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Pathology > Pathology of Immunologic Injury 1 - mechanisms of immune injury > Flashcards

Pathology of Immunologic Injury 1 - mechanisms of immune injury Flashcards

1
Q

Most women prefer the smell of dirty t-shirts from the men whose

A

HLA antigens differ most from hers

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2
Q

The one thing that actually seems to help older folks immune response is

A

physical exercise

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3
Q

Haptens

A

atoms or little molecules that bind to some body protein. the adduct may then be attacked by the immune system. On becomes allergic to nickel jewelry, poison ivy, penicillin, or whatever

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4
Q

The basis of adaptive immunity is

A

the precursors of our B and T lymphocytes developing specific and diverse receptors to deal with particular antigens that they may encounter in life

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5
Q

Effector cell: B lymphocyte

A

function = neutralization of microbe, phagocytosis, complement activation

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6
Q

Effector cell: Helper T lymphocyte

A

function = activation of macrophages, inflammation, activation (proliferation and differentiation) of T and B lymphocytes

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7
Q

Effector cell: Cytotoxic T lymphocyte

A

function = killing of infected cell

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8
Q

Effector cell: Regulatory T lymphocyte

A

function = suppression of immune response

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9
Q

Effector cell: Natural killer cell

A

function= killing of infected cell

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10
Q

pathologists distinguis different types of lymphocytes ising

A

special stains

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11
Q

CD8 stain illustrates

A

cytotoxic T lymphocytes (CTLs)

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12
Q

NK cells light up with

A

CD57

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13
Q

Natural killer cells exhibit _________ which signals that it has become infected by a virus

A

surface changes

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14
Q

_______ cells for processing antigens are abundant in ______

A

dendtritic

outer skin

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15
Q

B cells undergo maturation in the ________.

A

germinal follicles of lymph nodes. when you find a new node in your neck, this is what’s happening

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16
Q

Plasma cells, which make ______ are found mostly in the

A

antibodies

tissues rather than the blood

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17
Q

Hypersensitivity

A

a term used for disease cause by the immune system itself harming the body. The mechanisms are the same as those that protect us from invaders.

the immune system may be attacking antigens from the environment (microbes, non microbial antigens) and/or the body’s own antigens

the hypersensitivity reactions probably represent failures of control by the immune system’s feedback mechanisms.

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18
Q

Type I immune injury (atopy, immediate hypersensitivity, anaphylactic type)

A

is inappropriate function of the Th2/IgE/mast cell/ eosinophil system that is our major defense against worms. (i.e. peanuts or shellfish)

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19
Q

Type I immune injury - the immediate response
histamine
leukotrienes
PGD2

A

histamine is already present in the mast cell granules (vessels dilate and leak)
so are tryptase and chymase, strong proteases

The leukotrienes (made to order) contract smooth muscle and make vessels leak

Prostaglandin D2( made to order) causes bronchospasm and much mucus production

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20
Q

Three mediators of immediate responses of Type I hypersensitivity

A

histamine,
leukotriense,
PGD2

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21
Q

Late phase reaction of Type I hypersensistivity

A

goes on even after the allergen is gone

eosinophils brough to the site probably mediate much of the damage.

