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Hypersensitivity & Immunodeficiency Flashcards

1
Q

Type 1 hypersensitivity is [time frame], [Ig]-mediated, and can lead to anaphylaxis

A

Type 1 hypersensitivity is immediate, IgE-mediated, and can lead to anaphylaxis

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2
Q

Type 1 hypersensitivities always begin with [stage]

A

Type 1 hypersensitivities always begin with sensitization

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3
Q

Asthma and allergic rhinitis are examples of [Type] hypersensitivity

A

Asthma and allergic rhinitis are examples of Type 1 hypersensitivity

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4
Q

In a type 1 hypersensitivity reaction, mast cells are activated by _

A

In a type 1 hypersensitivity reaction, mast cells are activated by cross-linking of bound IgE

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5
Q

The immediate response in a T1 hypersensitivity reaction involves activation of mast cells followed by release of _

A

The immediate response in a T1 hypersensitivity reaction involves activation of mast cells followed by release of pre-formed granules (histamine, proteases)
* This immediate phase is what can cause anaphylactic shock

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6
Q

Histamine effects include:
* Smooth muscle _
* Vascular permeability _
* Vascular smooth muscle tone _
* Mucus secretion _
* Pruritus

A

Histamine effects include:
* Smooth muscle contraction (wheezing)
* Vascular permeability increases (swelling, hives)
* Vascular smooth muscle tone decreases (hypotension)
* Mucus secretion increases
* Pruritus

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7
Q

Also part of the immediate response, _ and _ are synthesized and act as potent bronchial constrictors and increase vascular permeability

A

Also part of the immediate response, prostaglandins and leukotrienes are synthesized and act as potent bronchial constrictors and increase vascular permeability
* Neutrophils and macrophages also get recruited to the site

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8
Q

The release of [cytokine] from Th2 cells stimulates eosinophils

A

The release of IL-5 from Th2 cells stimulates eosinophils

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9
Q

The late phase of a T1 hypersensitivity reaction is focused on synthesizing _ to further amplify the immune response

A

The late phase of a T1 hypersensitivity reaction is focused on synthesizing cytokines to further amplify the immune response

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10
Q

Mast cells make [cytokines] in the late phase

A

Mast cells make IL-4, IL-5, IL-13, TGF-b in the late phase
* IL-5 recruits eosinophils which further tissue damage

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11
Q

(True/False) Chronic urticaria is Ig-E mediated

A

False; if the patient has hives daily/ continuously it cannot be IgE-mediated
* IgE mediated means immediate response –> degranulation of mast cells
* It then takes time to make granules again

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12
Q

In order to diagnose anaphylaxis, there must be signs of _

A

In order to diagnose anaphylaxis, there must be signs of 2 systems involved
1. Cutaneous
2. Respiratory
3. GI
4. Cardiovascular

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13
Q

(True/False) Only use Epi when a patient has respiratory involvement

A

False; it is anaphylaxis once two systems are involved- don’t wait to use Epi

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14
Q

Epinephrine treats anaphylaxis via its affect as an _

A

Epinephrine treats anaphylaxis via its affect as an alpha and beta agonist
* In addition to treating hypotension and bronchoconstriction it mitigates some mast cell degranulation directly via unknown mechanism

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15
Q

Why are anti-histamines and steroids not indicated for treatment of anaphylaxis?

A

Why are anti-histamines and steroids not indicated for treatment of anaphylaxis?
* Anti-histamines only help the pruritus symptoms and steroids do not work acutely

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16
Q

Steroids are more helpful in the late phase of T1 hypersensitivity; explain

A

Steroids affect transcription in the nucleus which takes time, only helps in the late phase to reduce cytokine synthesis

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17
Q

_ is a monoclonal antibody that binds free IgE to prevent its binding to mast cells and basophils; it can be given to patients with allergies to improve reaction threshold

A

Omalizumab is a monoclonal antibody that binds free IgE to prevent its binding to mast cells and basophils; it can be given to patients with allergies to improve reaction threshold

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18
Q

The first line treatment for allergic rhinitis is _

A

The first line treatment for allergic rhinitis is intranasal steroid (fluticasone, budesonide, triamcinolone)
* Most effective if taken over time, does not work immediately

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19
Q

Azelastine and olopatadine are [drug category] which are second-line options for allergic rhinitis

