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int med exam 0828 > Allergy and Immunology > Flashcards

Allergy and Immunology Flashcards

1
Q

Describe the innate immune system and its 3 main components of the innate immune system?

A

rapid-acting, non-specific no memory with complement, macrophages, and NK cells.

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2
Q

what are the two parts of the adaptive immune system?

A
  1. Humoral: B-cells, plasma cells, and immunoglobulins
  2. Cell-Mediated: T-cells, activated macrophages and NK cells.
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3
Q

what are the components of myeloid cells?

A
  • Granulocytes (neutrophils, basophils, eosinophils)
  • Antigen-Presnting cells (monocytes/macrophages/dendritic cells)
  • Others: mast cells, erythrocytes, platelets
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4
Q

where are MHC cells located?

A

chromosome 6

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5
Q

what are class I HLA antigens?

A
  • these are types of MHC to differentiate self vs. nonself
  • Class I includes HLA-A/B/C on most nucleated cells
  • Present non-self material to CD8 T cells and play role in transplant rejection, neoplasms, and viral infections
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6
Q

what are class 2 HLA antigens?

A
  • HLA-DP/DQ/DR
  • On antigen-presenting cells
  • mediate reaction between macropahges, T and B-cells
  • CD4 cells recognize material presented only on Class 2 HLA antigens
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7
Q

what are class 3 HLA antigens?

A

consist of a few cytokines like TNF and lymphotoxin, some complement structures

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8
Q

what are the CD markers for T-cells/

A

CD2, CD4, CD4 and CD8

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9
Q

What are the types of CD4 cells?

A
  • TH1 - Activates CD8 cells and leads to cell-mediated immunity
  • TH2 - activates B cells to produce antibody and leads to humoral immunity
  • Th17- plays in role in immunity against fungi, bacteria, and in auto-immune disorders
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10
Q

what is the role of CD8 T-cells?

A

cytotoxic T cells, important against viruses and neoplastic cells.

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11
Q

what are natural killer T-cells?

A

they have the CD16 and CD56 like natural killer lymphoid cells but has a MHC molecule of CD1 which recognizes primarily lipids and glycolipids

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12
Q

describe the B-cell lineage and diseases associated in the blood and bone marrow?

A
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13
Q

describe the B-cell lineage and diseases associated in the periphery?

A
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14
Q

describe the B-cell lineage and diseases associated in the bone marrow?

A
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15
Q

what are eosinophils involved with?

A

allergic reactions and immunologic defense of parasites

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16
Q

what are the 3 antigen-presenting cells?

A
  • b-cells (most specific)
  • monocytes/macrophages - eat opsonized cells, stimulate interleukin 1, which stimulates T-cells
  • Dendritic cells - ingest pathogen, change conformation, travel to lymph node and activate lymphocytes
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17
Q

key things about IgG?

A
  • contains kappa and lambda light chains
  • crosses placenta
  • activates complement
  • Main antibody in serum
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18
Q

Key things about IgA?

A
  • main igG in secretions
  • Has 2 immunoglobulins (dimer) with J chain and secretory component
  • Main igG secreted in breast milk
  • Does not activate complement
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19
Q

Key things about IgM?

A
  • 1st immunoglobulin produced in infection
  • pentamer
  • Useful in dx of recent illness
  • Activates complement
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20
Q

what are the 3 complement pathways and leads to?

A
  • classical pathway
  • Lectin (mannose-binding) pathway
  • Alternative pathway
  • These all lead to the common terminal pathway (membrane attack complex)
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21
Q

what function do the 3 complement pathways all perform?

A
  1. opsonizing target cells with C3b
  2. inducing more inflammation with anaphylatoxins C3a, C4a, and C5a
  3. forming the “membrane attack complex”
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22
Q

describe the classical complement pathway?

A
  1. immunoglobulin (IgG/IgM) activate the classical pathway.
  2. C1 complex (q,r,s subunits) initiates response when a C1q subunit attaches to the antibody in an antigen-antibody complex
  3. C1q binds to Fc portion at least 2 igGs for 1 IgM.
  4. Binding activate C1q
  5. Activated C1q cleaves C2 and C4 forming C4b2A (c3 convertase)
  6. Activates C3
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23
Q

Describe the common terminal pathway?

A
  • C3 when combined with either factor C4b2a or factor b activates C5
  • Cause formation of C5-C9 MAC
  • Mac pokes hole in bacterial cell membranes and cause the bacteria to lyse
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24
Q

What condition is associated with C1 inhibitor? clinical presentation?

