & vessels
30
Genetic factor associated with autoimmune
HLA alleles
31
HLA alleles
locus on genes on chromosome 6 | regulate immune system by encoding for antigen-presenting proteins
32
these special T cells are able to present antigens to other cells to stimulate specific antibody production
T cells that have HLA genes
33
If someone comes back with a positive ANA test, they most likely have _____
Lupus
34
lupus is most common in what demographic?
African American women of childbearing age
35
Autoantibody-mediated tissue injury
autoantibodies against various cells (type II) | immune complex deposition (type III)
36
Lupus causes vessel injury by:
increasing risk of thrombosis with fibrinoid necrosis acute necrotizing vasculitis intimal thickening
37
Lupus causes renal failure by:
Glomerulonephritis characterized by proteinuria, hematouria, and urinary red blood cell casts which can pass through the glomerulus if it is damaged
38
Lupus can only be diagnosed if the patient presents with at least _ out of 11 of the criteria
4
39
photosensitivity caused by lupus can present as
``` Malar rash (butterfly) Discoid rash (erythema, raised, scaling) dermoepidermal degeneration caused by IgG deposits ```
40
serositis caused by lupus can present as:
pluritis or pericarditis | atypical chest pain
41
This causes verrucous (wart-like) vegetations on the mitral valve and is a symptom of lupus
Libman-Sacks Endocarditis
42
Pancytopenia
decrease in red blood cells, white blood cells, and platelets
43
Risks for developing Lupus
sex hormones (estrogen - hormone replacement therapy), UV light, smoking, infections
44
most common causes of death in lupus patients are:
renal failure, coronary artery disease, infection due to pancytopenia
45
Having lupus puts you at an increased risk for this type of cancer
B cell lymphoma
46
Sjogren Syndrome
CD4+ T cells (Type IV) unknown antigen | damage ductal epithelial cells
47
Sjogren syndrome can cause damage in these two glands most commonly
Lacrimal and salivary
48
Lacrimal gland destruction
called keratoconjunctivitis sicca | dry eyes --> inflammation, erosion, ulceration
49
Salivary gland destrution
called xerostomia | dry mouth --> fissuring, ulcerations
50
Sjogren syndrome can less commonly affect
vagina, nasopharynx (laryngitis), upper airways (bronchitis), kidneys, CNS, Muscles
51
Diagnosis for Sjogren syndrome
+ ANA
52
Isolated Sjogren syndrome
Sicca syndrome
53
Sjogren can be secondary to what autoimmune disorder most commonly
RA
54
Age range for women to develop Sjogren
35-45 years
55
Sjogren increases risk by 40x for this cancer
B cell lymphoma
56
Systemic Sclerosis (scleroderma)
extensive fibrosis in multiple tissues | vascular destruction of small arteries
57
Systemic sclerosis most commonly is found in what demographic?
Women age 40-60
58
Limited Systemic sclerosis
CREST Syndrome
59
CREST syndrome
Calcinoisis, Raynaud, esophageal dismotility (fibrosis of lower 2/3), sclerodactyly (hard, eroded skin), telangiectasia (spider veins)
60
diffuse systemic sclerosis
rapid/widespread skin involvement, early visceral involvement, aggressive
61
Congenital immune deficiency disorders
rare, early onset
62
X-linked agammaglobulinemia
``` Bruton disease 6 months male failed B cell maturation bacterial/viral infections: otitis media, pharygitis, sinusitis treatable with IgG infusions ```
63
Common variable immunodeficiency
decreased antibody response to infection normal B cells, no plasma cells increased GI infections increased risk for autoimmunity
64
Isolated IgA deficiency
decrease IgA production in mucous membranes can be asymptomatic recurrent URTIs or Diarrhea very common in caucasians
65
Hyper-IgM syndrome
High or nomral IgM Low IgG, IgA, IgE recurrent pyogenic bacterial infections 70% are x linked (male)
66
severe combined immunodeficiency
bubble boy lyphopenia (low T & B cells) & lymphoid atrophy highly vulnerable to all microbial infections most common among Native Americans
67
Examples of secondary immunodeficiency
infection, malnutrition, aging, cancer | Therapy-induced immunosuppression (MC)
68
Mechanisms of acquired immunodeficiency
suppression of marrow | lymphocyte dysfunction
69
AIDS
caused by HIV | destroys CD4+ T cells & macrophages via apoptosis or cytotoxicity
70
screening for HIV in blood transfusions
p24 antigen via ELISA or western blot
71
HIV resistance gene
CCR5
72
Stages of AIDS
Acute, Chronic, Crisis
73
Acute stage AIDS
pyrexia, pharygitis, myalgia, viremia ~3-6 weeks after infection decreased viremia after 12 weeks
74
Chronic stage AIDS
2-10 years after infection MC general lymphadenopathy steady decline of CD4+ T cells, steady incline of viral load infections: candidiasis, VZV
75
Crisis stage AIDS
1mo), diarrhea, weight loss, CNS defects | opportunistic infections & neoplasms
76
Cachexia
loss of lean muscle mass
77
common opportunistic neoplasms in crisis stage AIDS
Kaposi sarcoma, Burkitt Lymphoma, Primary CNS lymphoma, Cervical cancer
78
Ontogenic viruses
Kaposi sarcoma herpes virus, Epstein barr virus, HPV
79
Amyloidosis is caused by (2)
1. many inflammatory or inherited conditions | 2. failed phagocytosis
80
Amyloid
non-branching fibrillar proteins
81
Test for Amyloidosis
Congo Red Dye = apple-green birefringence | tissue biopsy, serum & urine
82
Three types of Amyloid protiens
1. Amyloid Light (AL) 2. Amyloid Associated (AA) 3. β-amyloid (Aβ)
83
Amyloid Light (AL)
B Cell proliferation: plasma cells (multiple myeloma) | immunoglobulin light chains, Bence-Jones protiens
84
Amyloid-Associated (AA)
Liver: Serum-Associated Amyloid (SAA) | Chronic inflammation: TB, RA, Ankylosing spondylitis, IBD, osteomyelitis
85
β-Amyloid (Aβ)
amyloid precursor protein: cerebral plaques | alzheimer disease
86
People with Down Syndrome have a 100% chance of developing ________ by age 40, why?
Alzheimer Disease due to the multiplication of the genes that are in charge of amyloid production
87
Primary Systemic Amyloidosis
``` (MC) malignant plasma cells AL proteins (multiple myeloma) ```
88
Secondary (reactive) Systemic Amyloidosis
Chronic inflammation | AA proteins
89
Aging Associated Systemic Amyloidosis
Elderly Patients, Senile Systemic Amyloidosis
90
Localized Amyloidosis
single organ/tissue | AL proteins
91
Localized Amyloidosis in tongue
macroglossia
92
Localized Amyloidosis in kidney
enlarged, pale, firm, decreased function | most common organ associated, very severe
93
Localized Amyloidosis in Brain
Aβ plaques, Alzheimer Disease
94
Localized Amyloidosis in Spleen
Splenomegaly, firm, decreased function
95
Localized Amyloidosis in Liver
massive hepatomegaly, pale, decreased function
96
Localized Amyloidosis in Heart
Cardiomegaly, decreased function | Restrictive Cardiomyopathy
97
Localized Amyloidosis in Wrist Ligaments
Carpal tunnel syndrome Seen in patients on long term dialysis since the Amyloid proteins are not completely filtered out and can accumulate in the body
98
Amyloidosis is most likely to be lethal if it involves
Kidney or heart
99
Prognosis of amyloidosis
1-3 years post diagnosis | worse if associated with multiple myeloma