A

Azelastine and olopatadine are intranasal antihistamines which are second-line options for allergic rhinitis
* Work immediately but only 50% as effective as intranasal steroids

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20
Q

Cetirizine, fexofenadine, and loratadine are [drug category] which are third-line options for allergic rhinitis

A

Cetirizine, fexofenadine, and loratadine are 2nd gen antihistamines which are third-line options for allergic rhinitis
* Minimal effect on congestion

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21
Q

[Drug class] should not be used for more than 3 days in a row due to risk of rebound vasodilation, “rhinitis medicamentosa”

A

Intranasal alpha-agonists (Oxymetazoline) should not be used for more than 3 days in a row due to risk of rebound vasodilation, “rhinitis medicamentosa”
* Generally avoid

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22
Q

Albuterol is a drug that improves asthma via _

A

Albuterol is a drug that improves asthma via beta-agonism

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23
Q

Allergic contact dermatitis is primarily mediated by [cells]

A

Allergic contact dermatitis is primarily mediated by CD4+ T cells
* Poison ivy reaction is another example

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24
Q

Type 4 hypersensitivity is a [time frame], _ mediated reaction

A

Type 4 hypersensitivity is a delayed, T cell mediated reaction
* Time course 24-72 hours

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25
When CD8+ cells recognize foreign cells they release _ and _ to perforate the cell membrane and induce apoptosis
When CD8+ cells recognize foreign cells they release **perforin** and **granzymes** to perforate the cell membrane and induce apoptosis
26
Dendritic cells present antigen that is recognized by CD4+ cells which secrete _ and _ to activate CD8+ cells and macrophages in a type 4 hypersensitivity reaction
Dendritic cells present antigen that is recognized by CD4+ cells which secrete **IL-2** and **IFN-gamma** to activate CD8+ cells and macrophages in a type 4 hypersensitivity reaction
27
_ is the test used for evaluation of contact dermatitis
**Patch testing** is the test used for evaluation of contact dermatitis
28
SJS/TEN is a severe cutaneous adverse reaction in which skin sloughs off, DRESS stands for _ ; both are Type 4 reactions involving T cells
SJS/TEN is a severe cutaneous adverse reaction in which skin sloughs off, DRESS stands for **drug rash with eosinophilia and systemic symptoms** ; both are Type 4 reactions involving T cells * SJS: 1-4 weeks * DRESS: 2-6 weeks
29
Transfusion reactions are an example of [Type] hypersensitivity
Transfusion reactions are an example of **Type 2** hypersensitivity
30
Glomerulonephritis, RA, and SLE are examples of [Type] hypersensitivity reactions
Glomerulonephritis, RA, and SLE are examples of **Type 3** hypersensitivity reactions
31
B lymphocytes, aka "humoral immunity" is most important in fighting _ infections
B lymphocytes, aka "humoral immunity" is most important in fighting **bacterial** infections * *Without humoral immunity expect chronic sinusitis and pneumonia*
32
T lymphocytes or cell-mediated immunity is most important in fighting _ infections
T lymphocytes or cell-mediated immunity is most important in fighting **fungal and viral** infections * *Particularly important for intracellular pathogens* * Also helps in bacterial infections
33
When it comes to fighting off skin and surface infections, [immune cells] are most important
When it comes to fighting off skin and surface infections, **granulocytes** (eosinophil, basophil, neutrophil) are most important
34
Recurrent _ or _ infections do not indicate immune deficiency; however other recurrent infections might
Recurrent **UTIs** or **strep throat** infections do not indicate immune deficiency; however other recurrent infections might
35
Warning signs of primary immunodeficiency include: * More than _ ear infections in a year * More than _ sinus infections in a year * More than _ pneumonias in a year
Warning signs of primary immunodeficiency include: * More than **4** ear infections in a year * More than **2** sinus infections in a year * More than **2** pneumonias in a year *Really you should have concern if you see infections equal to or greater than these numbers*
36
Lack of antibodies will lead to recurrent bacterial infections, especially with _ type bacteria
Lack of antibodies will lead to recurrent bacterial infections, especially with **encapsulated** bacteria * *SHiN: Strep pneumo, H flu, Neisseria meningitidus*