A
  • Hereditary angioedema is an autosomal dominant disorder caused by a decrease in C1 inhibitor activity?
  • recurrent non-pitting edema with each episode lasting 1-3 days
  • NO ITCHING or urticaria
  • Attacks may include laryngeal obstruction and affect GI tract (abdominal pain)
  • minor trauma from dental procedures can precipitate attacks
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25
Q

how would you diagnose hereditary angioedema?

A
  • First, check C4 levels, which would be low
  • Check C1-INH functional assay
  • If C4 and C1-INH low, type I HAE
  • If C4 low, and C1-INH normal, it is due to non-functional C1-INH, then it’s type 2.
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26
Q

what is the treatment of hereditary angioedema?

A
  • Epinephrine is not effective
  • Androgens (danazol) increase C1-INH levels and decrease swelling episodes (preventative med)
  • Can use kallikrein inhibitor and bradykin receptor antagonist for acute attacks
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27
Q

what does C1, C2, or C4 deficiencies cause?

A
  • decreased activation of complement via the classical pathway.
  • Can have recurrent sinopulmonary disease with encapsulated bacteria
  • increased incidence of rheumatoid diseases (SLE)
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28
Q

what do C3 deficiency presentation?

A

C3 is complete absence, results in severe pyogenic (bacterial) infections

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29
Q

how do you diagnose C5-C9 MAC deficiency? what is the presentation?

A
  • called terminal complement deficiency
  • Results in increased Neisseria meningococcal/gonococcal infections (especially meningitis/septicemia)
  • Screen for terminal complement deficiency with CH50
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30
Q

what does CH50 assay measure?

A
  • measures total complement hemolytic activity of the classical pathway
  • CH50 assay levels can still be normal even if C3 or C4 levels are lower
  • Good screen for complement deficiencies
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31
Q

what are the 3 conditions that result in immune complexes that are INCREASED in the seurm?

A
  • Hepatic vein thrombosis (Budd-Chiari)- decreased clearance
  • PNH - - results in decreased binding
  • SLE - results in a decreased amount of CRI on RBCs
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32
Q

what are the four types of hypersensitivities?

A
  1. Type I: IgE mediated - immediate (anaphylactic, atopic)
  2. Type II: IgG or IgM mediated - cytotoxic
  3. Type III: immune complex (antibody-antigen) mediated
  4. Type IV: Cell-mediated - delayed-type
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33
Q

Describe the classic response of type I hypersensitivity acute response? mechanism?

A
  • acute phase of immediate IgE hypersensitivity reactions within 1 hour after exposure
  • allergen reacts to FAB portion of IgE causing mast cell stimulation, releasing histamine
  • Measure tryptase to confirm anaphylactic reactions
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34
Q

Describe the histamine receptors?

A
  • H1: receptor activation causes the wheal and flare, bronchoconstriction and puritis
  • H2: receptor activation causes increased gastic acid
  • H3: activation causes decreased histamine synthesis and release (negative feedback)
  • H4: immunomodulatory effect and affects eosinophil and mast cell recruitment
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35
Q

Describe the late-phase response of type I hypersensitivity? mechanism?

A
  • late phase response occurs 3-12 hours after acute response, lasting hours to days.
  • Caused by an immediate IgE reaction stimulating synthesis of cytokines, recruitment of eosinophils and basophils
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36
Q

how do you diagnose anaphylaxis?

A

1 of 3 criteria of either:

  1. Sudden onset of skin/mucosal tissue with either sudden respiratory symptoms or hypotension
  2. 2 or more following exposure of skin/mucosal involvement, respiratory involvement, GI symptoms, hypotension
  3. Hypotension after exposure to a known allergen.
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37
Q

what is the tx for anaphylaxis?

A
  1. Epinephrine 1:1000 IM
  2. H1 and H2 antiganoists (diphenhydramine/cimetidine)
  3. steroids may help prevent delayed late-phase reactions
  4. If significant hypotension, Epi 1:10K IV
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38
Q

what do you need to watch out for in treating anaphylaxis?

A
  • Epinephrine affects alpha and beta-adrenergic systems.
  • If the patient is on beta-blockers, these are relatively contraindicated in patients at risk for anaphylaxis
  • Can give glucagon or vasopressin injections after epinephrine is given
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39
Q

what are type 2 hypersensitivity reactions?

