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Mechanisms of Disease > Immune and Soft Tissue Diseases > Flashcards

Immune and Soft Tissue Diseases Flashcards

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1
Q

What are two potential therapies for osteoporosis?

A

Selective estrogen receptor modulators (SERMs)

Bisphosphonates (induce osteoclast apoptosis)

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2
Q

Where are Rheumatoid nodules typically found?

A

Regions subjected to pressure

Ex: elbows and lumbosacral region

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3
Q

What are Rheumatic diseases? Are they autoimmune?

A

Connective tissue disorders, mainly bone/cartilage

Not all are autoimmune

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4
Q

True or false. In chronic autoimmune diseases, relapses are typically milder.

A

False. Immune memory makes it so relapses have a more robust response

(In a normal immune system, amplification mechanisms are beneficial to eliminated pathogens)

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5
Q

Describe a type I hypersensitivity

A

Immediate hypersensitivity

Production of IgE and later recruitment of inflammatory cells

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6
Q

What are some profibrotic cytokines? (3)

A

Transforming Growth Factor (TGF-β)

IL-13

Platelet-derived growth factor (PDGF)

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7
Q

Excessive fibrosis throughout the body is known as?

A

Systemic sclerosis

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8
Q

Glomerular Lupus Nephritis results in?

A

Compromised kidney function

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9
Q

Describe mast cell-dependent/IgE-independent Urticaria.

A

Direct degranulation of mast cells

Induced by opioids, antibiotics, curare, contrast media

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10
Q

What is allergic rhinitis? Cause?

A

Immediate hypersensitivity to inhaled antigens

Sustained IgE release in response to antigen

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11
Q

Secondary immunodeficiency syndromes are?

A

An effect of another disease like cancer, infection, or malnutrition

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12
Q

What is osteomyelitis?

A

Inflammation of bone and/or marrow

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13
Q

Are autoimmune diseases typically monogenic or complex multigenic disorders?

A

Complex multigenic disorders

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14
Q

Increased production of IgE leads to?

A

Immediate release of vasoactive amines and other mediators from mast cells

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15
Q

What are the clinical characteristics of Bruton agammaglobulinemia?

A

Absent/decreased circulatory B-cells

Low Ig levels of all types

Germinal centers underdeveloped (lymph nodes, tonsils, etc.)

Plasma cells absent throughout

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16
Q

What type of autoimmune disease is Systemic lupus erythematosus (SLE)?

A

Type III hypersensitivity

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17
Q

Describe the etiology acute necrotizing vasculitis

A

Type III hypersensitivity

Inflammation induced at the site of immune complex deposition

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18
Q

What are some consequences of fibrosis in regard to the GI tract?

A

Progressive atrophy/fibrous replacement of muscularis (especially in esophagus)

Weakens esophageal sphincter (causes GERD)

Malabsorption due to loss of villi/microvilli in small intestine

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19
Q

Describe the progression of joint damage?

A
  1. Lymphatic infiltration of synovium
  2. Vasodilation and angiogenesis
  3. Fibrin aggregates overlying synovium and free floating in fluid
  4. Surface synovial neutrophil accumulation
  5. Pannus formation
  6. Osteoclastic destruction
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20
Q

Describe the pathology of erythematosus

A

Degeneration of stratum basale

Edema in epidermis and dermis

Vasculitis

Immune complex deposition at epi:dermis junction

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21
Q

Describe the environmental etiology of SLE

A

UV irradiation (altered DNA becomes immunogenic)

Hormones and drugs

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22
Q

Of the five patterns of Lupus Nephritis, how many involve deposition of immune complexes into the glomerulus and how many involve deposition into the mesanginum

A

2 in glomerulus

3 in mesanginum

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23
Q

Antibody:antigen complexes form in the presence of?

A

excess antigen after antibody production

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24
Q

Uric acid levels increase in the body due to? (4)

