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Pathology I Test II > Disorders of the immune system > Flashcards

Disorders of the immune system Flashcards

1
Q

Immunity is from a latin term that means what?

A

Exemption from duty.

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2
Q

What are the 2 types of immune responses?

A
  1. Natural immunity (non-specific). 2. Acquired immunity (Specific).
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3
Q

What are the 3 proteins that work under the natural immunity response?

A
  1. Complement. 2. Properdin. 3. Lysozyme.
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4
Q

What is the general concept of acquired immunity?

A

Self vs. non-self.

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5
Q

What is the 1st, 2nd, and 3rd lines of defense in natural protection?

A
  1. Mechanical/ chemical barrier. 2. inflammatory/ Phagocytosis. 3. Specific immune responses.
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6
Q

What are the different kinds of T-Lymphocytes?

A

T-helper cells (CD4+), T-suppressor or cytotoxic cells (CD8+), and Natural killer cells.

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7
Q

B-lymphocytes will become what in tissues?

A

Plasma cells.

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8
Q

Where will T and B lymphocytes and Natural killer cells come from?

A

Bone marrow.

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9
Q

Basophils become what in tissues?

A

Mast cells.

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10
Q

Monocytes become what in tissues?

A

Macrophages.

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11
Q

All antibodies are composed of what?

A

Light and heavy chains.

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12
Q

Which chains of antibodies are changeable and which chain is the same?

A

Light- same. Heavy are specific for each Ig.

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13
Q

What is another name for light and heavy chains?

A

Light-Fc. Heavy-Fab.

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14
Q

What is the largest Ig?

A

IgM.

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15
Q

What is the function of the IgM?

A

To neutralize microorganisms.

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16
Q

The IgM has how many complement binding sites?

A

five.

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17
Q

What is the first Ig to appear?

A

IgM.

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18
Q

IgM is the natural antibody against what?

A

ABO blood group ag.

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19
Q

Which Ig has the smallest molecular weight?

A

IgG.

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20
Q

When will IgG be produced?

A

Small amounts produced on initial immunization and boosted on re-exposure.

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21
Q

IgG’s act as an opsonin which is what?

A

bacteria coating and phagocytosis.

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22
Q

IgA will be mainly found where?

A

In mucosal secretions; milk, tears, respiratory, GI tract.

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23
Q

What is the function of IgA?

A

Protective.

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24
Q

What Ig is secreted by sensitized plasma cells in tissues?

A

IgE.

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25
Q

IgE are attached locally to what?

A

Mast cells.

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26
Q

What is the function of IgE’s?

A

mediates allergic reactions in tissues, and to protect against parasites.

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27
Q

Where are IgD’s found at?

A

Cell membrane-bound found exclusively on B cells.

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28
Q

What is the function of the IgD?

A

participates in antigenic activation of B cells

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29
Q

Which of the Ig’s will not be released in the serum?

A

IgD.

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30
Q

What is the Major Histocompatiblity complex essential for?

A

presentation of antigens to T cells.

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31
Q

The major histocompatibility complex is AKA?

A

human leukocyte antigen (HLA).

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32
Q

What is an immunologic finger print unique to me?

A

my major histocopmatibility complex.

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33
Q

What are the 2 groups of the major histocompatibilty complex?

A

Type I and Type II.

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34
Q

The type I major histocompatibility complex has receptors for what?

A

CD8+ or the T suppressor or cytotoxic cells.

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35
Q

The type II major histocompatibility complex reacts with what?

A

CD4+ or the T-helper cells.

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36
Q

What are the antigen-presenting cells of the major histocompatibility complex?

A

Macrophages, and B cells if antigen is internalized.

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37
Q

What is the function of the Major histocompatibility complex (MHC)?

A

To present antigens to T cells.

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38
Q

T cells can only react to membrane-bound antigens and this means what?

A

Without Antigen presenting cells T cell will have no reaction to antigens.

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39
Q

MHC type I is a receptor for the CD8+ cells and are found where?

A

On all nucleated cells of the body.

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40
Q

MCH type I links what to what?

A

CD8+ or the T suppressor or cytotoxic cells to antigen presenting cells (APC).

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41
Q

MCH type II react with the CD4+ or T helper cells and this will lead to what?

A

antigen presenting cells to Helper T lymphocytes. This serves as a presentation of exogenous antigens that are first internalized and processed.

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42
Q

MHC is AKA?

A

HLA or human leukocyte antigen.