A
  • Type 2 reactions occur when an IgG or IgM antibody binds to a fixed tissue antigen or cell receptor creating autoantibodies.
  • Binding of antibody results in target cell destruction via complement
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40
Q

what are examples of type 2 reactions involving fixed tissue antigens?

A
  • Goodpasture - target antigen is basement membrane of lung and kidney
  • Myasthenia gravis - AcH receptors on muscle cells
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41
Q

what type hypersensitivity reactions are vasculitis?

A

type 3

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42
Q

what are type 3 hypersensitivity reactions?

A
  1. antibody (usually IgG) reacts with target antigen to form immune complexes that precipitate and activate complement with subsequent small vessel inflammation and necrosis.
  2. start to see more antigen than antibody then IC form and quickly cleared
  3. IC interlace and become bigger/less soluble, precipitates in small vessels
  4. Complement is activated, cytokines, see leukocytoclastic vasculitis (hemorrhagic indurated lesions)
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43
Q

what are the 2 models for what happens clinically in type 3 HSN?

A
  1. Serum sickness with systemic activation, within 1-2 weeks, necrotic vasculitis
  2. Arthrus reaction - IC at injection site, within 4-12 hours, painful indurated lesions appears and may progress to sterile abscess
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44
Q

what is the difference between type i and type IV HSN?

A
  • Type 1 is food and occurs earlier
  • Type 2 - contact dermatitis, tuberculin sensitivity, peaks 24-72 hours
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45
Q

what is the difference between type 2 and type 5 HSN?

A
  • type V has autoimmune IgG has a stimulatory effect on receptor while type 2 has a destructive effect.
  • Graves is type 5
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46
Q

what causes cholinergic urticaria?

A
  • precipitated by heart
  • presents as punctate lesions that are pruritic.
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47
Q

what is chronic urticaria?

A

hives last >6 weeks, resolves to minute to hours or migrates to other areas. check for thyroid antibodies.

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48
Q

what is urticarial vasculitis?

A

urticaria that lasts >24 hours in a fixed location, dx ith skin biopsy.

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49
Q

what is vasomotor rhinitis?

A

sneezing attacks followed by nasal congestion on exposure to a stimuli

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50
Q

what is rhinitis medicamentosa?

A

rebound congestion caused by prolonged use of vasoconstricting nasal drops (phenylephrine or oxymetazoline). Treat by stopping drug.

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51
Q

what is atrophic rhinitis?

A

atrophy of nasal mucosa, crusting, fetor, loss of smell.

patients are typically younger and from warmer climates

some are colonized by klebsiella ozanae

treat with nasal saline lavage

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52
Q

what is the tx of rhinitis?

A

antihistamines is first line

intranasal steroids are the most effective for allergic rhinitis

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53
Q

what are the first generation H1 blockers? Side effects?

A
  • diphenhydramine, chlorpheniramine, and hydroxyzine
  • cross BBB, interacts with acetylcholine receptors causing blurry vision, dry mouth, and urinary retention
  • Avoid in elderly
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54
Q

which rhinitis medications can you use in pregnancy?

A
  • H1: chlorpheniramine, diphenhydramine, tripelenamine
  • H2: lortaradine and cetirizine
  • monteleukast, cromolyn, and budenosine (preferred)
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55
Q

why should you avoid oral decongestants in pregnancy?

A
  • can cause congenital malformations like gastroschisis and small intestine atresia.
  • Gastroschisis is where baby’s small intestines grow outside the abdomen through hole near belly button.
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56
Q

what are the 2 major components of assessing asthma control?

A

impairment (symptoms) and risk (exacerbations)

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57
Q

step up therapy for asthma for which of the following (simple)?

A
  1. symptoms during the day>2x/week
  2. night time awakenings >2x/month
  3. ED visits/admissions >2x/year
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58
Q

describe the difference between SJS and TENs?

A
  • SJS = epidermal detachment <10%
  • Overlap syndrome 10-30%
  • TEN = >30%
59
Q

what is DRESS syndrome?

A
  • Drug rash with eosinophilia and systemic symptoms
  • occur 2-8 weeks after exposure
  • typically anti-convulsants, minocycline, and allopurinol
  • can see the reactivation of HHV6
  • Symptoms may worsen after stopping drug
  • Glucocorticoids and IVIG are beneficial
60
Q

what symptoms do you see SJS/TEN?

