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From Flashcardlet > Patho 2 > Flashcards

Patho 2 Flashcards

1
Q

What is immunity?

A

Special function of lymphocytes and macrophages that defends the body against foreign threats, mainly microbes by attacking and destroying the foreign substance - prevents or limits infections

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2
Q

What is autoimmunity?

A

The body will attack its own tissues in addition to foreign threats

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3
Q

What is self?

A

Each person’s normal DNA and the proteins made in accordance

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4
Q

What is non self?

A

Proteins of other living things

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5
Q

What are three body systems that work in defense against non self threats?

A
  • Physical and chemical barriers
  • Lymphatic system
  • Immune system
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6
Q

What are some examples of physical and chemical barriers?

A
  • Skin and sclerae
  • Respiratory, GI, and GU mucosae
  • Gastric acid
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7
Q

Why do smokers have weakened immune mechanisms in their respiratory mucosae?

A

Smoke damages cilia, making them prone to infection

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8
Q

What mechanism is lacking in a UTI?

A

Flushing mechanism of urinating, if someone is not drinking enough

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9
Q

What is a non immune defense mechanism?

A

Physical and chemical barriers

They do not improve after exposure to an antigen and create no memory

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10
Q

What are three functions of the lymphatic system?

A
  • House and support immune cells
  • Filter tissue fluid for non self content
  • Absorb dietary fat and deliver it into the blood
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11
Q

What is MALT?

A

Mucosal associated lymphoid tissue - consists of nodules of immune system cell s situated at sites where pathogens frequently enter the body

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12
Q

What is red pulp?

A

Composed of broad venous spaces filled with slowing moving blood, lymphocytes, and macrophages, through which blood filters as old red blood cells are removed and non self content is detected

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13
Q

What is white pulp?

A

Consists of nodules of lymphocytes and macrophages that function much like lymph nodes to filter blood for non self content

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14
Q

Where are the main lymph nodes located?

A
  • Cervical
  • Submandibular
  • Axillary
  • Inguinal
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15
Q

What is innate immunity?

A

Present from birth and consists of cellular and molecular defense capabilities that have an evolved ability to attack any non self substance

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16
Q

What are the characteristics of innate immunity?

A

Rapid and broad

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17
Q

What is adaptive immunity?

A

Programmable system that interacts with invading non self material, learns its characteristics, and manufactures a targeted, highly specific response designed to fight that specific invader

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18
Q

What are the characteristics of adaptive immunity?

A

Slower, programmable, specific

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19
Q

Which type of immunity refers to the immune response?

A

Adaptive immunity

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20
Q

What is the difference between innate and adaptive immunity?

A

Innate attacks any non self substance, while adaptive attacks a specific invader

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21
Q

Which immunity has memory?

A

Adaptive

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22
Q

What is an antigen?

A

Any substance capable of inciting an adaptive immune response

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23
Q

What is a happen?

A

Small nonprotein molecule that can stimulate an immune reaction by combining with a normal self protein in such a way that the combination becomes non self

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24
Q

What is the primary immune response?

A

Initial reaction to an antigen exposure

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25
Q

How long does a primary immune response take?

A

About a week because the immune system has not previously encountered the antigen

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26
Q

What is the secondary immune response?

A

All subsequent exposures

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27
Q

How long does a secondary immune response take?

A

Much quicker because the immune system has memorized the first encounter and is able to spring into action instantly

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28
Q

What are the immune cells?

A

White blood cells

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29
Q

What are the specialized cells of the immune system?

A
  • Macrophage
  • Dendritic cells
  • Lymphocytes
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30
Q

What are macrophages?

A

Large tissues phagocytic cells derived from blood monocytes that ingest and destroy microbes and other non self antigens

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31
Q

What are the macrophages of the brain?

A

Microglia

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32
Q

What are the macrophages of the liver?

A

Kupffer cells

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33
Q

What are dendritic cells?

A

Type of macrophage that can evolve from monocytes or lymphocytes, but remain fixed in place

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34
Q

Where are dendritic cells found?

A

Fixed in place, concentrated in lymphoid organs and in tissues exposed to the environment

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35
Q

What is a general term to describe macrophages and dendritic cells?