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43
Q

What chromosome are the HLA subtypes found on?

A

6 regions A,B, and DR.

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44
Q

HLA A3 is assoicated with what?

A

Hemochoromatosis, myathenia gravis, Multiple sclerosis.

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45
Q

HLA B27 is associated with what?

A

Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reiter’s syndrome.

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46
Q

HLA B8 is associated with what?

A

Grave’s disease, celiac sprue.

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47
Q

HLA DR2 is associated with what?

A

Multiple sclerosis, hay fever, SLE, Goodpasture.

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48
Q

HLA DR3 is associated with what?

A

Diabetes Mellitus type I.

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49
Q

HLA DR4 is accoicated with what?

A

Rheumatoid arthritis, DM type I.

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50
Q

HLA DR5 is associated with what?

A

Pernicious anemia, hasimoto’s throiditis.

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51
Q

HLA DR7 is assoicated with what?

A

Steroid-responive nephrotic syndrome.

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52
Q

Pernicious anemia is caused by what?

A

A B12 deficinecy.

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53
Q

What is an epitope?

A

An antigenic site.

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54
Q

How many epitopes can be on an antigen?

A

Many.

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55
Q

Antibodies to soluable antigens form what?

A

Soluable complexes that may be found in circulation.

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56
Q

What do antibodies that are bound to fixed antigens on cells do?

A

Coat the cell surface.

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57
Q

What happens when antigen-antibody complexes bind?

A

This activates the complement system.

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58
Q

The complement system does what?

A

Lysis of cells, agglutination or recruitment of inflammatory cells.

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59
Q

What is immune hemolysis?

A

The immune system breaking down RBC.

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60
Q

Immune hemolysis is what type of reaction?

A

A hypersensitive one.

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61
Q

How many types of immune hemolysis are there?

A

types I-IV.

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62
Q

Which types of immune hemolysis are caused by antibodies?

A

I,II, III.

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63
Q

Type I hypersensitive reaction is due to what?

A

Anaphylactic.

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64
Q

Type II hypersensitive reaction is due to what?

A

Cytotoxic antibody mediated.

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65
Q

Type III hypersensitive reaction is due to what?

A

Immune complex mediated.

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66
Q

Type IV hypersensitive reaction is due to what?

A

Cell mediated, delayed type.

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67
Q

Type I hypersensitivity is mediated by what?

A

IgE, mast or basophils.

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68
Q

Type I hypersensitivity takes how long to respond?

A

4-6 hours.

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69
Q

Is hay fever always seasonal?

A

No.

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70
Q

What are the treatments for Type I hypersensitivity?

A

anti-histamines, Vitamin C, Desensitization.

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71
Q

Asthma is what type of hypersensitivity?

A

Type I.

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72
Q

Type I hypersensitivty associated with asthma affects what?

A

Bronchi.

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73
Q

Will asthma always be a hypersensitivty disease?

A

No there are many types.

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74
Q

Hypersensitive asthma is due to an inhaled antigen mediated by what?

A

SRS-As a slow release.

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75
Q

What supplement can relax the airways?

A

Magnesium.

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76
Q

What is a side effect of magnesium?

A

It relaxes the smooth muscle and can lead to a warm feeling.

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77
Q

Atopic dermatitis is a type I hypersensivity and it is typically a _____ disease.

A

Childhood.

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78
Q

Atopic dermatitis is aka?

A

Eczema.

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79
Q

what % of children get atopic dermatitis?

A

10%.

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80
Q

OF the 10% of children that get atopic dermatitis how many of them have family history of atopic dermatitis?

A

50%.

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81
Q

How will allergen that causes atopic dermatitis enter the body?

A

inhaled, ingested in food, or skin contact.

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82
Q

Atopic deramtitis is sometimes treated with corticosteroids and this can cause what?

A

Asthma/hay fever later in life.

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83
Q

What is a severe sytemic response to an allergen called?

A

Anaphylactic shock.

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84
Q

Anaphylactic shock is what type of hypersensitve reaction?

A

Type I.

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85
Q

What happens with anaphylactic shock?

A

A massive release of histamine/other vasoactive substances.

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86
Q

What are the signs of anaphylactic shock?

A

chocking, wheezing, shortness of breath.

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87
Q

What is the treatment of anaphylactic shock?

A

epinephrine STAT, high flow O2 non-rebreather.

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88
Q

What type of hypersensitivity is associated with autoimmune diseases?

A

Type II.