A
  • severe sloughing away of the burn
  • mucosal involvement eyes, mouth and lips
  • Nikolsky sign - removal of epidermis with slight tangential pressure
  • IVIG may be beneficial
  • glucocorticosteroids are contraindicated.
61
Q

what type of HSN is hypersensitivity pneumonitis?

A

immune complex and cell mediated (3 and 4)

62
Q

what type of HSN is ABPA?

A

IgE and immune complex mediated (type 1 and 3)

63
Q

why does ABPA and hypersensitivity pneumonitis not respond to allergy injections?

A
  • Hypersensitivity pneumonitis is not IgE mediated
  • ABPA can be worsened by allergy injections as they could induce the production of more aspergillus immune complexes.
64
Q

what does a RAST test measure?

A

these are serum tests (CAP-FEIA/RAST) used when skin testing cannot be performed like if patient has :

  • extensive skin disease
  • dermatographism
  • anaphylactic sensitivity to an allergen
  • on-going histamine use (depresses skin test response) that cannot be held for 1-2 weeks
65
Q

what is mastocytosis?

A

abnormal mast cell proliferation and accumulation within various organs

66
Q

what are the 3 types of mastocytosis? Test for diagnosis?

A
  • cutaneous mastocytosis: mast cells only in dermis
  • Systemic mastocytosis: increased mast cells in tissues and organs
  • Malignant mastocytosis: severe systemic symptoms with no skin changes
  • elevated tryptase>20
67
Q

what is urticaria pigmentosa?

A
  • seen in cutaneous and systemic mastocytosis
  • brownish macules
  • formation of wheal upon gentle stroking of macule (darier sign)
68
Q

bruton’s agammaglobulinemia presentation?

A
  • increased susceptibility to pyogenic and encapsulated organisms
  • recurrent sinopulmonary and ear infections
  • okay for fungi and gram negatives
  • more susceptible to enteroviral infections and giardia
69
Q

dx of bruton agammaglobulinemia? tx?

A
  • Ig assay shows very low or no Immunoglobulins
  • No B-cells (no SmIg+ or CD19+)
  • Treat with IVIG
70
Q

what is CVID?

A
  • deficiency of IgG +/- IgA
  • increased susceptibility to encapsulated organisms
  • recurrent sinopulmonary infections and bronchiectasis
  • Can get giardiasis and enterovirus
  • Unlike XLA, increased incidence of autoimmune disease and malignancy
71
Q

Dx of CVID? tx?

A
  • Ig assay showing low IgG +/- low IgA and/or IgM
  • Unlike XLA, CVID patients have mature B cells present (CD19+)
  • Tx with IVIG
72
Q

what is IgA deficiency?

A
  • most common IgG deficiency
  • recurrent sinopulmonary infections
  • recurrent giardiasis
  • association with autoimmune diseases liek celiac and hashimotos
  • Tx with prophylatic abx
73
Q

Wiskott Aldrich syndrome?

A
  • Low IgM and elevated igA and IgE
  • WISK through the EXIT
  • Eczema, x-linked, immunodeficiency, thrombocytopenia
  • tx with bone marrow transplant
74
Q

what is SCID? TX?

A
  • deficiency in b and t cells
  • treat with BMT
75
Q

Digeorge syndrome?

A
  • CATCH 22
  • cardiac
  • Abnormal facies
  • Thymic hypoplasia
  • cleft lip
  • hyopocalcemia
  • chromosome 22
76
Q

what is ataxia telangiectasia?

A
  • AR disease
  • cellular and IgG deficiency
  • recurrent sinopulmonary infections, bronchiectasis, and progressive telangiectasias
  • progressive neurologic deterioration with cerebellar ataxia and mental deterioration
77
Q

what types of cancer is interleukin 2 used to treat?

A
  • lymphokine that activates natural killer T-cells
  • Treat melanoma and RCC
78
Q

what does alpha interferon used to treat?

A
  • generally cytostatic (not cidal)
  • causes symptoms like viral infections
  • used to treat hepatitis C and hairy cell leukemia
79
Q

what are the 2 general dysfunctions in which normal defense mechanisms cause disease?

A
  1. An overexubertant response to foreign antigen
  2. autoimmune disease develops in which the body see a self antigen as foreign
80
Q

what are the 4 types of immunologic hypersensitivity reactions?

