Immunology - Exam 2

Front 1

(Anaphylactic) - mediated by IgE

Back 1

1

Front 2

(Cytotoxic) - mediated by IgG and IgM - cytolytic response

Back 2

2

Front 3

(immune complex) - Ag+Ab+complement cause injury to blood vessels and other tissues

Back 3

3

Front 4

(Cell-Mediated) - mediated through T cells, cell-mediated immunity - or when it causes
Injury it is called delayed hypersensitivity

Back 4

4

Front 5

the result of the binding of antigen to antigen specific IgE bound to its Fc receptor on mast cells and basophils; this result in the degranulation of the cells with release of inflammatory mediators. An example would be allergic rhinitis due to inhaled pollens.

Back 5

Type I hypersensitivity reaction (immediate hypersensitivity)

Front 6

are caused by small molecules that bond covalently to cell-surface components of human cells, producing modified structures that are perceived by the immune system as foreign. B cells respond to these new epitopes with the production of IgG or IgM which binds to the modified cell with complement activation and phagocytosis resulting in cell destruction. An example would be the hypersensitivity reaction to the small molecules of penicillin.

Back 6

Type II hypersensitivity reactions

Front 7

are due to small soluble immune complexes formed by soluble protein antigens binding to the IgG made against them. These initiate the complement cascade and produce an inflammatory response that damages tissues. An example of this vasculitis as seen in a condition known as serum sickness.

Back 7

Type III hypersensitivity reactions

Front 8

are caused by the products of antigen-specific T cells. Most are caused by CD4 Th1 cells, a minority are due to CD8 cytotoxic cells. These reactions do not occur immediately and are known as delayed hypersensitivity reactions. For example poison ivy.

Back 8

Type IV hypersensitivity reactions unlike the types I, II, and III where the effector molecules initiating the reactions are antibodies, the type IV

Front 9

which phagocytes are involved in:
acute inflammatory processes

Back 9

polymorphonuclear leukocytes

Front 10

which phagocytes are involved in:
chronic inflammation

Back 10

macrophage/circulating monocytes

Front 11

which phagocytes are involved in:
parasitic infections and Type I mediated injury

Back 11

eosinophils

The allergic individual (for example, ragweed allergy) has plenty of these eosinophils in the blood and nasal secretions which are of diagnostic and pathogenic importance.

Front 12

types of chemical mediators:
a) histamine, (causes the leaking of blood vessels, edema, and the shock of anaphylaxis) b) heparin, c) ECF-A (eosinophilic chemotactic factors of anaphylaxis which brings in eosinophils c) PAP (platelet activating factor).

Back 12

Preformed

Front 13

types of chemical mediators:
the products of arachadonic acid pathways (both lipoxygenase and cyclooxygenase pathways) including leukotrienes C, D, E, the slow reacting substance of anaphylaxis (SRSA), and prostaglandins and thromboxanes

Back 13

Newly synthesized

Front 14

summary of type I anaphylactic response:

Immune reactant:
Antigen:
Effector mechanism: Example:

Back 14

Immune reactant: IgE
Antigen: soluble antigen
Effector mechanism: Mast-cell activation
Example: allergic rhinitis, asthma, systemic anaphylaxis

Front 15

what are the 3 components of the immune system

Back 15

can divide the immune system into three compartments. The first compartment is non-specific immunity (mostly phagocytosis)

The second is specific immunity involving B and T cells.

It is in the third compartment that immunologically mediated diseases are produced.

Front 16

all blank are black but not all blank are blank

Back 16

all allergens are antigens, but not all antigens are allergens.

Front 17

Onset All Ages

Duration Transient or Permanent

Skin Tests Positive

Mucosa Erythema, edema***** mucus

Back 17

Food Sensitivity: Reaginic
*********

Front 18

Onset Infancy, childhood

Duration Transient , except gluten

Skin Tests Negative

Serum Antibodies Elevated

Mucosa Villous atrophy, infiltration

Back 18

Food Sensitivity: Not Reaginic

Front 19

what immunologic causes of urticaria are NOT mediated by IgE??

can you use skin test?