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89
Q

What causes Type II hypersensitivity?

A

Cytotoxic antibody that reacts to antigen in cells or tissue components.

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90
Q

With type II hypersensitivity the antigen can be where?

A

Extrinsic or intrinsic.

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91
Q

Type II hypersensitivity is mediated by what Ig’s?

A

IgG or IgM.

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92
Q

Type II hypersensitivity activates the complement system which will do what?

A

Lysis of cell.

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93
Q

Give an example of a type II hypersensitive reaction?

A

Blood transfusion mismatch.

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94
Q

What type of hypersensitive reaction is hemolytic anemia?

A

Type II.

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95
Q

What is hemolytic anemia?

A

A systemic autoimmune disorder can be caused by foreign chemicals.

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96
Q

Goodpasture’s syndrome involves what pathologies?

A

renal and pulmonary.

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97
Q

What causes goodpastures syndrome?

A

autoimmune to component of Type IV collagen.

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98
Q

What type of hypersensitivity is goodpasture’s syndrome?

A

Type II.

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99
Q

What are the signs and symptoms of goodpastures syndrome?

A

Hemoptysis (coughing of blood), and hematuria.

100
Q

What will cause Grave’s disease?

A

Autoantibody against the thyroid receptor for thyroid-stimulating hormone.

101
Q

How will the autoantibody for the thyroid receptor for thyroid-stimulating hormone be affected with Graves disease?

A

It will be stimulated to make more T3 and T4.

102
Q

Graves disease will cause exopthalmus which is what?

A

Protrusion of the eyeball.

103
Q

What is myasthenia gravis?

A

Episodic muscle weakness and easy fatigability.

104
Q

What causes myasthenia gravis?

A

Autoantibody and cell-mediated destruction of acetylcholine receptors.

105
Q

What type of hypersensitivity is myasthenia gravis?

A

Type II.

106
Q

What will worsen and lessen symptoms of myasthenia gravis?

A

Worsen-muscle activity. Lessen-rest.

107
Q

How is myasthenia gravis tested?

A

By antibody testing to aceylcholine receptors.

108
Q

Initially and eventually what % of ocular muscles are affectd by myasthenia gravis?

A

initially-40%. Eventually-85%.

109
Q

Type III hypersensitive reactions cause what?

A

Acute inflammation in response to circulating antigen-antibody immune complexes deposited in vessels or tissues.

110
Q

The antigen-antibody complex that are circulating around that casue Type III hypersensitive reactions activate what?

A

complement system, or they bind to and activate certain immune cells. This results in release of inflammatory mediators.

111
Q

When will type III hypersensitive reactions become systemic?

A

When antigen and antibody are more balanced instead of when there is much more antigen than antibody. When we get a balanced amount of antigen and antibodies there will be lots of complexes formed which tend to be deposited in various tissues and this leads to a systemic reaction.

112
Q

Poststerptococcal glomerulonephritis typically follows what?

A

Upper respiratory tract infection by a nephritogenic streptococcal strain.

113
Q

Poststerptococcal glomerulonephritis is when the antigen from the upper respiratory tract infection gets onto the glomerulonephritis during filtration of plasma and what happens?

A

The Complement system is evoked, and this leads to a type III hypersensitive reaction.

114
Q

What Type III hypersensitive reaction was discovered by injecting horse serum into rabbits repeatedly?

A

Arthus reaction.

115
Q

What happens with arthus reaction?

A

The antigen/antibody complexes collect in the vascular walls, serosa, and glomeruli.

116
Q

What did the CDC have to say about arthus reaction?

A

Rarely reported after vaccination, but can happen after tetanus or diphtheria vaccinations.

117
Q

What is the arthus phenomenon?

A

Polyarteritis Nodosa (Many arteries Knotty).

118
Q

What disease can cause arthus phenomenon?

A

Unknown antigen, but seen with chronic hepatitis B virus.

119
Q

What is SLE?

A

Systemic Lupus erythematosus.

120
Q

What is SLE glomberulonephritis?

A

A deposition of complement-activating immune complexes.

121
Q

Type IV hypersensitive reactions are reactions of what?

A

T cell mediated. Not antibodies

122
Q

How will Type IV hypersensitive reactions in general happen?

A

T cells get sensitized and after second contact they are activated and damage tissue by direct toxic effects or through release of cytokines.

123
Q

What will T cell cytokines do?

A

activate eosinphils, monocytes, macrophages, neutrophils, or Killer cells.