A
  1. TYpe I: IgE-immediate (anaphylatic, atopic) - minutes to hours, triggered by foreign allergens w/mast cell degranulation
  2. TYpe 2: IgG or IgM - cytotoxic/auotimmune (thrombocytopenia/hemolytic anemia)
  3. type 3: immune complex (antibody-antigen mediated) - vasculitis/drug fever/serum sickness/arthrus reaction
  4. type 4: delayed, 4 subtypes (a,c,d) - contact dermatitis/TB sensitivity
81
Q

what are the 4 histamine receptors and what does their activation do?

A
  1. H1 - wheal and flare, bronchoconstriction, pruritus
  2. H2: gastric secretions
  3. h3 - histamine synthesis and release (negative feedback)
  4. h4 - immunomodulatory and affects eosinophils and mast cell chemotaxis
82
Q

What are the 4 types of type I responses?

A
  1. Acute response - minutes to hours, mast cell degranulation, the allergen binds Fc portion, histamine release, mastocytosis…
  2. Late response - 3-12 hours, hours to days. caused by an initial immediate IgE reaction that stimulates cytokines and subsequent cellular recruitment of eosinophils and basophils. Results in the eosinophilic inflammatory infiltrate. Think asthmatics
  3. Anaphylaxis - 5-30 minutes, up to 2 hours. Immunologic (IgE, Complement activation with release of C3a, C4a, C5a or non-immunologic (contrast, drugs -vanc/opioids)
83
Q

diagnose anaphylaxis?

A

any one of 3 criteria is fulfilled

  1. Sudden onset with skin/mucosal tissue + hypotension/respiratory symptoms.
  2. >2 organ symptoms after exposure of antigen (skin/mucosal, respiratory, hypotension, GI symptoms)
  3. Hypotension after exposure to known allergen.
84
Q

what is the biphasic phase of anaphylaxis?

A

up to 20% of patients who experience IgE-mediated anaphylaxis have the 2nd episode within 1-30 hours after the initial event, caused by recruitment of inflammatory cells similar to LPR of type I HSN.

85
Q

who must be observed for biphasic response?

A

anyone treated for anaphylaxis or provided with emergency self-medications if discharged.

86
Q

which factors increase likelihood of biphasic phase of anaphylaxis?

A
  1. delayed epi administration
  2. severe initial symptoms
  3. delayed resolution of initial symptoms
  4. co-existence of asthma
  5. oral ingestion of allergens
  6. b-blocker meds
87
Q

what is the treatment for type I HSN?

A
  1. avoidance of the allergen,
  2. antihistamine (occasional glucocorticoids)
  3. allergen -specific immunotherapy (immunotherapy can take up to 1 year, cause an increase in Treg secretion of IL-10 and blocking of IgG isotype. Only IgE mediated reactions benefit. )
88
Q

Anaphylaxis treatment and dose? what happens if refractory hypotension?

A
89
Q

describe type 2 HSN?

A
90
Q

give examples of type 2 HSN target cell receptors and type 2 reactions?

A
91
Q

what is unique about penicillin in terms of HSN reactions?

A

can cause an immediate IgE mediated reaction and delayed IgG mediated reaction

92
Q

describe type 3 HSN?

A
  • immune complex, seen in autoimmune diseases and reaction to drugs.
  • Immune complex form when antibodies combine with antigen (self or foreign)
  • a HSN occurs when an antibody (usually IgG) reacts with antigen to form IC, and precipitates/activates complement with subsequent small vessel inflammation and necrosis.
    *
93
Q

Describe the pathophys of type 3 HSN?

A

Precipitation occurs when there is slight antigen excess in relation to antibody hence occuring in 1-2 weeks, where complement starts to get activated and IC become less soluble.

94
Q

Give examples of type 3 reactions?

A
95
Q

describe type 4 HSN reactions?

A
96
Q

clinically, describe the HSN reactions for:

  1. Contact dermatitis
  2. Chronic allergic asthma/rhinitis
  3. ABPA
  4. hypersensitivity pnuemonitis
A
97
Q

Describe symptoms of serum sickness and arthrus reaction?

A
  1. Serum sickness - systemic reaction in which large amount of antigen injected into a nonimmunized host and within 1-2 weeks, see a necrotic vasculitis, fever, and joint pain.
  2. Arthrus reaction - local reaction when patient is first hyperimmunized (increase in IgGs) and then given a small intradermal injection of the target antigen. Many ICs are made at the injection site, induce complement cascade and inflammatin. Within 4-12 hours, a painful, indurated lesion appears and may progress to a sterile abscess.
98
Q

define acute urticaria vs chronic uticaria?