A

Antigen presenting cells

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36
Q

What are antigen presenting cells?

A

Capture antigens and prepare them for presentation to T lymphocytes

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37
Q

Where are T lymphocytes matured?

A

Thymus

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38
Q

Where are B lymphocytes matured?

A

Bone marrow

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39
Q

Which adaptive immune response do T lymphocytes belong to?

A

Cellular/delayed

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40
Q

Which adaptive immune response do B lymphocytes belong to?

A

Humoral/antibody

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41
Q

What are NK cells?

A

Natural killer lymphocytes that do not require education and have an innate capacity to instantly recognize, attack, and kill cells

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42
Q

What kind of cells do NK cells target?

A

Virus infected cells and tumor cells

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43
Q

Which immune response do NK cells belong to?

A

Adaptive immune response

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44
Q

What are CD proteins?

A

Cluster differentiation proteins - clusters of proteins on cell membranes used for identification, capable of inciting an immune reaction in another person

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45
Q

How do B cells have their effect on non self antigens?

A

Secretion of antibodies

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46
Q

What is another term for the B cell system?

A

Humoral immunity

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47
Q

When do B cells turn into plasma cells?

A

Upton antigen contact

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48
Q

What are plasma cells

A

Antibody secreting B cells that reproduce a clone of identical cells to amplify their antibody producing power

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49
Q

What is clonal expansion?

A

When plasma cells reproduce a clone of identical cells to amplify their antibody producing power

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50
Q

What kind of B cells do not secrete antibodies?

A

Memory cells

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51
Q

What is a memory B cell?

A

B cell which lingers in the body, preprogrammed and ready to quickly multiply and release a flood of antibodies the next time the antigen appears

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52
Q

What is antibody production critically dependent on?

A

Helper T cells

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53
Q

What is another name for antibody?

A

Immunoglobulin

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54
Q

What are the immunoglobulins?

A

G, A, M, D, E

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55
Q

Which Ig is the first one to respond?

A

M

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56
Q

Which is the smallest and most abundant Ig?

A

G

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57
Q

What is IgG?

A

Neutralizes microorganisms

  • Produced slowly
  • Lasts long time
  • Confers permanent immunity against reinfection
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58
Q

Where is IgA most abundant?

A

Mucosal secretions where MALT tissue is abundant

GI tract, respiratory tract, tears, mother’s milk

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59
Q

What is an example of a disorder where there would be high levels of IgA?

A

Celiac’s disease and gluten sensitivity, because the cilia in the GI tract are blunted

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60
Q

Which Ig is on the surface of B cells?

A

IgD - not located in blood

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61
Q

What is the function of IgD?

A

Participates in the process of activating B cells to recognize an antigen and undergo clonal expansion

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62
Q

Which Ig is produced slowly and lasts a longer time, conferring permanent immunity?

A

IgG

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63
Q

Which Ig temporarily transfers a mother’s immunity?

A

IgA

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64
Q

Which Ig is seen in allergic responses?

A

IgE

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65
Q

What is IgE?

A

Attaches to mast cells, important in allergic reactions

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66
Q

What would the labs of an immune response look like, immediately and shortly after?

A

Soar in IgM - quick protection

Soar in IgG - permanent immunity

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67
Q

What Ig level would rise on reexposure?

A

IgG

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68
Q

How are antibodies effective?

A
  • Neutralize function of antigen
  • Cause cell death by rupturing cell membrane of microbe where antigen is a part of
  • Incite inflammatory reaction
  • Make microbe more susceptible to phagocytosis
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69
Q

What is the immune complex?

A

When antibodies attach to the target antigen

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70
Q

Why is the immune complex made?

A

So the antibodies achieve their full effect on the antigen

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71
Q

What is active immunity?

A

Endogenous production of antibodies by the person’s own immune system

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72
Q

What is passive immunity?

A

Antibodies are transferred to confer temporary immunity (vaccines or immunity transfer from mother to baby)

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73
Q

What are B cells stimulated by?

A

Freely circulating antigen

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74
Q

What are T cells stimulated by?