37
The most common B-cell deficiency is _
The most common B-cell deficiency is **IgA deficiency** * Recall that IgA is in the mucosa * Many cases asymptomatic or presents with sinopulmonary infections or anaphylaxis to blood * Associated with celiac, GI disorders
38
The most common symptomatic immune deficiency is _
The most common symptomatic immune deficiency is **common variable immune deficiency (CVID)**
39
Symtoms of CVID most commonly present at age _
Symtoms of CVID most commonly present at age **20-40** * Presents with recurrent sinopulmonary infection * Bronchiectasis affects 30-50% of patients
40
CVID is caused by _
CVID is caused by **faulty B cell differentiation into plasma cells**
41
How do you work up a possible B-cell deficiency?
42
DiGeorge is caused by chromosome deletion at _ ; it is [inheritance pattern]
DiGeorge is caused by chromosome deletion at **22q11** ; it is **autosomal dominant**
43
DiGeorge syndrome is ultimately caused by a failure of _ development
DiGeorge syndrome is ultimately caused by a failure of **pharyngeal pouch** development, *pouches 3, 4* * Pouch 3 --> **thymus + inferior parathyroid** * Pouch 4 --> **superior parathyroid**
44
The downstream effect of absent thymus is _
The downstream effect of absent thymus is **improper T cell differentiation** * *Recall that the T cells go from bone marrow --> thymus to mature* * These patients get recurrent viral infections and CMV, EBV, JC virus, VZV + fungal infections, Candida, PJP, Crypto
45
The mneumonic to remember DiGeorge symptoms is _
The mneumonic to remember DiGeorge symptoms is **CATCH22** * Cardiac * Abnormal facies * Thymic hypoplasia * Cleft palate * Hypoparathyroidism * Chromosome 22q11
46
SCID is often caught in newborns but at least seen by _
SCID is often caught in newborns but at least seen by **year 2 of life** * *Recall that newborns get maternal antibodies for the first 6 months*
47
Signs of SCID
SCID presents with: * Recurrent, severe infections (T cell, B cell, NK cell dysfunction) * Chronic diarrhea, failure to thrive * Absence of lympoid tissue (tonsils, adenoids, axilla)
48
The most common cause of SCID is a _ defect which is [inheritance pattern]
The most common cause of SCID is a **IL-2 receptor gamma chain** defect which is **X-linked recessive**
49
The less common, autosomal recessive form of SCID is caused by _
The less common, autosomal recessive form of SCID is caused by **ADA deficiency** * Build up of metabolic toxins that destroy T and B cells
50
MMR is a [type] vaccine
MMR is a **live attenuated vaccine**
51
Varicella is a [type] vaccine
Varicella is a **live attenuated** vaccine
52
Live attenuated vaccines induce [immune response]
Live attenuated vaccines induce **humoral IgG** and **cellular** * MHCI presents pathogen to CD4+ * CD4+ activates B cell and allows class switching --> IgG * Dendritic cell can be infected and also present via MHCII --> cellular response
53
Whole inactivated vaccines will induce [immune] response
Whole inactivated vaccines will induce **humoral IgG** response * *Cannot infect the dendritic cells to trigger cellular response (CD8+)* * However, can be presented via MHC-I, activate CD4+, class switch
54
Subunit protein inactivated vaccines induce [immune] response
Subunit protein inactivated vaccines induce **humoral IgG** response * *Cannot infect the dendritic cells to trigger cellular response (CD8+)* * However, can be presented via MHC-I, activate CD4+, class switch
55
Subunit polysaccharide inactivated will induce [immune response]
Subunit polysaccharide inactivated will induce **humoral IgM only** * *Its an inactivated vaccine, so it cannot infect dendritic cell = no MHC-II and no cellular response* * *MHC I can only present protein so it cannot present it either; no class switching, IgM only*
56
Subunit polysaccharide + conjugate inactivated vaccines will induce [immune response]
Subunit polysaccharide + conjugate inactivated vaccines will induce **humoral IgG** * *Because the polysaccharide has been conjugated to a protein we can get class switching*
57
The MMR and varicella vaccine can be given to HIV+ patients if CD4+ cell count is at least _
The MMR and varicella vaccine can be given to HIV+ patients if CD4+ cell count is at least **200** * *Live vaccines are contraindicated in pregnancy and patients with immunodeficiency because they can revert to a virulent form*
58
[Coombs test] detects antibodies attached to the RBC surface
**Direct coombs test** detects antibodies *directly* attached to the RBC surface
59