Back 19

Drugs (mediated by IgE)
exception: serum sickness (mediated by IgG)
Foods (mediated by IgE)
Parasitic infestation (mediated by IgE)
dander, pollen
wheat, fish
Insect stings and bites (mediated by IgE)
Transfusion reaction
Cryopathies
cryoglobulinemia (mediated by IgG and IgM)
cryofibrinogenemia
cold hemolysin syndrome (mediated by IgG)
Collagen-vascular disease

can test for with skin test

Front 20

what are the non-immunologic causes of urticaria

can you use skin test?

Back 20

Drugs
Histamine liberators
Acetylsalicyllic acid and related anti-inflammatory compounds
Iodinated dyes
Foods
Histamine liberators
Hereditary angioedema (not true urticaria)
Angioedema due to acquired C1 esterase deficiency
Stress
Hyperthyroidism

Blackberries, blueberries and strawberries
No skin test can be done for Aspirin, radioactive dye, etc.

Front 21

Drug Causes of Urticaria

Back 21

Opiates
Antibiotics,especially penicillin
Aspirin and other NSAIDS

Cause non-immunologic urticaria. Can’t do a skin test for most.
PCN is the main drug and can be skin-tested for. Aspirin is 2nd.

Front 22

eg of essential (acquired) urticaria

Back 22

man jumps into cold pool, and, due to massive release of histamine, dies. (MC type)

Front 23

classification of cold urticaria

Back 23

Familial
Essential (acquired)
Secondary
cryoglobulinemia
cryofibrinogenemia
cold hemolysin syndrome

Front 24

ice cube tests for what

Back 24

cold urticaria

Lesions will be somewhat large (larger than those of cholinergic urticaria).

Front 25

how to test for cholinergic urticaria and what does it look like

Back 25

Due to heat (also, possibly stress or exercise). Lesions are small (like pencil erasers), NO massive release of histamine.
Test by having them break into a sweat (or, in Hx, they’ll tell you about coming out of a hot shower looking like this).

Front 26

50 yo pt presents with angioedema and no urticaria
no family history of symptoms
swollen everywhere
the swelling was precipitated by trauma and it has lasted between 48-72 hours
you give him epi --> no relief
what is it

Back 26

acquired angioedema

Front 27

20 yo pt presents with angioedema and no urticaria
some family history of symptoms
swollen everywhere
the swelling was precipitated by trauma and it has lasted between 48-72 hours
you give him epi --> no relief
what is it

Back 27

hereditary angioedema (no underlying disease)

Front 28

35 yo pt presents with angioedema and urticaria
some family history of symptoms
swollen on face and lips
the swelling was not precipitated by trauma and it has lasted between about 10 hours
you give him epi --> relief
what is it

Back 28

allergic/histamine mediated angioedema

no underlying disease

Front 29

how to distinguish between type 1 HAE and acquired HAE

Back 29

HAE type 1 -- C1 is normal
in acquired C1 is decreased

Front 30

what is the screening test for HAE

Back 30

C4 (complement)

Front 31

what does a decreased C1q level indicate

Back 31

it distinguishes AAE (decreased C1) from HAE (normal C1)

Acquired AE is due to presence of underlying disease.

Treatment of underlying condition may result in resolution

For acute attacks, C1 inhibitor concentrate, where available should be used

Attenuated androgen may be useful in Type 1

Immunosuppressive therapy for Type 2

Front 32

talk about darer's line as a part of urticaria pigmentose

what type of cells do you see in skin?

Back 32

Part of urticaria pigmentosa; see a tremendous amount of mast cells in skin.
If stroked, see Darer’s line, get an urticaria with erythema along the line.
If in skin, benign; if widespread, in internal organs, it is MALIGNANT.

Front 33

how long to wait until you suspect vasculitis

Back 33

Urticarial vasculitis.
Any lesion that doesn’t clear in 48 hrs, or leaves petechiae or ecchymoses (bruise), could be a vasculitis.