A

Contact with an antigen bound the a cell membrane of an antigen presenting cell

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75
Q

Why is T cell immunity called delayed immunity?

A

T cells need to travel to the site of the offending antigen to attack it, which usually takes a few days

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76
Q

What are cytotoxic T cells?

A

“Effector T cells” - target and destroy cells that have been identified as containing alien antigens

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77
Q

How do cytotoxic T cells relate to runaway reactions?

A

They suppress unnecessary antibody production to prevent runaway reactions and autoimmune disease

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78
Q

What CD antigen type do cytotoxic T cells have?

A

CD8

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79
Q

Which MHC type do cytotoxic T cells interact with?

A

Type I MHC

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80
Q

What are helper T cells?

A

Faciliate the immune activities of B cells and other T cells

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81
Q

What CD antigen type do helper T cells have?

A

CD4

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82
Q

Which MHC type do helper T cells interact with?

A

Type II MHC

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83
Q

What are regulatory/suppressor T cells?

A

Modulate the immune response to shut down the immune response after successful defense to maintain immune homeostasis

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84
Q

What are memory T cells?

A

Enable the cellular immune system to mount a rapid secondary immune response

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85
Q

Which T cells are the generals?

A

Regulatory or suppressor T cells

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86
Q

How else are T cells stimulated, other than B cells presenting to them?

A
  • Cells with corrupted DNA

- Mediate immune rejection of tissue transplants

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87
Q

What is an MHC?

A

Major histocompatibility complex - mechanism by which antigens are displayed to immune cells - allows immune cells to recognize cell as self of nonself

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88
Q

What is another term for MHC?

A

HLA - human leukocyte antigens (because they were first discovered on WBCs)

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89
Q

What types of cells do not have MHC I?

A

Red blood cells

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90
Q

What types of cells have MHC II?

A

Dendritic and macrophages only

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91
Q

What do MHC I glycoproteins display?

A
  • Non self, alien antigens synthesized inside a virus infected or cancerous cell
  • Normal, self antigens in healthy cells
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92
Q

What do MHC II glycoproteins display?

A

Macrophages and dendritic cells capture the antigen and then display it to warn T cells to look around for cells to kill

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93
Q

What is the difference between MHC I and II?

A
  • Immune system attacks the cell with MHC I display

- Immune system reads MHC II display and goes looking for cells to attack

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94
Q

What is hypersensitivity?

A

Reactions that are the result of an abnormally active immune system and are the cause of allergy and autoimmune disease

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95
Q

What is another name for type I immune reaction?

A

Immediate hypersensitivity

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96
Q

What is another name for type II immune reaction?

A

Cytotoxic hypersensitivity

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97
Q

What is another name for type III immune reaction?

A

Immune complex hypersensitivity

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98
Q

What is another name for type IV immune reaction?

A

Cellular hypersensitivity

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99
Q

What is a type I immune reaction?

A

Occurs within a few minutes after an antigen combines with a preformed antibody that was created from an earlier exposure

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100
Q

What is the sensitizing exposure?

A

The initial exposure to an antigen where IgE antibodies are secreted and attach to mast cells

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101
Q

Does the initial, sensitizing exposure cause symptoms?

A

No

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102
Q

What happens during subsequent exposure?

A

Antigen combines with IgE antibodies already present on the surface of mast cells and triggers mast cell release of histamine and inflammatory mediators

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103
Q

What does the release of histamine cause?

A
  • Congestion
  • Hives
  • Increased vascular permeability
  • Bronchospasm
  • Watery eyes
  • Edema
  • Itching
  • Wheezing
  • Shortness of breath
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104
Q

What causes hives?

A

Release of histamine causes increased H2, which causes increased HCl acid in the stomach, which causes hives

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105
Q

What cells are activated in type I immune responses?

A
  • Increase in eosinophils and basophils
  • Platelet activation
  • Increased prostaglandins
106
Q

What is a bronchospasm?

A

Increased smooth muscle construction in the bronchi

107
Q

What is edema in a allergic response due to?

A

Increased vascular permeability and congestion due to the release of histamine

108
Q

What drugs can we prescribe for a type I immune reaction?