124
Q

Caseating granuloma is seen in what?

A

TB.

125
Q

How will Type I DM be triggered?

A

Autoimmune response.

126
Q

What type of reaction is Type I DM?

A

Type IV hypersensitive.

127
Q

What is an autograph, isograft, homograft, and xenograft?

A

auto-self to self. Iso-identical twin or clone. Homo-within species. Xeno-outside of species.

128
Q

What is a hyperacute reaction to a transplant?

A

reaction during operation; have antibodies to donors antigen, like a reaction to wrong blood type.

129
Q

What is the time frame for an acute reaction to a transplant?

A

first few weeks.

130
Q

How long will chronic transplant rejections last and they can casue what?

A

months to years, obliteration of arterial lumen.

131
Q

What types of transplants are used clinically?

A

kindey, skin, liver, heart, lung, pancreas, bone marrow.

132
Q

Graft-versus-host reaction is mediated by what?

A

Transplanted T lymphocytes.

133
Q

Graft-versus-host reaction is most often a complication of what?

A

Bone marrow transplantation.

134
Q

What are the organs most commonly effected by graft-versus-host reactions?

A

skin, intestines, liver.

135
Q

What is the most common minor blood group antigen?

A

Rh.

136
Q

What is the major blood group antigens?

A

A and B.

137
Q

Blood type A can give blood to who?

A

A and AB.

138
Q

Blood type A can get blood from who?

A

A,O.

139
Q

Blood type B can give blood to who?

A

B, AB.

140
Q

Blood type B can get blood from who?

A

B, O.

141
Q

Blood type AB can give blood to who?

A

Type AB.

142
Q

Blood type AB can get blood from who?

A

Universal (so A,B,AB, O).

143
Q

Bood type O can give blood to who?

A

Universal (so A,B,AB, O).

144
Q

Bood type O can get blood from who?

A

O.

145
Q

Rh factor is important in what?

A

Mother being - and baby being +, but only after mother is sensitized so can affect second birth.

146
Q

The Rh factor causing problems with pregnancy is prevented by what?

A

Rhogam.

147
Q

Fetal hydrops is caused by Rh factor incompatibility and leads to what?

A

Pleural effusion, ascites, scalp edema.

148
Q

In general what is an autoimmune disease?

A

Abnormal response to self-antigen.

149
Q

What are 3 things that make autoimmune diseases more common?

A
  1. Familial predisposition. 2. Certain HLA-haplotypes. 3. Sex differences more common in females than males.
150
Q

Name 5 systemic autoimmune diseases?

A

sle, rheumatic fever, rheumatoid arthritis, systemic sclerosis, polyarteritis nodosa.

151
Q

Name 5 autoimmune diseases that are limited to a single organ?

A

multiple sclerosis, Hashimotos thyroiditis, autoimmune hemolytic anemia, pemphigus vulgaris, myasthenia gravis.

152
Q

Then next many question will give the autoantibody and you must give the associated disorder.

A

ok

153
Q

antinuclear antibodies (ANA)?

A

SLE.

154
Q

Anti-dsDNA, Antio-smith?

A

Specific for SLE.

155
Q

Antihistone?

A

Drg-induced lupus.

156
Q

Anti-IgG?

A

Rhematoid arthritis.

157
Q

anticentromere?

A

scleroderma.

158
Q

Anti-Scl-70?

A

scleroderma (diffuse).

159
Q

Antimitochondrial?

A

primary biliary cirrhosi.

160
Q

antigliadin?

A

Ciliac disease.

161
Q

anti-basement membrane?

A

goodpasture.

162
Q

anti-epithelial cell?

A

pemphigus vulgaris.

163
Q

antimicrosomal, antithyroglobulin?

A

hashimotos.

164
Q

anti-jo-1?

A

polymyositis dermatomyositis.

165
Q

anti-ss-A?

A

Sjogren syndrome.

166
Q

Anti-ss-B?

A

Sjogren syndrome.

167
Q

Anti-U1 RNP?

A

Mixed Connnective tissue.

168
Q

Anti-smooth muscle?

A

Autoimmune hepatitis.

169
Q

Anti-glutamate decarboxylase?

A

Type I DM.

170
Q

C-ANAC?

A

Wegner’s granulomatosis.

171
Q

P-anca?

A

Other vasculitides.

172
Q

Virtually all Systemic Lupus Erythematosus (SLE) will have what?

A

ANA or the antinuclear anitbodies.