Front 34

The best TX for HAE

Back 34

– replace the C1-INH, or we block Bradykinin, or prevent Bradykinin’s attachment to the cell. It is NOT Tx’d by epinephrine/steroids.

Front 35

tx of ACUTE HAE

Back 35

Tx for acute episode is epinephrine (as long as you maintain an airway).
Give epinephrine to raise the blood pressure, and keep patient alive.

Front 36

main difference between type I and type II HAE

Back 36

In HAE Type I, there is a C1-esterase inhibitor deficiency; in Type II, there is a functional abnormality of C1-esterase inhibitor

Front 37

most important thing to do with anaphylactic rxn

Back 37

maintain airway
ABCs

Front 38

anaphylactoid rxns are mediated by

Back 38

NOT BY IgE!!!

Results from the release of mast-basophil mediators

Anaphylaxis – a syndrome with varied mechanisms, clinical presentations, and severity.

An acute life-threatening reaction.

Front 39

talk about trend of anaphylactic rxns vs anaphylactoid rxns

Back 39

The milder the case, the more likely it is to be anaphylactoid.
As the rxn gets more violent, it is more likely anaphylaxis.
Hard to test for anaphylactoid rxns.

Front 40

anaphylactoid/anaphylactic rxns type

begins rapidly with clinical manifestations short-lived

Back 40

Unimodal ***

Keep pts in office/hospital for some time, bc of the possibility of the bimodal or protracted rxn.

Front 41

anaphylactoid/anaphylactic rxns type

can begin within minutes of exposure, but after a transient clinical improvement the reactions return in 1 to 8 hours later

Back 41

BIMODAL ****

Keep pts in office/hospital for some time, bc of the possibility of the bimodal or protracted rxn.

Front 42

anaphylactoid/anaphylactic rxns type

can begin suddenly or gradually, but clinical manifestations are prolonged

Back 42

Protracted

ep pts in office/hospital for some time, bc of the possibility of the bimodal or protracted rxn.

Front 43

Gell and Coombs’ Hypersensitivity (immunopathologic reactions)

Immediate

Back 43

Type I

Types I, II and III can result in immunologically-induced or allergic anaphylaxis

Front 44

Gell and Coombs’ Hypersensitivity (immunopathologic reactions)

Cytotoxic

Back 44

Type II

Types I, II and III can result in immunologically-induced or allergic anaphylaxis

Front 45

Gell and Coombs’ Hypersensitivity (immunopathologic reactions)

Immune Complex

Back 45

Type III

Types I, II and III can result in immunologically-induced or allergic anaphylaxis

Front 46

Gell and Coombs’ Hypersensitivity (immunopathologic reactions)

Delayed Hypersensitivity

Back 46

Type IV

Types I, II and III can result in immunologically-induced or allergic anaphylaxis

Front 47

sx:

Diffuse erythema
Diffuse pruritus
Diffuse urticaria
Angioedema
Bronchospasm
Laryngeal edema*
Hyperperistalsis
Hypotension*
Cardiac arrhythmias*
Nausea
Vomiting
Lightheadedness
Headache
Feeling of impending doom
Unconsciousness
Flushing

Back 47

Signs and Symptoms of Anaphylaxis



MC manifestations of anaphylaxis are DERM-related.
The most dangerous things are laryngeal edema and hypotension.

Front 48

Physician-Supervised Management of Anaphylaxis

Back 48

Assessment of airway, breathing, circulation, and mentation.

b) Administer EPI, 1:1000 dilution, 0.3 - 0.5 ml
(0.01 mg/kg in children, max 0.3 mg dosage) IM, to control SX and BP. Repeat, as necessary.
Aqueous EPI 1:1000, 0.1- 0.3ml in 10ml NS (1:100,000
to 1:33,000 dilution), IV over several minutes prn.