A
  • H2 blockers (antacids) - hives
  • Antihistamine
  • Prednisone
109
Q

What do systemic type I immune reactions result in?

A
  • Shock
  • Suffocation
  • Death
110
Q

Does a type I immune reaction have to produce symptoms only on second exposure?

A

No, you could be naturally sensitized

111
Q

What do IgE antibodies do in a type I immune reaction?

A

Attach to mast cells and sensitize them

112
Q

What makes a mast cell release histamine?

A

A subsequent exposure to an antigen binds to the antibodies present on the mast cell

113
Q

What is a type II immune reaction?

A

Self antigens become seen as non self by the immune system and become targets for attack:

  • Antibodies attach to target cell and endure phagocytosis or an anti-inflammatory response causing cell death
  • Antibodies attach to target cell receptors and interfere with target cell function
114
Q

What are two examples of type II immune reactions?

A

Myasthenia gravis

Grave’s disease

115
Q

What is a type III immune reaction?

A

Antigen and antibody combine to form an immune complex that deposits in tissue, damaging it and inciting an inflammatory reaction

116
Q

What is a systemic hypersensitivity?

A

Complex forms in blood and is deposited in tissue

117
Q

What is local hypersensitivity?

A

Complex forms and remains at the site of antigen introduction

118
Q

What does the deposit of an immune complex in a tissue stimulate?

A

Complement system

119
Q

What are the steps of the complement system?

A
  • Activation
  • Infammation
  • Opsonization
  • MAC
120
Q

What is the activation of the complement system?

A

Antigen and antibody binding

121
Q

What is opsonization?

A

Pathogen is marked for phagocytosis and destruction

122
Q

What is a MAC?

A

Membrane attack complex - directly acts on microbe cell membrane which further lyses and destroys cells

123
Q

What is an example of a type III immune reaction?

A

Lupus

124
Q

What type of cells do types I-III immune reactions involve?

A

B cells

125
Q

What type of cells do type IV immune reactions involve?

A

T cells

126
Q

What is a test for lupus?

A

ANA - antinuclear antibody

127
Q

What is a type IV immune reaction?

A

T cells produce clone cytotoxic T cells to attack invader, but they attack normal self antigens instead

128
Q

What is the time frame for type IV immune reactions?

A

More delayed because T cells need to be produced after antigen contact

129
Q

What are two examples of type IV immune reactions?

A

TB, poison ivy

130
Q

What is an allergy?

A

Any exaggerated but otherwise normal immune response to a foreign antigen regardless of the type of hypersensitivity reaction

131
Q

What is an allergen?

A

Any sustenance that induces an allergic reaction

132
Q

What is atopy?

A

Allergy due to type I hypersensitivity

133
Q

What are some areas that atopy effects?

A
  • Nose
  • Skin
  • Airway
134
Q

What are some examples of atopy?

A
  • Asthma
  • Eczema
  • Hay fever
  • Urticaria
135
Q

What is anaphylaxis?

A

Type I, acute, potentially fatal, IgE mediated

136
Q

What does anaphylaxis require in order to happen?

A

Prior sensitization

137
Q

What is the atopic triad?

A

Rhinitis, dermatitis, and asthma

138
Q

What are the most common allergens?

A
  • Dust
  • Animal dander
  • Mold
  • Pollen from trees, grass, and weeds
139
Q

What is autoimmunity?

A

Our own tissues and self antigens become targets of the immune system

140
Q

What are some mechanisms that cause autoimmune disease?

A
  • Imperfect fetal B and T cell programming
  • Inaccessible self antigens
  • Molecular mimicry
  • Infection and inflammation
141
Q

How does imperfect fetal B and T cell programming cause autoimmune disease?

A

Immune function hinges on self tolerance, the ability to recognize self and not attack - a few non tolerant T and B cells may survive maturation and escape suppression

142
Q

How do inaccessible self antigens cause autoimmune disease?

A

An antigen that has been hidden from contact with immune cells since conception may become unmasked - attacked because they were never designated as self antigens in the embryo

143
Q

What is molecular mimicry?

