Immune Response and Altered Immunity

1. type I: allergy

2. type II: cell/tissue targeted

3. type III: circulating cells and immune-complex precipitates in capillaries

4. type IV: cytotoxic t-cell mediated, delayed hypersensitivity reactionAntib

Four types of hypersensitivity reactions:

IgE

Antibody involved in allergies

Atopic individuals

Individuals with a genetic predisposition to produce IgE to an allergen

Anaphylaxis

severe allergic reaction

On the second exposure. After the first, IgE sits on mast cells and basophils and waits for antigen (allergen)

when does first allergic reaction happen? why?

the allergen binds to IgE on mast cells and basophils. The mast cells/basophils degranulate, releasing histaminelocal

How do allergic reactions happen on the second/subsequent exposures?

Local: angioedema, uticaria

Anaphylactic: widespread edema, pulmonary edema

increased vascular permeability symptoms (local and anaphylactic) in allergy

local: local redness and warmth

anaphylactic: flushed, warm shock, hypotension

vasodilation symptoms (local and anaphylactic) in allergy

local: depends on area (ex: diarrhea)

Anaphylactic: bronchoconstriction (wheezing), tracheal constriction (stridor), increased peristalsis (vomiting and diarrhea)

smooth muscle contraction symptoms (local and anaphylactic) in allergy

local mucous production

anaphylactic: widespread mucous

goblet cell symptoms (local and anaphylactic) in allergy

vomiting

histamine2 receptors stimulated in the stomach during allergies leads to what?

1. increased vascular permeability

2. vasodilation

3. smooth muscle contraction

4. stimulates goblet cells

5. stimulates itch receptors

6. stimulates H2 receptors in the stomach

actions of H1 in allergies [6]

uticaria

medical name for hives

1. local allergy testing

2. serum IgE levels to specific antigens

allergy tests [2]

epinephrine injection IM

Main treatment for anaphylaxis

if the antigen (allergen) is similar

cross-sensitivity occurs in allergies if what?

–Warm, flushed skin (vasodilation)

–Systemic angioedema, urticaria (increased vascular permeability)

–Bronchial, laryngeal, tracheal spasm (smooth muscle contraction)

–Pruritus (stim. of itch receptors)

–Low BP (vasodilation, low PVR, relative hypovolemia)

–GI upset (stim of smooth muscle)

early S+S of anaphylaxis: [6]

•decreased BP, increased HR, cool pale skin, diaphoretic,

•decreased urine output, increased RR, altered LOC

•…with peripheral edema, bronchospasm

HPA and fluid shift symptoms of early anaphylaxis:

•Epinephrine (IM)…stops release of H₁ (stabilizes basophils/mast cells)

•Stop exposure

•Airway management

•IV fluids and oxygen

•Antihistamines (blocks action of circulating H₁)

•Steroids (reduce inflammation)

•Bronchodilators

•H₂ Receptor Antagonists

Anaphylaxis treatment [7]

Epinephrine IM stops the release of histamine and stabilizes basophils/mast cells

How does epinephrine treat anaphylaxis

Blocks action of circulating histamine

how do antihistamines treat anaphylaxis/allergies?

the target is a cell or tissue antigen.

Target in type II hypersensitivity reactions:

IgM/IgG

Mediators in type II hypersensitivity reactions: [2]

Compliment and ag-depending cytotoxic T-cells

IgM/IgG causes antigen-antibody complex to activate what? [2]

Damage to target cell and inflammation

Result of compliment and cytotoxic t-cells in type II hypersensitivity reactions:

Grave’s disease (target is the thyroid)

Example of a type II hypersensitivity reaction:

The antigen in circulation. A worse reaction than type II

Target in type III hypersensitivity reactions:

Forms in the blood and precipitates out in capillary beds in tissues (kidneys, joints, skin, lungs, heart)

In type III reactions, where do Ag-Ab complexes form?

Compliment. Attracts WBCs. It degranulates basophils so histamine1 is released. Tissue around complex gets damaged. prostaglandin synthesis

In type III reaction, Ag-Ab complexes activate what, causing what to be released? [4]

Raynaud disease, celiac

examples of type III hypersensitivity reactions:

Gluten. Not an allergy because not IgE mediated. Si

what is the antigen in Celiac disease?

Largely related to inflammation and loss of tissue function from

1. destroyed target cells in type II

2. injured and destroyed capillaries/tissues/organs in type III

Signs and symptoms of type II and III reactions come from what? [3]

anti-B

Type A blood has which antibodies?

anti-A

Type B blood has which antibodies?

None

Type AB blood has which antibodies?

anti-A and anti-B

Type O blood has which antibodies?

None

Rh+ blood has which antibodies?

anti-Rh

Rh- blood has which antibodies?

none

Rh- blood will have which antigens?

None

O blood will have which anitgens?