For potentially moribund subjects, tubercular syringe, EPI 1:1000, 0.1 ml, insert into vein (IV), aspirate 0.9 ml of blood (1:10,000 dilution). Give as necessary for response.

notes:
IMMEDIATE Tx: Assess and maintain an airway, then epinephrine, 1:1000 IM (in the thigh).
At certain times, epinephrine is NOT given sub-Q; in those times, it is given IV (HUGE RISK of ventricular tachycardia).
In most severe cases, pull up blood with epi, and shoot epi straight into vein.

Front 49

Non-allergic reaction characterized by slow pulse, nausea, pallor, sweating, clammy skin, and/or hypotension.

Back 49

Vasodepressor (Vaso-Vagal)

SLOW, BOUNDING pulse is key (normally, in an anaphylactic rxn, the pulse is RAPID and hard to feel)
See this with dental injections, removing stitches
Will NOT start itching and feeling a sense of impending doom (MC with anaphylaxis)
Do NOT Tx with epinephrine (not needed)

Front 50

General Measures to Reduce the Incidence of Drug- Induced Anaphylaxis and Anaphylactic Deaths

Back 50

General Measures

Obtain thorough history for drug allergy.

Avoid drugs with immunological or biochemical cross-reactivity with any agents to which the patient is sensitive.

Administer drugs orally rather than parenterally when possible.

Check all drugs for proper labeling

Keep patients in clinic for 20 to 30 minutes after injections.

Front 51

Measures to Reduce the Incidence of Anaphylaxis and Anaphylactic Deaths


at risk pt's

Back 51

Measures for Patients at Risk
Avoid causative factor/s.
Have patient wear and carry warning identification.
Teach self-injection of epinephrine and caution patient
To keep epinephrine kit with them.
Discontinue -adrenergic blocking agents, ACE inhibitors (controversial), monoamine oxidase inhibitors, and tricyclic antidepressants, where possible.


note:
Discontinue beta blockers (bc epi can’t be given in the rare event that pt has anaphylactic rxn).

Front 52

understand good and bad prognoses in terms of anaphylaxis

large/small dose of antigen
onset of symptoms early/late
initiation of tx early/late
route of exposure parental - good/bad ; oral - good/bad (think food and drugs)
beta blocker use good/bad
presence of underlying diseae - good/bad

Back 52

Prognosis

Factor Poor Good

Dose of antigen (allergen) Large Small

Onset of symptoms Early Late

Initiation of treatment Late Early

Route of exposure

Parenteral Yes No

Oral* No Yes

β-adrenergic blocker use Yes No

Presence of underlying disease Yes No

* True for drugs, not foods

Front 53

urticaria - mediated by what

Back 53

IgE

Front 54

anaphylaxis - mediated by what

Back 54

IgE

Front 55

when someone comes in with a snake bite
mechanism?
skin testing indicated?
acute therapy?
immunotherapy?

Back 55

pharm effects of venom
NO
tx: supportive
immuno: NO

Front 56

someone comes in with large local inflammation
mechanism?
skin testing indicated?
actue therapy?
immunotherapy?

Back 56

local inflammation
none indicated
cool packs NSAIDs, antihistamines
NO

Front 57

someone comes in with urticaria
mechanism?
skin testing?
acute therapy?
immunotherapy?

Back 57

IgE mediated of complement activation
adults - yes (skin testing) ; children - NO
tx: antihistamine, close observation
immuno- adults - YES ; children (NO TESTING DONE SO NO!)

Front 58

anaphylactic pt comes in
mechanism?
skin testing?
acute therapy?
immunotherapy?

Back 58

IgE mediated mechanism
adults nad child get skin testing
tx: epi, sub-Q and other resuscitation as needed
immuno- YES (if skin tests are positive)

Front 59

Risk factors for adverse drug rxns

Back 59

HIV Infections
Cystic Fibrosis
Multiple Drug Allergy
Familial Drug Allergy


Others include: topical drugs are most likely to cause rxns, as are high/prolonged doses.

MC drugs that cause rxns: PCN, aspirin, sulfonamides

Children are LESS susceptible to adverse drug rxns than are adults. (weird)

Front 60

Classification of Adverse Drug Reactions

Back 60

Overdose or toxicity
Side effects
Secondary effects
Drug Interactions
Intolerance
Idiosyncratic (pharmacogenetic) reactions
Allergy or hypersensitivity


NOTE
True “allergy” is the least likely cause of adverse drug rxn; it is pretty much the most dangerous, but it isn’t very likely to occur.