A

Antigens in some infectious agents may share antigenic molecular features that are similar to certain self antigens - immune response directed at foreign antigen also attacks the self antigen like it

144
Q

How does infection and inflammation cause autoimmune disease?

A

Tissue injury and inflammation may alter self antigens in a way that makes them appear to be nonself

145
Q

How can we test to see if a patient is genetically more susceptible to autoimmune diseases?

A

MHC/HLA genotyping

146
Q

What is SLE?

A

Systemic lupus erythematosus

147
Q

What type of immune reaction is lupus?

A

Type III

148
Q

Describe the characteristic rash of lupus

A

Rash on cheeks resembling a wolf (lupus), also known as malar or butterfly rash because it spreads across the bridge of the nose from one cheek to the other

149
Q

What are the diverse manifestations of lupus?

A 
May affect any organ or tissue especially"
Sin
Serosal membranes
Kidney
Joints
Brain
150
Q

Why is lupus unpredictable?

A

It waxes and wanes in intensity and manifestations

151
Q

What antibodies are associated with lupus?

A

ANA - antinuclear antibodies

152
Q

What do ANAs target?

A

DNA or RNA

153
Q

What is the ratio of women to men that have lupus?

A

9:1

154
Q

Why might women more commonly have lupus?

A

Maybe has to do with estrogen? Estrogen increases inflammatory response, while androgens typically decrease it

155
Q

What are some examples of systemic diseases?

A 
SLE
Rheumatic fever
Rheumatoid arthritis 
Systemic sclerosis (scleroderma)
Polyarteritis nodosa
156
Q

What are some examples of organ specific diseases?

A 
MS (brain)
Hashimoto thyroiditis
Autoimmune hemolytic anemia
Glomerulonephritis
Primary biliary cirrhosis
Dermatomyositis
Myasthenia gravis (skeletal muscle)
157
Q

What is the loss of self tolerance in SLE mainly due to?

A

Overactive helper T cells that stimulate B cell production of antiself antibodies (ANAs)

158
Q

What is arthritis?

A

Disease of joint inflammation; painful joint condition associated with joint abnormalities

159
Q

What is osteoarthritis?

A

Progressive, noninflammatory erosion of joint cartilage

160
Q

What is osteoarthritis caused by?

A

Wear and tear

161
Q

What joints are mainly affected by osteoarthritis?

A

Weight bearing joints - hip, knee, spine

162
Q

What is the pathophysiology behind osteoarthritis?

A

Cartilage becomes thin or worn away and bone surfaces begin to rub painfully against each other. In advanced disease cases, bone cysts and jagged growth of new bone (osteophytes/bone spurs) project into adjacent soft tissue and cause inflammation, swelling, and pain

163
Q

What is the most common sign and symptom of osteoarthritis?

A

Activity related joint pain is relieved by a short rest (other arthritis conditions have pain that lasts an hour or so despite rest)

164
Q

What is rheumatoid arthritis?

A

Chronic, systemic autoimmune disease involving mainly inflammation of synovial joints, but which regularly affects other tissues

165
Q

Who is affected more by rheumatoid arthritis?

A

2-3 times more women than men (80% of RA occurs in women)

166
Q

Why do we think rheumatoid arthritis occurs?

A

Not sure, but maybe a virus or other agent tigers a T lymphocyte autoimmune reaction that attacks the synovial membrane

167
Q

Is there a genetic predisposition to RA?

A

Yes

168
Q

How are B lymphocytes involved in RA?

A

Circulating antibody complex called rheumatoid factor is detected in 75% of patients

169
Q

What is a pannus?

A

The inflammatory reaction stimulates growth of blood vessels and fibrous tissue into the synovium and joint cartilage; pannus is the highly vascular inflammatory membrane

170
Q

How does the pannus damage the synovium?

A

It forms over cartilage and oozes destructive enzymes and other agents that dissolve the cartilaginous plate

171
Q

What is ankylosis?

A

Overgrowth of the synovium results in complete destruction of the joint, which can undergo fibrous repair that welds together the ends of bones to produce an immovable joint

172
Q

What is the Z deformity?