[Coombs test] detects presence of unbound antibodies in the serum
**Indirect coombs test** detects presence of unbound antibodies in the serum
60
Rheumatoid arthritis is an example of a [hypersensitivity reaction]
Rheumatoid arthritis is an example of a **type III hypersensitivity**
61
[Transfusion rxn] involves urticaria, pruritis, wheezing, hypotension, respiratory arrest within minutes to 3 hours of receiving blood products
**Allergic/anaphylactic reaction** involves urticaria, pruritis, wheezing, hypotension, respiratory arrest within minutes to 3 hours of receiving blood products
62
Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinuria, and jaundice within 24 hours of blood transfusion may be [transfusion reaction]
Fever, hypotension, tachypnea, tachycardia, flank pain, hemoglobinuria, and jaundice within 24 hours of blood transfusion may be **acute hemolytic transfusion reaction**
63
Acute hemolytic transfusion reaction is a [type HS reaction]
Acute hemolytic transfusion reaction is a **type II hypersensitivity** * *Which typically causes intravascular hemolysis- hemoglobinuria*
64
Acute hemolytic transfusion reactions typically occur secondary to _
Acute hemolytic transfusion reactions typically occur secondary to **ABO blood group incompatability**
65
[Transfusion reaction] occurs when cytokines created by donor WBCs accumulate during storage of blood products
**Febrile nonhemolytic transfusion reaction** occurs when cytokines created by donor WBCs accumulate during storage of blood products
66
Febrile nonhemolytic transfusion reactions will present as _
Febrile nonhemolytic transfusion reactions will present as **fever, headachem chills, fushing within 1-6 hours** * *From preformed cytokines*
67
Respiratory distress and noncardiogenic pulmonary edema following a transfusion is likely _
Respiratory distress and noncardiogenic pulmonary edema following a transfusion is likely **Transfusion related acute lung injury (TRALI)**
68
Transfusion related acute lung injury (TRALI) occurs due to _
Transfusion related acute lung injury (TRALI) occurs due to **neutrophil activation by a product in the blood --> inflammation --> pulmonary edema** * *Neutrophils sequestered in pulmonary vasculature get released*
69
[Transfusion rxn] is a response to a foreign antigen on donor RBCs that was previously encountered by recipient and presents within 1-2 weeks
**Delayed hemolytic transfusion reaction** is a response to a foreign antigen on donor RBCs that was previously encountered by recipient and presents within 1-2 weeks
70
Thrombosis of graft vessels is most indicative of [transplant rejection]
Thrombosis of graft vessels is most indicative of **hyperacute transplant rejection** * Pre-existing recipient antibodies
71
Vasculitis of graft vessels is most indicative of [transplant rejection]
Vasculitis of graft vessels is most indicative of **acute transplant rejection** * Cellular or humoral response
72
[Transplant rejection] is dominated by arteriosclerosis
**Chronic transplant rejection** is dominated by arteriosclerosis
73
Graft-vs-host disease is caused by _
Graft-vs-host disease is caused by **grafted immunocompetent T cells proliferating in the host and targeting host**
74
Name (3) B cell disorders and what patients most often present with
1. **Bruton agammaglobulinemia**: defect in BTK results in no B-cell maturation --> recurrent bacterial and enteroviral infection after 6 months of age 2. **Selective IgA deficiency** mostly asymptomatic; GI infections, atopy/anaphylaxis/autoimmune 3. **Common variable immunodeficiency** defect in B-cell differentiation --> sinopulmonary infections, increased risk of autoimmune
75
_ is a deficiency of Th17 cells due to STAT3 mutation which impairs the recruitment of neutrophils to sites of infection
**Autosommal dominant hyper-IgE syndrome** is a deficiency of Th17 cells due to STAT3 mutation which impairs the recruitment of neutrophils to sites of infection * *Also called Job syndrome*
76
Failure to thrive, chronic diarrhea, thrush, and recurrent infections (all kinds) is a common presentation of _
Failure to thrive, chronic diarrhea, thrush, and recurrent infections (all kinds) is a common presentation of **SCID** * *Also decreased TRECs, absent thymic shadow and germinal centers*
77
Hyper IgM syndrome is most commonly due to defective _
Hyper IgM syndrome is most commonly due to defective **CD40L on Th cells** * *Will present with severe pyogenic infections early in life*

Integrated systems (8 decks)

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