173
Q

75% of SLE patients will have what involvment?

A

KD.

174
Q

What is the major sign of SLE?

A

Butterly rash.

175
Q

What type of people most often get SLE?

A

Females in late 30-40s

176
Q

What are the treatments of SLE?

A

Vacation, Yoga (breathing helps shift from acid to alkalosis), drinking backing soda, more vegatables, reduce stress.

177
Q

The first episode of acute rhematic fever occurs most often?

A

between 5 and 15 years old.

178
Q

Acute rhematic fever is uncommon when?

A

Before 3 and after 21.

179
Q

What is the precursor of acute rhematic fever?

A

GAS (group A strptococcal). An infection.

180
Q

What infection will share an epitope with GAS?

A

GAS M.

181
Q

What is most often affected by rhematic fever?

A

Joints, heart, skin, CNS.

182
Q

joints are ______ ________ with rheumatoid arthritis.

A

symmetrically inflamed.

183
Q

Symmetrically inflamed joints with rheumatoid arthritis leads to what?

A

progressive destruction of aticular structures.

184
Q

What are 3 ways to treat rheumatoid arthritis?

A

drugs, physical measures, and surgery.

185
Q

What type of drug is used for rheumatoid arthritis?

A

DMAR disase-modifying antirheumatic drugs.

186
Q

What part of the population is affected with rheumatoid arthritis?

A

1% of population with 2-3 times more women than men. Can happen at any age, but most often between 35-50.

187
Q

Antibody known as anti-IgG is aka?

A

Rheumatoid factor.

188
Q

What type of cells make rheumatoid factor?

A

plasma cells.

189
Q

Can rheumatoid arthritis occur without anti-IgG aka rheumatoid factor?

A

Yes.

190
Q

What are the symptoms of Rheumatoid arthritis?

A

Early morning stiffness, joint pain swelling and stiffness.

191
Q

Rheumatoid artritis will have symetric pain and the stiffness lasts how long in the mornings?

A

more than 60 min.

192
Q

How can we treat rheumatid arthritis?

A

No red meat in diet, Rust Ox/poison ivy.

193
Q

How will fingers drift with rheumatoid arthritis?

A

Ulnar drift.

194
Q

What are the 2 types of immuneodeficiency diseases?

A
  1. Primary (congenital=present at birth). 2. Secondary (aquired).
195
Q

What is the secondary or aquired immunodeficiency?

A

AIDS aquired immunodeficiency syndrome.

196
Q

What will cause severe combined immunodeficiency, and what type of immunodeficiency is it?

A

It is primary and caused by a defect of lymphoid stem cells pre-B, Pre-T cells.

197
Q

What is the most common type of primary immunodeficiency diseases?

A

Isolated deficiency of IgA.

198
Q

What % of people have Isolated deficiency of IgA?

A

1 out of every 700 people

199
Q

What is isolated deficiency of IgA like in the population?

A

Often asymptomatic.

200
Q

What type of immunodeficiency disease is DiGeorge’s syndrome and what causes it?

A

It is a primary one caused by T-cell deficiency related to aplasia of thymus associated with aplasia of parathyroid glands.

201
Q

What type of virus is HIV aka Human immunodeficiency virus?

A

RNA retrovirus.

202
Q

AIDS infects what?

A

T helper Cells (CD4+).

203
Q

Where is AIDS stored at?

A

Macrophages and related phagocytic cells.

204
Q

What are the clinical presentations of HIV/AIDS?

A

acute illness, asymptomatic infection, persistent generalized lymphadenopathy.

205
Q

What are 5 pahtologic findings in AIDS?

A
  1. Lymphadenopathy. 2. Kaposis sarcoma. 3. Nephrophaty. 4. Weakness. 5. oral thresh.
206
Q

What type of infections happen with AIDS?

A

Opportunistic.

207
Q

What 3 places are prone to opportunisitic infections?

A
  1. Lungs. 2. GI tract. 3. CNS.
208
Q

What are the 3 tumors that develop with AIDS?

A
  1. Lymphoma of lymph nodes or GI tract. 2. Lymphoma of the CNS. 3. Kaposis sarcoma.
209
Q

What type of cell is deficient with immune deficiencies?

A

Phagocytic.

210
Q

What immune deficiency will cause a decreased production of B cells?

A

Bruton’s agammaglobulinemia.

211
Q

How is Bruton’s agammaglobulinemia caused and who can get it?