A

Deviation of the bones of the hand toward the radial side of the arm, with deviation of the fingers in the ulnar direction

173
Q

What are rheumatoid nodules?

A

Painless 1-2 cm subcutaneous inflammatory nodules not found in other forms of arthritis except for RA

174
Q

What are the most commonly affected joints in RA?

A 
Joints where the fingers meet the hand
Next join in the finger
Wrist
Elbow
Shoulder
Ankle
175
Q

What other tissues does RA affect besides joints?

A 
Heart
Blood vessels
Eyes
Skin
Lungs
Skeletal muscle
176
Q

When is RA most flaring?

A

Mornings (as opposed to osteoarthritis in which pain is equal all day)

177
Q

What is juvenile idiopathic arthritis?

A

Any arthritis arising in someone less than 16 years old that lasts for 6 weeks

178
Q

What are the characteristics of JIA?

A
  • One or few joints
  • Actue, systemic, toxic onset
  • Large joints
  • ANA present
  • Nodules and RF are absent
179
Q

What are spondyloarthropathies?

A

Several related types of autoimmune, genetically, influenced, vertebral arthritis that occur in patients who do not have a specific antibody in their blood

180
Q

Which type of arthritis experiences no inflammation?

A

Osteoarthritis

181
Q

What is gout?

A

Chronic metabolic disease associated with

  • High blood uric acid levels
  • Joint deposits of uric acid crystals
  • Inflammatory nodular subcutaneous deposits of uric acid crystals
182
Q

What do uric acid crystals do?

A

Sharp and incite intense inflammation, causing sever acute and chronic relapsing arthritis

183
Q

How is the kidney affected in gout?

A

Kidney excretes uric acid, which, when it causes renal deposits of irate crystals, may result in renal failure

184
Q

Where does gout usually manifest?

A

Big toe

185
Q

What are the risk factors to gout?

A
  • Alcohol use

- Diet of high fish and animal flesh

186
Q

What substance causes uric acid crystals?

A

Purines (found in fish and animal flesh)

187
Q

How does diabetes relate to gout?

A

Diabetics have high uric acid levels

188
Q

Why don’t you check the uric acid levels of someone with gout during a flare up?

A

Because the uric acid is being pulled into the joints at that time, and the reading will be falsely low

189
Q

What is a natural remedy to fight inflammation?

A

Cherry juice

190
Q

What is myasthenia gravis?

A

Acquired autoimmune disease of the neuromuscular junction

191
Q

How is the neuromuscular junction affected in myasthenia gravis?

A

Antibodies block acetylcholine receptors on the muscle side of the synapse, thus interrupting the transmission of the nerve impulse

192
Q

What organ is also affected in myasthenia gravis?

A

Thymic hyperplasia or thymoma is present in most patients

193
Q

What are some signs and symptoms of myasthenia gravis?

A 
Drooping eyelids
Double vision
Eye muscle weakness
Slack facial muscles
Difficult chewing
Proximal limb muscles
Respiratory failure
194
Q

What is systemic sclerosis?

A

Scleroderma - microvascular damage and inflammation and fibrosis of the support in fibrous intercellular tissue of many organs, especially the dermis

195
Q

Where does sclerosis affect tissues?

A 
Gi tract
Lungs
Kidney
Heart
Skeletal muscle
Small blood vessels
196
Q

What is the distinctive characteristic of scleroderma?

A

Uniform presence of Raynaud phenomenon

197
Q

What is the Raynaud phenomenon?

A

Condition resulting from spasm of small blood vessels that causes coldness, blanching, bumbles, and pain in the fingers and toes

198
Q

Why do patients with systemic sclerosis have trouble swallowing?

A

Dysphagia from esophageal involvement

199
Q

What is polyarteritis nodosa?

A

Autoimmune disease dominated by generalized blood vessels inflammation

200
Q

What is amyloidosis?

A

Dysfunction associated with systemic deposition of amyloid protein (local amyloid deposits in some organs are usually innocuous)

201
Q

What is an amyloid?

