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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
Q

hay fever

A

this and the host of food allergy problems actually do bring out the eosinophils, again it’s all about IgE

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26
Q

Eosinophilic gastroenteritis

A

the first consideration is food allergy

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27
Q

Allergic astma has a component of _______

though this is not the entire story

A

IgE and plenty of Eosinophils

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28
Q

anaphylaxis

A

often due to massive IgE mediated response

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29
Q

atopic dermatitis is seen mostly in folks with

A

allergies

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30
Q

atopic dermatitis, keep your attention on

A

FcER1 on dendritic macrophages in allergy folks

now links to several interleukins and other molecules

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31
Q

chronic urticary is____

causes include

A

a nuisance illness

autoimmunity (igE or its receptor), food, and unknown

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32
Q

non-atopy allergy

A

chronic urticaria

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33
Q

uritcaria not immune mediated

A 
cold urticaria
cholinergic urticaria (due to wet heat)
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34
Q

what two things tend to run with urticaria? cause?

A

dermatographism, readheadedness

reasons unknown

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35
Q

Type II immune injury

A

antibodies attack a fixed agent

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36
Q

coombs test

A

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
Q

Goodpastures’s disease is caused by

A

antibodies against the basement membranes of lung and kidney

38
Q

Transfusion related acute lung injury is caused by

A

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
Q

The most common came of hypothyroidism from illness is

A

autoimmunity.

40
Q

most often patients with autoimmune hypothyroidism have

A

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
Q

Addison’s (classic)

A

adrenal being destroyed by T cells in classic addisons. Type II, though no one knows which arm of immunity starts the trouble

42
Q

young diabetic

A

islet of langerhans being destroyed. both antibodies and angry T cells are generally present

43
Q

Myasthenia gravis

A

antibodies and sometimes angry on-scene T cells. If not, the antibodies can still interfere with function

44
Q

Patients such as _____ who develops a _______or ________ who develops such_____ have a circulating anticoagulant, and are in serious trouble.

A

a hemophiliac who develops antibodies against factor viii,

or a lups patient who develops such antibodies

45
Q

Graves antibodies cause hyperthyroidism by

A

binding to and turning on the TSH receptors that drive thyroid hormone production

46
Q

Graves antibodies cause proliferation of

A

loos CT behind the eyes and on the shins

47
Q

Isaac’s dz

A

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
Q

Type III immune injury

A

immune complex disease

49
Q

Type III immune injury mechanism

A

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
Q

Type III immune injur involves

A

deposition of complexes of a soluble antigen and antibodies, generally in vessel walls.

51
Q

Type III immune injury we’ve all experienced during a viral illness

A

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
Q

immune complex definition

A

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
Q

Arthus reaction

A

antigen sensitization
antibody formation (day 4-17?)
antigen challenge
immune complex formation and inflammation

54
Q

Immune complex disease

A

inject antigen
8-14 days serum sickness
joints, heart, kidneys (deposition?)

55
Q

serum sickness

A

antigen sensitzation
antibody fromation
re-exposure to antigen
immune comples formation and inflammation

56
Q

In the old days, al we had for diphtheria was ____ and ____ was a dreaded side effect

A

antibodies from horses that had been immunized with toxin

serum sickness

57
Q

The most hated of all type III immune-mediated reactions is

A

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
Q

Type IV immune injury

A

T cell mediated injury

59
Q

delayed hypersensitivity in the skin

A

H & E stain for CD4 cells

60
Q

anergy tester

A

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
Q

anergy

A

no response to things you MUST have already met. Something’s wrong with this person’s T helper cells

62
Q

anergy - think of

A

sarcoidosis, lymphomas or other cancers, HIV infection, measles, or really bad disseminated infections

63
Q

poison ivy - the happen is

A

urushiol

64
Q

Tests for T cell hypersensitivity

A

patch tests

65
Q

Vitiligo

A

CD4 and CD8 stains ???

66
Q

halo nevus

A

the cells destroy melanocytes near a regressing nevus

67
Q

allergy to nickel watchband

A

T cell mediated, no antibodies

68
Q

infamous armpit sarcoid of the 50s

A

allergy to zirconium

69
Q

Granuloma formation

A

often done by Th1 clls. No antibody required

70
Q

Suture granuloma

A

granulomas form to wall off foreign objects even in the absence of an immune response

71
Q

T cell mediated hypersensitivity (Th1 or Th17) suspects…

A 
psoriasis
rheumatoid arthritis
multiple sclerosis
Crohns
ulcerative colitis
sarcoid
72
Q

Our ability to overcome/ manage hypersensitivity most of the time has made

A

organ transplantation routine in the 21st century.

73
Q

Transplant rejection key features

A

Cd8 cells - acute cellular rejection

antibodies - acute humoral rejection

74
Q

hyperacute rejection

A

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
Q

acute cellular rejection

A 
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
Q

chronic transplant rejection

A

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
Q

chronic kidney transplant rejection

A

transplant glomerulopathy

vessels, tubules

78
Q

chronic liver transplant rejection

A
  • little arteries gone
79
Q

Graft vs host following

A

marrow, stem cell, or organ transplant

80
Q

acute graft vs host disease takes

A

days to weeks after transplant

81
Q

acute graft vs host signs/symptoms

A

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
Q

acute graft vs host often starts

A

on the palms

83
Q

chronic graft vs host disease appears

A

later (after 100 days)

84
Q

chronic graft vs host signs/symptoms

A

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
Q

Stress is good - it’s lfe’s way of telling you

A

that you are not dead

86
Q

stress becomes distress only when

A

it is unmanageable

87
Q

eustress makes a person

A

productive.

88
Q

the worst way to deal with distress is to

A

accept bad advice or to become avoidant

89
Q

even distress does not always make

A

disease more likely.

Pathology (15 decks)

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