A

Associated with recurrent Bacterial infections after 6 months of age when maternal IgG levels drop off. It is a X-linked recessive gene that occurs in boys.

212
Q

What immune deficiency will cause a decreased production of T cells?

A

Thymic aplasia (DiGeorge syndrome).

213
Q

T cell deficiency will present as what?

A

Tetany

214
Q

What is tetany?

A

a state marked by severe, intermittent tonic contractions and muscular pain, due to hypocalcemia.

215
Q

What immune deficency will cause a decreased production of both T and B cells?

A

SCID (severe combined immunodeficiency).

216
Q

What immune deficency will cause a decreased T cell activation?

A

IL2 receptor deficency.

217
Q

What will cause a IL2 receptor deficency?

A

Infections due to decreased Th1 response.

218
Q

What immune deficiency will cause a decreased activation of B cells?

A

Hyper IgM syndrome, and Wiskott-aldrich syndrome.

219
Q

What causes Hyper IgM syndrome?

A

Defect in CD40 ligand on CD4 + T helper cell.

220
Q

What causes Wiskott-aldrich syndrome?

A

X-linked defect in the ability to mount an IgM response.

221
Q

What is the triad of symptoms for Wiskott-aldrich syndrome?

A

WIPE. Wiskott. Infections. Purpura. Eczema.

222
Q

What immune deficiency will cause a decreased activation of Macrophages?

A

Job’s syndrome.

223
Q

Job’s syndrome presents with what?

A

FATED. Facies, Abscesses, Teeth, increased IgE, Dermatologic problems.

224
Q

What is the leukocyte adhesion deficiency syndrome?

A

An immune deficiency leading to phagocytic cell deficiency because of a LFA-1 defect.

225
Q

How will leukocyte adhesion deficiency syndrome present?

A

With recurrent bacterial infections, absent pus formation, and delayed separation of umbilicus.

226
Q

What is Chediak-higashi disease?

A

An immune deficiency leading to phagocytic cell deficiency because of autosomal recessive defect in microtubular function and lysosomal emptying of phagocytic cells.

227
Q

How will Chediak-Higashi’s disease present?

A

with recurrent pyogenic infections by staphylococci and strptococci, partial albinism, and peripheral neuropathy.

228
Q

What is Chronic granulomatous disease?

A

An immune deficiency leading to phagocytic cell deficiency because of lack of NADPH oxidase activity or similar enzymes.

229
Q

How will chronic granulomatous disease present?

A

Marked opportunisitic infections with bacteria, especially S. aureus, E. coli, and Aspergillus.

230
Q

What does idiopathic mean?

A

Of unknown cause.

231
Q

What is an idiopathic dysfunction of T cells?

A

Chronic mucocutaneous candidiasis.

232
Q

Chronic mucocutaneous candidiasis is a T cell dysfunction against what?

A

Candida albicans.

233
Q

How will Chronic mucocutaneous candidiasis present?

A

With skin and mucous membrane candida infections.

234
Q

There are 3 B cell idiopathic dysfunctions is due to a deficiency in a specific class of immunoglobins?

A

Selective immunoglobulin deficiency.

235
Q

How will selective immunoglobulin deficiency present?

A

Siuns and lung infections, Milk allergies and diarrhea are common.

236
Q

What B cell idiopathic dysfunction is due to a defect in DNA repair enzymes?

A

Ataxia-Telangiectasia.

237
Q

Ataxia-Telangiectasia is associated with what deficiency?

A

IgA.

238
Q

How will ataxia-Telengiectasia present?

A

with cerebellar problems and spider angiomas.

239
Q

What B cell idiopathic dysfunction has normal numbers of circulating B cells?

A

Common variable immunodeficiency.

240
Q

When can common variable immunodeficiency be acquired?

A

20s-30s.

241
Q

What is an Amyloid?

A

A space occupying lesion that is an inert protein.

242
Q

What are amyloid fibers like?

A

7.5 nm thick when seen by elctron microscopy.

243
Q

How will amyloids stain and be seen?

A

Stain congo red and appears apple green under polarized light.

244
Q

What type of sheets will Amyloids have by radiographic cyrstallography?

A

Beta-pleated.

245
Q

What is the usual cause of systemic amyloidosis?

A

Deposition of AA or AL amyloid in various organs, like; liver, kidney, adrenals, spleen, or heart.

246
Q

Give an example of localized organ-specific amyloid deposits?

A

Brain-alzheimers.

Pathology I Test II (4 decks)

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