A

Mixture of insoluble proteins, some of which may be Ig fragments; misfolded mutant or normal proteins

202
Q

What is the difference between misfolded mutant and normal proteins in amyloidosis?

A

Misfolded mutant proteins are the cause of primary amyloidosis. Normal proteins are the cause of amyloidosis secondary to some other disease

203
Q

What happens when proteins misfiled?

A

Cell quality control mechanisms degrade them into waste products, and if this mechanism is overwhelmed, amyloid accumulates

204
Q

What is light chain amyloidosis?

A

Most common type; secondary, with B cell malignancies where the lymphocytes secrete a great excess of abnormal Ig, which is degraded into its heavy and light chain components (light chain is deposited as amyloid)

205
Q

What is hereditary amyloidoisis?

A

Primary, rare caused by gene defects like hereditary Mediterranean fever; increased production of inflammatory cytokines associated with fever and synovial, pleural, and peritoneal inflammation

206
Q

What does successful tissue transplantation require?

A

Donor and recipient be as much alike anitgenically as possible to avoid immune refection of the donated organ

207
Q

What characteristics do we look at when determining a good transplant match?

A
  • MHC/HLA

- ABO blood group types

208
Q

Is a blood transfusion a tissue transfusion?

A

Yes, a temporary liquid tissue transplantation

209
Q

What is an autograft?

A

IF the patient is both the donor and recipient

210
Q

What is a homograft?

A

Transplant between individuals (aka allograft)

211
Q

What is a xenograft?

A

Transplantation across species

212
Q

What is a hyper acute rejection?

A

Reaction that occurs within minutes or hours when preformed antibodies in the recipients blood react immediately with graft

213
Q

What is an acute rejection?

A

Usually occurs within a few weeks, owing to an immune vasculitis

214
Q

What is a chronic transplant rejection?

A

Develops over a period of months to years and is mainly the result of prolonged T cell assault on donor cells

215
Q

What are the four blood groups?

A

A, B, AB, O

216
Q

What is the most common blood type?

A

O

217
Q

What type of antibodies does A blood group have?

A

Anti-B antibodies

218
Q

What type of antibodies does AB blood group have?

A

Neither antibodies

219
Q

What type of antibodies does O blood group have?

A

Both anti-A and anti-B antibodies

220
Q

What blood type is the universal donor?

A

O

221
Q

What blood type is the universal recipient?

A

AB

222
Q

What type of blood can O blood type patients receive?

A

O only (because type O has anti-A and anti-B antibodies)

223
Q

What is erythroblastosis fetalis?

A

Rh- mother, Rh+ fetus
Fetus’s RBC leak into maternal circulation at delivery and stimulate production of material anti-Rh antibodies
Second pregnancy with Rh+ fetus will be attacked by mother’s antibodies, causing hemolysis

224
Q

What kind of antibodies do Rh- blood types have?

A

No antibodies, unless exposed to Rh+ blood

225
Q

What is a cross match?

A

Blood from potential donor is mixed with recipient bloodroot see if agglutination occurs

226
Q

What is major crossmatch?

A

Mix of donor RBCs with recipient plasma to check for agglutination

227
Q

What is the major cross match used for?

A

If a clerical lab test or error has occurred such that the donor and recipient blood are incompatible, the major crossmatch reveals the incompatibility

228
Q

What is a minor crossmatch?

A

Mix of donor plasma with recipient RBC

229
Q

What is the minor crossmatch used for?

A

Backup test to reconfirm that the original laboratory typing of donor and recipient was correct

230
Q

Transfusing blood incompatible by major/minor crossmatch is acceptable?

A

Transfusing by minor crossmatch - there is little danger in transfusing incompatible PLASMA because antibody is greatly diluted by recipients plasma (allowed in urgent situations)

231
Q

What is the difference between primary and acquired immunodeficiency disorders?

A

Primary is caused by inherited genetic defects, while acquired deficiencies occur secondary to another disease

232
Q

What is the most common immunodeficiency disorder?

A

AIDS

233
Q

What are opportunistic infections?

A

Organisms that ordinarily do not cause infection in people with healthy immune systems are the cause of many infections in immunodeficient patients

234
Q

When do immunodeficient disorders usually become apparent?