Some drugs have “predictable” effects: expected side effects (drowsiness with anti-Histamine), expected secondary effects (use ABX and see overgrowth of bacteria), also D-D int.

Front 61

most drug allergy manifestations are ...

Back 61

cutaneous!!!

Exanthematous eruptions
Urticaria and angioedema
Contact dermatitis
Erythema multiforme
Stevens-Johnson syndrome
Exfoliative dermatitis
Fixed drug eruption
Non-thrombocytopenic purpura
Henoch-Schonlein syndrome
Photosensitivity reactions

Front 62

these clinical manifestations of what?

Anaphylaxis
Serum sickness-type reactions
Drug fever
Hematologic reactions
Thrombocytopenia
Hemolytic anemia
Agranulocytosis
Eosinophilia

Back 62

Drug Allergy Systemic Reactions



Serum sickness is Type III
Drug fever – pt was Tx’d for pneumonia, and now drug causes fever and high WBC count

Front 63

serum sickness is type ....

Back 63

3!

Front 64

breakdown products of penicillin are broken down into what groups

what type of rxns are seen from each group?

how to test for them?

Back 64

Major haptenic group (95%) – causes derm manifestations
Minor haptenic group (5%) – causes anaphylactic rxns
Can skin test for MAJOR group, but not for minor.

Front 65

PCN can cause what type of hypersensitivity rxns?

Back 65

PCN can cause ANY of the four rxns


1 - igE - urticaria, systemic anaphylaxis

2 - igm,igg - hemolytic anemia

3 - igg - serum sickness, glomerulonephritis

4 - T dth cells - contact dermatitis

Front 66

One test to determine if an anaphylactic rxn occurred/is occurring....

Back 66

Tryptase; must be done within 2 or 3 hrs (draw blood as ER doc)

Front 67

hypersensitivity rxns
which are IgG mediated

Back 67

II and III

Front 68

hypersensitivity rxns
which are IgE mediated

Back 68

I

Front 69

hypersensitivity rxns
which have soluble antigens

Back 69

I
III
IV (Th1 and Th2 cells)

Front 70

hypersensitivity rxns
immune reactant
antigen
effector mechanism
example

TYPE I

Back 70

IgE
soluble
mast-cell activation
allergic rhinitis, asthma, systemic anaphylaxis

Front 71

hypersensitivity rxns
immune reactant
antigen
effector mechanism
example

TYPE II

Back 71

2 types - both use IgG as its immune reactant

A = cell or matrix associated antigen
effector mechanism is complement FcR cells (phagocytes, NK cells)
example: some drug allergies (PCN)

B - cell surface receptor
effector mechanism - antibody alters signalling
example - chronic urticaria (antibody to Fce Ralpha)

Front 72

hypersensitivity rxns
immune reactant
antigen
effector mechanism
example

TYPE III

Back 72

IgG
soluble antigen
mechanism: complement phagocytes
example - serum sickness, arthus rxn

Front 73

hypersensitivity rxns
immune reactant
antigen
effector mechanism
example

TYPE IV - Th1 cells

Back 73

Th1 cells are reactant
they are soluble
mech: macrophage activation
example: contact dermatitis, tb rxn

Front 74

hypersensitivity rxns

immune reactant
antigen
effector mechanism
example

TYPE IV - Th2 cells

Back 74

reactant cell - Th2
they are soluble
EOSINOPHIL activation
example: chroni asthma, chronic allergic rhinitis

Front 75

hypersensitivity rxns
immune reactant
antigen
effector mechanism
example

TYPE IV - CTL

Back 75

cell-associated antigen
mech: cytotoxicity
eg: contact dermatitis

Front 76

hypersensitivity rxns

which is contact dermatitis an example of

Back 76

IV - Th1 cells

IV - CTL

Front 77

mediator of type I rxn
found where?
granules?

