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Mechanisms of Disease > Immune and Soft Tissue Diseases > Flashcards

Immune and Soft Tissue Diseases Flashcards

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
Q

How can Glomerular Lupus Nephritis be detected?

A

Detected as hematuria and proteinuria

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26
Q

Urticaria (aka Hives) is described as?

A

Acute inflammatory dermatosis

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27
Q

What are the consequences of chronic gout?

A

Joint damage and eventual joint deformity

Crystal deposition in subcutaneous areas (tophus)

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28
Q

What is the normal function of PDGF?

A

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

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29
Q

Autoimmune pathogenesis can be caused by?

A

Failure of self-tolerance

Defective regulation

Abnormal presentation of self-antigens

Inflammation

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30
Q

What is the mechanism by which IgE functions? In what cell type does this happen

A

Binds to dimer-receptor complex –> activates tyrosine kinase –> degranulation by the release of cytoplasmic vesicles (histamines)

Mast cells

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31
Q

What are the clinicopathologic manifestations of SLE?

A

Nephritis

Skin lesions

Arthritis

32
Q

What are some of the clinical presentations of an immediate hypersensitivity? (4)

A

Anaphylaxis

Bronchial asthma

Allergic rhinitis or sinusitis

Food allergies

33
Q

An immune response ends when?

A

Phagocytes clear all antigen

Lack of T-cell stimulation results in apoptosis

34
Q

Persistent hives may indicate?

A

Hodgkin lymphoma

35
Q

How can SLE be diagnosed?

A

Test for anti-nuclear antibodies to dsDNA

36
Q

In children with osteomyelitis, how do bacteria typically reach bone?

A

Bloodstream

37
Q

Pyogenic osteomyelitis is commonly caused by what bacteria?

A

S. Aureus

38
Q

Describe diffuse scleroderma. Is it more or less severe

A

Onset - widespread skin involvement

Rapid progression

Early visceral involvement

MORE SEVERE

39
Q

What is Gout? Is it autoimmune?

A

Inflammation of synovial joints induced by presence of uric acid crystals

40
Q

Compare and contrast acute vs. chronic rheumatic diseases

A

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
Q

What enzyme is responsible for the production of uric acid in purine catabolism? What drug can inhibit it?

A

Xanthine oxidase

Allopurinol

42
Q

Primary immunodeficiency syndromes are?

A

Genetic

43
Q

What is erythematosus?

A

Rash of the malar area (bridge of nose and cheeks)

44
Q

Ankylosis of joints refers to?

A

Abnormal stiffness and rigidity due to adhesion and fibrosis

45
Q

Antibody:Antigen complexes are normally cleared by macrophages, but become pathogenic when?

A

Deposited beneath the epithelium (oftentimes endothelium)

46
Q

What structures do anti-nuclear antibodies typically recognize?

A

DNA (native/dsDNA)

Histones

Non-histone RNA-bound proteins

Nucleolar antigens

47
Q

What occurs after the immediate hypersensitivity reaction (pathologically speaking)?

A

Infiltration of eosinophils, T-cells, and neutrophils

48
Q

Patients with BTK have ______ T-cell immunity

A

Normal

49
Q

What is the mechanism by which histamine functions?

A

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
Q

What gene is mutated in Bruton agammaglobulinemia? How is it inherited?

A

Mutation in Bruton Tyrosine Kinase (BTK)

X-linked

51
Q

What occurs during the early stage of an allergic response?

A

Release of histamine, leukotrienes, and prostaglandin D2 –> induces sneezing, nasal secretion, and mucosal swelling

(all in ~5 minutes)

52
Q

Describe a type III hypersensitivity

A

Immune complex-mediated

deposition of antigen-antibody complexes –> recruitment of leukocytes –> release enzymes and toxic molecules

53
Q

Describe the neutrophil, protein, and mucin counts in the synovial fluid of someone with Rheumatoid Arthritis

A

High neutrophil count

High protein count

Low mucin count

54
Q

What is the normal function of IL-13?

A

Activates TGF-β

55
Q

Why should patients with BTK never be given an immunization with a live virus?

A

Without any functional Ig, the virus can invade the bloodstream and cause the actual infection

56
Q

What is the primary cause of hives?

A

Localized mast cell degranulation

57
Q

Although it is not diagnostic, erythematosus could be an indicator of?

A

SLE

58
Q

What gene is typically associated with the etiology of SLE?

A

Major histocompatibility complex

59
Q

What is the normal function of BTK?

A

Part of the signaling pathway within maturing B-cells for quality control checkpoints

60
Q

What are some consequences of fibrosis in regard to skin?

A

Loss of elasticity/flexibility

Thinning of epidermis, loss of associated structures (hair and nails)

Development of calcifications and ulcerations

61
Q

In adults with osteomyelitis, how do bacteria typically reach bone?

A

Fractures

Surgery

Diabetic infections of the feet

62
Q

What is the normal function of TGF-β

A

Activates myofibroblasts to produce extracellular matrix leading to scar formation

63
Q

What is the most frequent site for systemic sclerosis?

A

Skin (Scleroderma)

64
Q

Describe mast cell-dependent/IgE-dependent Urticaria

A

Localized immediate hypersensitivity

Associated with exposure to pollen, food, drugs, insect venom

65
Q

What antigens are typically involved in SLE?

A

Nuclear antigens (circulating or “planted” in the kidney)

66
Q

Describe a type IV hypersensitivity

A

Cell-mediated

Activated T-lymphocytes release cytokines –> macrophage activation or T-cell mediated toxicity

67
Q

Describe limited scleroderma. Is it more or less severe?

A

Skin involvement is limited to fingers, forearms, and face

Visceral involvement is late (“benign”)

Slow progression

LESS SEVERE

68
Q

What occurs during the first hour of a hypersensitivity response (pathologically speaking)?

A

Vasodilation

Congestion

Edema

69
Q

A hypersensitivity is caused by?

A

An imbalance between effectors and limiters (failure of normal regulation)

70
Q

Describe a type II hypersensitivity

A

Antibody-mediated

Production of IgG and IgM –> opsonization –> phagocytosis or lysis

71
Q

Patients with BTK are at risk for? Specifically?

A

Recurrent respiratory tract infections

  • H. influenzae*
  • S. pneumoniae*
  • S. aureus*
72
Q

What occurs during the late stage of an allergic response? Chronic exposure?

A

Within 2-4 hours influx of eosinophils and monocytes

Chronic exposure changes tissue structure

73
Q

What are some consequences of fibrosis in regard to the lungs?

A

Interstitial fibrosis

Pulmonary hypertension

74
Q

Mast cell-independent/IgE-independent Urticaria is caused by

A

Chemicals or drugs that inhibit COX and arachidonic acid production

or

Hereditary disorder

75
Q

Describe the immunological etiology of SLE

A

Failure to eliminate self-reactive B-cells

Cytokines promoting unregulated B-cell activity

Mechanisms of Disease (13 decks)

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