1. degranulates basophils, causing release of histamine1

2. pokes holes in donor RBC (target tissue, but also circulating in blood)

Complement causes what to happen in type II ABO transfusion reaction?

1. hemolysis: decreased RBCs to carry O2

2. Free Hgb in urine

3. Increased circulating bilirubin

Complement poking holes in donor blood (transfusion rxn) causes what to happen? [3]ABO

1. hypotension

2. flushing

3. uticaria

4. hypoxia

5. fever

6. hemolytic anemia (maybe)

7. jaundice (maybe)

ABO transfusion rxn (type 2) s+s: [7]

Increased vascular permeability

What causes uticaria (hives)?

Immune complexes precipitate out into capillaries in kidneys, lungs, joints, skin, heart. INcreased inflammation in these areas

How does a transfusion reaction become type III?

1. flank pain

2. chest or back pain

3. SOB

4. joint pain

5. S+S of affected organ damage

S+S of type III ABO transfusion rxn: [5]

1. CNS toxicity

2. Jaundice

excess unconjugated bilirubin (type III transfusion rxn) can lead to what? [2]

Spleen enlargement

increased clearance of RBC debris in type III transfusion rxn can lead to what?

Hgb is a large molecule, damages nephron when trying to excrete. Renal damage.

trying to excrete Hgb in type III transfusion rxn can cause what? why??

1. S+S

2. re-test blood for ABO incompatibility

3. Hgb in the urine

Diagnosis of transfusion reaction: [3]

1. IV fluids to correct hypotension and clear hemoglobinuria

2. o2

Treatment for transfusion reaction: [2]

Rh

Which incompatibility is more severe: Rh or ABO?

Febrile non-hemolytic reaction

Transfusion reaction related to WBC reaction and not Ag-Ab

Hemolytic disease of newborn

Rh- mother has Rh+ baby for the second time. Maternal IgG crosses placenta, reacts to fetus. RBCs in the fetus get destroyed in the spleen.

anemia with excess erythroblasts and excess free hgb, so fetus gets increased bilirubin and jaundice

Hemolytic disease of Newborn results in what in the fetus?

KernicterusDiagn

CNS damage from excess bilirubin

1. S+S

2. Coombs test to detect anti-human Abs

3. bilirubin

4. blood group incompatibility

Diagnosis of hemolytic disease of newborn: [4]

Rhogam. Neutralizes fetal Rh antigen at exposure so mother does not form Anti-Rh antibodies

prevention of hemolytic disease of newborn:

Type IV hypersensitivity reactions:

Cytotoxic t-cell mediated hypersensitivity reactions. A delayed hypersensitvity that appears days post exposure.

1. transplant rejection

2. type I DM

3. contact dermatitis

4. reaction to vaccine/drug

Examples of type IV hypersensitivity reactions: [4]

Destruction of the target tissue

S+S from type IV hypersensitivity reactions are related to what?

Autoimmunity

Breakdown in tolerance to self anigens. Develop antibodies against self

Antibodyto antigen on GI mucosal cells

Antibodiy in Inflammatory bowel disease

Antibody to synovium antigen of joints (also antibody to iris, blood vessels, pleura)

Antibody in rheumatoid arthritis:

Antibody to DNA antigen so multi-system(all organs)

antibody in systemic lupus erythematosus (SLE)

antibody to spinal tissue antigen

antibody in ankylosing spondylitis:

Antibody to ACH receptor antigen

antibody in myasthenia gravis:

inflammation (prostaglandins) and compliment

which mediators cause tissue destruction and S+S

scar tissue formation

results in a loss of function in autoimmune disease

via blood and bodily fluids (including placenta, childbirth, breastmilk)

how is HIV transmitted?

1. attaches to CD4 receptors on helper T cells and enters cells

2. takes over host ribosome to produce new HIV

3. some DNA inserted into host genome and lies dormant

4. When reactivated, reproduces and ruptures helper cells to release new viruswhy

How does HIV invade cells?

T and B cells, lymphocytes, and macrphages are affected. Loss of immunity and inflammation

why are HIV patients more susceptible to infections?

1. colon, duodenum, rectum (weight loss and malnutrition)

2. Skin cells (Kaposi’s sarcoma)

3. Brain glial cells (dementia)

Cells affected in HIV: [3]

CD4 <500 (normal: 500-1200)

immunosuppression by HIV is defined when:

mild flu-like illness

Initial HIV infection S+S

200

risk of opportunistic infections happen when CD4 is below:

antibody produced like any viral exposure, but not protectice in HIV. Produced against a “decoy” antigen

Antibody produced in first HIV exposure:

lack of cell-mediated immunityy to infection because of a loss o necessary helper t cells and WBCs

How is HIV virus allowed to spread?

Seropositive. Means teere has been an exposure to HIV but do not have AIDS

blood test for HIV antibody

6 months

Window period for HIV