A

Excess purine catabolism

Defects in purine salvage

Diuretic administration

Reduced glomerular filtration in the kidneys

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25
How can Glomerular Lupus Nephritis be detected?
Detected as hematuria and proteinuria
26
Urticaria (aka Hives) is described as?
Acute inflammatory dermatosis
27
What are the consequences of chronic gout?
Joint damage and eventual joint deformity Crystal deposition in subcutaneous areas (tophus)
28
What is the normal function of PDGF?
Regulates proliferation and differentiation of stromal cells during embryogenesis May promote differentiation of adult stem cells or stimulate existing stromal cells Still not fully understood
29
Autoimmune pathogenesis can be caused by?
Failure of self-tolerance Defective regulation Abnormal presentation of self-antigens Inflammation
30
What is the mechanism by which IgE functions? In what cell type does this happen
Binds to dimer-receptor complex --\> activates tyrosine kinase --\> degranulation by the release of cytoplasmic vesicles (histamines) Mast cells
31
What are the clinicopathologic manifestations of SLE?
Nephritis Skin lesions Arthritis
32
What are some of the clinical presentations of an immediate hypersensitivity? (4)
Anaphylaxis Bronchial asthma Allergic rhinitis or sinusitis Food allergies
33
An immune response ends when?
Phagocytes clear all antigen Lack of T-cell stimulation results in apoptosis
34
Persistent hives may indicate?
Hodgkin lymphoma
35
How can SLE be diagnosed?
Test for anti-nuclear antibodies to dsDNA
36
In children with osteomyelitis, how do bacteria typically reach bone?
Bloodstream
37
Pyogenic osteomyelitis is commonly caused by what bacteria?
S. Aureus
38
Describe diffuse scleroderma. Is it more or less severe
Onset - widespread skin involvement Rapid progression Early visceral involvement MORE SEVERE
39
What is Gout? Is it autoimmune?
Inflammation of synovial joints induced by presence of uric acid crystals
40
Compare and contrast acute vs. chronic rheumatic diseases
**Acute:** External initiation, stops after exposure (self-limiting), flares on re-exposure **Chronic****:** Remote initiation, autoimmune (self-propagating), frequent flares due to immune memory
41
What enzyme is responsible for the production of uric acid in purine catabolism? What drug can inhibit it?
Xanthine oxidase Allopurinol
42
Primary immunodeficiency syndromes are?
Genetic
43
What is erythematosus?
Rash of the malar area (bridge of nose and cheeks)
44
Ankylosis of joints refers to?
Abnormal stiffness and rigidity due to adhesion and fibrosis
45
Antibody:Antigen complexes are normally cleared by macrophages, but become pathogenic when?
Deposited beneath the epithelium (oftentimes endothelium)
46
What structures do anti-nuclear antibodies typically recognize?
DNA (native/dsDNA) Histones Non-histone RNA-bound proteins Nucleolar antigens
47
What occurs after the immediate hypersensitivity reaction (pathologically speaking)?
Infiltration of eosinophils, T-cells, and neutrophils
48
Patients with BTK have ______ T-cell immunity
Normal
49
What is the mechanism by which histamine functions?
Diffuses through bloodstream --\> binds to G protein-coupled receptor H1-3 on endothelial, nerve, and smooth muscle cells --\> increases vascular permeability by dilation blood vessels
50
What gene is mutated in Bruton agammaglobulinemia? How is it inherited?
Mutation in Bruton Tyrosine Kinase (BTK) X-linked
51
What occurs during the early stage of an allergic response?
Release of histamine, leukotrienes, and prostaglandin D2 --\> induces sneezing, nasal secretion, and mucosal swelling (all in ~5 minutes)
52
Describe a type III hypersensitivity
Immune complex-mediated deposition of antigen-antibody complexes --\> recruitment of leukocytes --\> release enzymes and toxic molecules
53
Describe the neutrophil, protein, and mucin counts in the synovial fluid of someone with Rheumatoid Arthritis
High neutrophil count High protein count Low mucin count
54
What is the normal function of IL-13?
Activates TGF-β
55
Why should patients with BTK never be given an immunization with a live virus?
Without any functional Ig, the virus can invade the bloodstream and cause the actual infection
56
What is the primary cause of hives?
Localized mast cell degranulation
57
Although it is not diagnostic, erythematosus could be an indicator of?
SLE
58
What gene is typically associated with the etiology of SLE?
Major histocompatibility complex
59
What is the normal function of BTK?
Part of the signaling pathway within maturing B-cells for quality control checkpoints
60
What are some consequences of fibrosis in regard to skin?
Loss of elasticity/flexibility Thinning of epidermis, loss of associated structures (hair and nails) Development of calcifications and ulcerations
61
In adults with osteomyelitis, how do bacteria typically reach bone?
Fractures Surgery Diabetic infections of the feet
62
What is the normal function of TGF-β
Activates myofibroblasts to produce extracellular matrix leading to scar formation
63
What is the most frequent site for systemic sclerosis?
Skin (Scleroderma)
64
Describe mast cell-dependent/IgE-dependent Urticaria
Localized immediate hypersensitivity Associated with exposure to pollen, food, drugs, insect venom
65
What antigens are typically involved in SLE?
Nuclear antigens (circulating or "planted" in the kidney)
66
Describe a type IV hypersensitivity
Cell-mediated Activated T-lymphocytes release cytokines --\> macrophage activation or T-cell mediated toxicity
67
Describe limited scleroderma. Is it more or less severe?
Skin involvement is limited to fingers, forearms, and face Visceral involvement is late ("benign") Slow progression LESS SEVERE
68
What occurs during the first hour of a hypersensitivity response (pathologically speaking)?
Vasodilation Congestion Edema
69
A hypersensitivity is caused by?
An imbalance between effectors and limiters (failure of normal regulation)
70
Describe a type II hypersensitivity
Antibody-mediated Production of IgG and IgM --\> opsonization --\> phagocytosis or lysis
71
Patients with BTK are at risk for? Specifically?
Recurrent respiratory tract infections ## Footnote * H. influenzae* * S. pneumoniae* * S. aureus*
72
What occurs during the late stage of an allergic response? Chronic exposure?
Within 2-4 hours influx of eosinophils and monocytes Chronic exposure changes tissue structure
73
What are some consequences of fibrosis in regard to the lungs?
Interstitial fibrosis Pulmonary hypertension
74
Mast cell-independent/IgE-independent Urticaria is caused by
Chemicals or drugs that inhibit COX and arachidonic acid production or Hereditary disorder
75
Describe the immunological etiology of SLE
Failure to eliminate self-reactive B-cells Cytokines promoting unregulated B-cell activity

Mechanisms of Disease (13 decks)

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