Back 77

MAST CELLS
in tissue
YES GRANULES

Front 78

a mediator of type I rxn but found in BLOOD, not tissue

Back 78

BASOPHIL

Front 79

when is histamine released?
released with what?
what does it do?

Back 79

type I hypersensitivity rxn
with serotonin, esoinophil chemotactic factors, proteases

it increase vascular permeability, smooth muscle contraction

ITS PREFORMED and released IMMEDIATELY in type I rxn

Front 80

what does bradykinin do

Back 80

its a secondary mediator in type I rxns - is major cause of life-threatening anaphylactic rxn

Front 81

what interleukens are "popular"

Back 81

2,3,4,5,6 - they bring cells to the site!

Front 82

not a lot of cells present
erythema surrounds edema (like a mosquito bite)

what is this?

Back 82

type I rxn

NOT TYPE III (arthus)
NOT TYPE IV

Front 83

describe the PK reaction - prausnitx-kutsner rxn

what type is it?

Back 83

Prausnitz-Kutsner (PK) Reaction or Passive Cutaneous Anaphylaxis – Type I
Inject anti-serum (IgE) into skin and follow with Ag + dye; due to vasodilation, dye will leak out quickly.

Front 84

what is the schultz-dale rxn

what type of rxn are you trying to imitate?

Back 84

Smooth muscle (ileum) from actively sensitized animal (has Ab) put in solution. Adding Ag causes muscle to contract (explains “smooth muscle contraction” of Type I reaction).

Front 85

MUST KNOW THE STEPS OF THE INHALED ALLERGEN FOLLOWED BY IMMUNE RXN

Back 85

Pollen enters body, picked up by APC, presented in conjunction w/ MHC-II to T-helper cell (TH2, also CD4), which contacts B-cell, thru IL-4, to produce IgE (typical Type I reaction).

It is the IgE that sits on the mediator cells (mast cells and basophils); IgE is created by the *contact* between the TH2 cell and the B cell.

IgE can attach to Fc (epsilon) region on mediator cells, and attach to mast cell/basophil, without an Ag being present.


VERY VERY VERY IMPORTANT

Front 86

what is going on in type IV reaction - contact dermatitis

Back 86

CELLS !! many many cells

Does not involve Immunogolbulins, but cells. Shows CELLULAR infiltration. (very little erythema/edema)

Front 87

good pasture's disease is what?

Back 87

Type II reaction; due to Rh factor – causes hemolytic disease of the newborn, characterized by autohemolytic anemia.


the same business with the

Front 88

what are transfusion rxns? (what type?)

Back 88

TYPE II

Front 89

what does the COOMBs test do?

Back 89

tests for agglutination of two blood samples

Type II reaction (autohemolytic anemia). This is the Coombs’ Test. If blood types match, no agglutination (test is negative); if they don’t, see picture on left (positive agglutination).

(Transfusion rxns are Type II)
slide 14


Mismatched blood types lead to agglutination, due to binding of Ab to Ag. (Type II rxn)

Front 90

example of type III rxn

Back 90

Type III is vasculitis. Can be local (Arthus rxn) or systemic (serum sickness; char by typical lesions – palpable purpura - on lower extremity)

Front 91

what will you see in type IV rxn?

Back 91

Typical Type IV Mantoux or tuberculin test. See some erythema, but the KEY is the nodular feel. Loaded with round MONOnuclear cells (lymphocytes, monocytes, and macrophages), not PMNs (how to diff. from Type III).

Front 92

what are the key mechanisms that contribue to immunological self-tolerance ********* memorize this answer

Back 92

neg selection in the BM and thymus

expression of tissue-specific proteins in the thymus

no lymphocyte acces to some tissues

SUPPRESSION OF AUTOIMMUNE RESPONSES BY REGULATORY T CELLS

induction of anergy in autoreactive B and T cells

Front 93

describe process of Thelper and B cells and how we can have autoimmune disease

Back 93

T and B cells are always present and can lead to autoimmunity; the T-helper cell is usually NOT active (bc of T-suppressor cells). If activated, it will stim either T or B cells to go on to autoimmunity. Bypass can occur to directly stim T effector cells to cause autoimmune dz. Recognition of self as Ag.