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22
Q

most important eosinophil attractant/ activator

A

IL-5

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23
Q

Urticaria is often (not always) about

A

igE, type I immune injury

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24
Q

allergy prick tests rely on

A

urticarial responses

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25
hay fever
this and the host of food allergy problems actually do bring out the eosinophils, again it's all about IgE
26
Eosinophilic gastroenteritis
the first consideration is food allergy
27
Allergic astma has a component of _______ | though this is not the entire story
IgE and plenty of Eosinophils
28
anaphylaxis
often due to massive IgE mediated response
29
atopic dermatitis is seen mostly in folks with
allergies
30
atopic dermatitis, keep your attention on
FcER1 on dendritic macrophages in allergy folks | now links to several interleukins and other molecules
31
chronic urticary is____ | causes include
a nuisance illness | autoimmunity (igE or its receptor), food, and unknown
32
non-atopy allergy
chronic urticaria
33
uritcaria not immune mediated
``` cold urticaria cholinergic urticaria (due to wet heat) ```
34
what two things tend to run with urticaria? cause?
dermatographism, readheadedness | reasons unknown
35
Type II immune injury
antibodies attack a fixed agent
36
coombs test
patient sample + anti HuIgG (coomb's reagent)= agglutination example - the baby's sample is positive for the presence of the mother's Ab on the surface of RBCs in erythroblastosis fetalis
37
Goodpastures's disease is caused by
antibodies against the basement membranes of lung and kidney
38
Transfusion related acute lung injury is caused by
antibodies in the donor plasma against HLA antigens that the recipient happens to have these antibodies are often there because donors previous pregnancy by the donor - hence the stron preference today for plasma donors being men.
39
The most common came of hypothyroidism from illness is
autoimmunity.
40
most often patients with autoimmune hypothyroidism have
antibodies and a mixed infiltrate of T and B cells. no one knows whether the antibodies are required (antibody-dependent cell mediated cytotoxicity) or whether the T cells are doing some of the damage on their own.
41
Addison's (classic)
adrenal being destroyed by T cells in classic addisons. Type II, though no one knows which arm of immunity starts the trouble
42
young diabetic
islet of langerhans being destroyed. both antibodies and angry T cells are generally present
43
Myasthenia gravis
antibodies and sometimes angry on-scene T cells. If not, the antibodies can still interfere with function
44
Patients such as _____ who develops a _______or ________ who develops such_____ have a circulating anticoagulant, and are in serious trouble.
a hemophiliac who develops antibodies against factor viii, | or a lups patient who develops such antibodies
45
Graves antibodies cause hyperthyroidism by
binding to and turning on the TSH receptors that drive thyroid hormone production
46
Graves antibodies cause proliferation of
loos CT behind the eyes and on the shins
47
Isaac's dz
antibodies keep the nerves firing muscle all the time. like this, there are a host of antibody mediated diseases that involve molecules rather than gross of histopathology
48
Type III immune injury
immune complex disease
49
Type III immune injury mechanism
the immune complexes form in the circulation and deposit in the vascular intima these syndromes produce vasculitis (including possible infarcts), arthritis, and/or glomerular nephropathies if the vessel undergoes necrosis, we speak of fibrinoid
50
Type III immune injur involves
deposition of complexes of a soluble antigen and antibodies, generally in vessel walls.
51
Type III immune injury we've all experienced during a viral illness
during the phase of an acute viral illness in which just enough antibodies have appeared to cause big immune complexes, which got deposited in your vessels and caused pain in the nearby nerves it ends when the antibody becomes more abundant and the immune complexes can melt away
52
immune complex definition
an immune complex is formed by an association between an antigen, its specific humoral antibody and portions of the complement system. may be small or very large
53
Arthus reaction
antigen sensitization antibody formation (day 4-17?) antigen challenge immune complex formation and inflammation
54
Immune complex disease
inject antigen 8-14 days serum sickness joints, heart, kidneys (deposition?)
55
serum sickness
antigen sensitzation antibody fromation re-exposure to antigen immune comples formation and inflammation
56
In the old days, al we had for diphtheria was ____ and ____ was a dreaded side effect
antibodies from horses that had been immunized with toxin | serum sickness
57
The most hated of all type III immune-mediated reactions is
hyperacute rejection of a donor kidney - the patient already had antibodies against the kidney. it turns white and bloodless before the surgeons eyes as the vessels plug up with complexes
58
Type IV immune injury
T cell mediated injury
59
delayed hypersensitivity in the skin
H & E stain for CD4 cells
60
anergy tester
the pricks contain things that you have almost certainly met - mumps candida, athlete's foot, tetanus toxoid, etc good responses to the mumps, athletes foot, candida, whatever
61
anergy
no response to things you MUST have already met. Something's wrong with this person's T helper cells
62
anergy - think of
sarcoidosis, lymphomas or other cancers, HIV infection, measles, or really bad disseminated infections
63
poison ivy - the happen is
urushiol
64
Tests for T cell hypersensitivity
patch tests
65
Vitiligo
CD4 and CD8 stains ???
66
halo nevus
the cells destroy melanocytes near a regressing nevus
67
allergy to nickel watchband
T cell mediated, no antibodies
68
infamous armpit sarcoid of the 50s
allergy to zirconium
69
Granuloma formation
often done by Th1 clls. No antibody required
70
Suture granuloma
granulomas form to wall off foreign objects even in the absence of an immune response
71
T cell mediated hypersensitivity (Th1 or Th17) suspects...
``` psoriasis rheumatoid arthritis multiple sclerosis Crohns ulcerative colitis sarcoid ```
72
Our ability to overcome/ manage hypersensitivity most of the time has made
organ transplantation routine in the 21st century.
73
Transplant rejection key features
Cd8 cells - acute cellular rejection | antibodies - acute humoral rejection
74
hyperacute rejection
IgG precipitates in gloms and arterioles (type III injury). fibrinoid in the arterial walls kidney blanched and ruined in minutes. with todays techniques of antibody detection, this is now mostly just a very bad memory
75
acute cellular rejection
``` T cells destroying a transplant. CD4 lights the vessels up heart kidney - tubulitis pancreas liver - endotheliitis intimal hyperplasia in the arteries artery in a transplanted lung capillaritis ```
76
chronic transplant rejection
vessels narrowed or totalled. The intima is most thickened, and (unlike in atherosclerosis), it tends to be concentric. T cells do cause thickening of intima/media
77
chronic kidney transplant rejection
transplant glomerulopathy | vessels, tubules
78
chronic liver transplant rejection
- little arteries gone
79
Graft vs host following
marrow, stem cell, or organ transplant
80
acute graft vs host disease takes
days to weeks after transplant
81
acute graft vs host signs/symptoms
generlized rash, sometimes loss of epidermis jaundice from damage to bile ducts ulcers along the GI tract, may bleed you'll only see a few donor lymphocytes, mostly CD8s doesn't take may of those CD8s to do the mischief
82
acute graft vs host often starts
on the palms
83
chronic graft vs host disease appears
later (after 100 days)
84
chronic graft vs host signs/symptoms
mor fibrosis and less obvious necrosis fibrosis of the dermis with loss of skin adnexal structures (resembles scleroderma) cholestatic jaundice from damage to bile ductules GI damage with possible malabsorption and/or esophageal stricture damage to host T cells with immunocompromise CMV pneumonitis is the most feared infection
85
Stress is good - it's lfe's way of telling you
that you are not dead
86
stress becomes distress only when
it is unmanageable
87
eustress makes a person
productive.
88
the worst way to deal with distress is to
accept bad advice or to become avoidant
89
even distress does not always make
disease more likely.

Pathology (15 decks)

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