A

When the patient repeatedly is infected with an unusual or persistent opportunistic infection

235
Q

What are patients with B cell deficiency prone to?

A

Do not produce effective antibody response and usually suffer from infections from pyogenic bacteria

236
Q

What are patients with T cell deficiency prone to?

A

Prone to virus and fungus infections, and envelopment of neoplasm as a result of failed immune surveillance

237
Q

What is AIDS?

A

Acquired immunodeficiency syndrome - caused by infection with HIV which infects T cells and related macrophages

238
Q

What are patients with AIDS prone to?

A

Severe infection
Secondary neoplasms
Nervous system symptoms

239
Q

What value determines a diagnosis of AIDS?

A

CD4 count of 200 or less

240
Q

How does the infection of T cells cause problems with AIDS?

A

HIV infects helper T cells, which suppress the immune system - Helper T cells can’t stimulate the B cells to make antibodies or initiate cytotoxic T cells to kill foreign invaders

241
Q

What are the risk factors to AIDS?

A
  • Homosexual or bisexual males
  • Intravenous drug abusers
  • Males with hemophilia
  • Recipients of transfusions of human blood or blood components
  • Heterosexual contacts of the above
242
Q

How is AIDS transmitted?

A

HIV is transmitted by close human contact that transfers body fluid, mainly semen and blood or blood products

243
Q

Does HIV infect non human cells?

A

No - no animal reservoirs

244
Q

What does HIV do once it infects a CD4 cell?

A

HIV RNA synthesizes abnormal DNA that merges with normal DNA to become part of a new corrupted T cell DNA.
Later, process is revered and corrupted DNA produces new HIV RNA, which becomes the core of a new virus particle

245
Q

What happens to infected CD4 cells that do not die?

A

Linger as a population of infected but inactive, or latent, cells that can be stimulated to become active again and resume the cycle of T cell destruction

246
Q

How is latent cell predication reactivated?

A

Non HIV infections stimulate latent cells and renewed internal HIV replication

247
Q

How is B cell immunity affected in HIV?

A

B cells are stimulated by HIV antigens and antigens of opportunistic infections. They produce large amounts of ineffective antibody

248
Q

How is the nervous system damaged by HIV?

A

HIV majorly targets the microglia nervous system macrophages

249
Q

What is the natural progression of HIV infection?

A
  • Acute viral syndrome - flu like
  • Chronic, latent, infection - asymptomatic
  • Progression to clinical AIDS
250
Q

What does a lower CD4 count signal?

A

Associated with more advanced disease and worse prognosis

251
Q

What do labs look like during the latent phase?

A

Helper T cell levels are moderately depressed, virus levels are low, anti-HIV antibodies present

252
Q

How long does the latent phase last?

A

Could last for many years (7-10); could last indefinitely and AIDS may never develop, which is rare

253
Q

What signs and symptoms do HIV infected patients present with?

A

People from one of the risk groups present with:

  • Fever
  • Weight loss
  • Diarrhea
  • Palpable lymph nodes
  • Infection
  • Neurologic symptoms
  • AIDS related secondary neoplasm
254
Q

What are three types of neoplasms developed in AIDS?

A
  • Kaposi sarcoma
  • B cell lymphoma
  • Cervical carcinoma
255
Q

What is Kaposi sarcoma?

A

Sluggish vascular tumor caused by herpesvirus

256
Q

What are neoplasms in AIDS due to?

A

Because of failed immune surveillance of T cells

257
Q

What virus may underlie B cell lymphomas?

A

Epstein-Barr virus

258
Q

What is an example of a common opportunistic infection?

A

Candidiasis - yeast

259
Q

What are the main goals of treatment of AIDS?

A

Control HIV virus, control other infections

260
Q

What is a common drug treatment for AIDS?

A

HAART - highly active antiretroviral therapy - combination of antivirus drugs given in high concentrations

261
Q

How does HAART help AIDS patients?

A
  • Limits virus proliferation
  • Decreases numer and seriousness of opportunistic infections
  • Prolongs life

From Flashcardlet (133 decks)

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