Front 94

what are the organ specific diseases ***

Back 94

THYROID - hashimoto's thyroiditis, primary myxoedema, thyrotoxicosis
STOMACH - pernicious anemia
ADRENAL - addison's
PANCREAS - juvenile diabetes

In the non-organ spec diseases, organs get attacked secondarily to autoimmune phenomenon. In organ-specific, the organ is seen as foreign, leading to attack.

Front 95

what are the NON-organ specific diseases ***

Back 95

MUSCLE - dermatomyositis
KIDNEY - lupus
SKIN - scleroderma
JOINT - rheumatoid arthritis


In the non-organ spec diseases, organs get attacked secondarily to autoimmune phenomenon. In organ-specific, the organ is seen as foreign, leading to attack.

Front 96

what is most important antigen on surface in autoimmunity

Back 96

MHC!!!!


(determine autoimmune reaction). Ag is presented to T cell with MHC. MHC I is a marker for death (on every cell), so we can kill those cells; MHC II does NOT mark for death; only found on immune cells, and these cells can’t be killed.

Front 97

what are major autoimmune diseases of endocrine glands?

THYROID

Back 97

hashimoto's thyroiditis
graves disease
subacute thyroiditis
idiopathic hypothyroidism

Front 98

what are major autoimmune diseases of endocrine glands?

islets of langerhans

Back 98

type 1 diabetes (insulin-dependent, juvenile-onset diabetes)
type 2 (insulin-resistant, adult-onset diabetes)

Front 99

what are major autoimmune diseases of endocrine glands?

adrenal gland

Back 99

ADDISON"s disease

Front 100

thyroid tissue is infiltrated with huge numbers of cells - what happens

Back 100

crowds out the normal fucntion --> HYPOTHYROIDISM

Front 101

whats going on in graves disease

Back 101

Grave’s disease
Abnormal IgG (against TSH) crosses placenta to baby.

Front 102

Grave’s disease
Instead of normal TSH allowing receptor to change thyroglobulin into thyroxine (some of which enters circ, some goes to pituitary). Auto-Ab stimulates the thyroid and causes constant pouring out of thyroxine (causes ....




what are TSH levels

Back 102

exophthalmos, sweating, loss of weight, high blood pressure, rapid heart beat) w/o quieting down. Akin to hyperthyroidism. TSH is LOW in blood

Front 103

how it graves different from myasthenis gravis

Back 103

Myasthenia Gravis – Ab does not stim receptor (instead, blocks Ach receptor), so muscles don’t contract


graves - antibody stimulates thyroxine (TSH is low in blood), but OVERactive thyroid is observed

Front 104

what happens in pernicious anemia

Back 104

Pernicious Anemia – Auto-Ab against Intrinsic factor made by parietal cells (such that B12 does not bind to IF; possible fatal anemia develops)

Front 105

with warm agglutinins....
antibody type?
ability to fix complement?

Back 105

With warm agglutinins, Ab is formed, does not fix complement, and agglutinates RBCs -> anemia. Mostly idiopathic.

(lymphoproliferative diseases, tumors, viral diseases, sarcoidosis, drugs, SLE)


Agglutination/hemolysis depends on temperature.

Front 106

with cold agglutinins....
antibody type
ability to fix complement?

Back 106

IgM -- YES IT FIXES COMPLEMENT

(infection MONO, M. pneumo, cold agglutinin disease)


Agglutination/hemolysis depends on temperature.

Front 107

with cold hymolysins....
antibody type?
ability to fix complements?

Back 107

IgG - YES it USUALLY fixes complement

(donath-landsetiner antibody - variable infections)


Agglutination/hemolysis depends on temperature.

Front 108

what is ice cube test used for in terms of agglutinins?

Back 108

used to assess agglutinins/hemolysis of previous slide - see if it activates complement... and so forth