A
  • superficial blanching transient pruritic wheel-and flare reaction(hives)
  • acute <6 weeks
  • chronic >6 weeks.
  • Treat addresses pruritus and swelling with H1 antihistamine (hydroxyzine) or newer 2nd generation H1 (cetirizine).
  • H2 antihistamines and glucorticoids reserved for refractory urticaria or angioedema
99
Q

describe urticarial vasculitis. Dx, tx?

A
100
Q

what is the presentation and first line tx for atopic dermatitis?

A
  • pruritic, dry thickened scaly rash on flexural skin surfaces.
  • First line tx is moisturizers
101
Q

describe the treatment approach to atopic dermatitis?

A
102
Q

new-onset eczema recurrent and refractory to conventional therapy. Next step?

A

referral to dermatology to r/o cutaneous T-cell lymphoma (mycosis fungoides)

103
Q

what should you do if you have a patient with a linear itchy rash just below the umbilicus where the belt buckle touches the abdomen?

A

order patch testing

104
Q

symptoms of allergic rhinitis?

A
  • congestion, sneezing, rhinorrhea, and nasal itching.
  • Eosinophils appear on nasal smear only when the patient is symptomatic.
105
Q

tx of allergic sinusitis?

A
  • mild - intranasal glucocorticoids
  • moderate/severe or refractory to glucocorticoids - intranasal antihistamine or intranasal histamine + intranasal glucocorticoids
106
Q

tx of allergic sinusitis during pregnancy?

A
107
Q

Describe the following nonallergic rhintiis:

  1. infectious rhintiis - symptoms/cause?
  2. vasomotor rhinitis
  3. NARES
  4. Rhinitis medicamentosa
  5. atrophic rhintiis
A
108
Q

Define acute rhinosinusitis?

A
  • rhinorrhea, nasal congestion, facial pain, and sinus tenderness <4 weeks.
  • clinical diagnosis
  • treat initially with nsaids, nasal saline washes and intranasal glucocorticoids
109
Q

when are antibiotics needed for acute rhinosinusitis? which ones?

A

Given only in the following scenario:

  • Severe initial symptoms with high fever, purulent nasal discharge, and facial pain
  • worsening symptoms after initial improvement (double sickening)
  • persistent symptoms with no improvement after 7-10 days
  • Tx with Augmentin/doxycycline.
110
Q

define chronic rhinosinusitis (CRS)

A
111
Q

what does recurrent episodes of acute sinusitis suggest?

A

selective IgA deficiency. Check an IgA level.

112
Q

describe DRESS syndrome?

A
113
Q

describe SJS/TENs?

A
114
Q

Treatment to decrease likelihood of radiocontrast media reactions?

A

these are non-immunologic reactions to parenteral iodine or gadolinium caused by direct interaction with msat cells. .

115
Q

what are the fruits and vegetables that cross react with latex allergens?

A
116
Q

what are the main risk factors for development of latex allergies?

A
117
Q

basics of hypersensitivity pneumonitis?

A
118
Q

3 types of presentation for hypersensitivity pneumonitis?

A
119
Q

diagnosis and treatment of hypersensitivity pneumonitis?

A
120
Q

presentation and treatment of ABPA?

A
121
Q

which one is better for allergy testing skin vs seurm?

A
122
Q

when is serum testing done in lieu of skin testing for allergies?

A
123
Q

name the live viral vaccines?

A
124
Q

when are live vaccine contraindicated?

A
125
Q

what are the vaccines recommended in pregnancy? which ones are contraindicated?

A
126
Q

which vaccines have interaction with immunoglobulin products? what are the recommended intervals between administration?

A
127
Q

what are mastocytosis and the types?

A
128
Q

how do you diagnosis systemic mastocytosis?

A
129
Q

how do you treat patient’s with cutaneous mastocytosis?

A
  • advise patients to stay away from cold, heat, alcohol, ASA, and opiates
  • oral cromolyn may help GI symptoms
  • Various chemotherapy regimens have been used in the past for systemic and malignant mastocytosis, but not successful.
130
Q

what is eosinophilic eosphagitis? symptoms, dx, and tx?

A
131
Q

what are the inherited immunoglobuin deficiencies?

A
  1. Congenital agammaglobulinemia
  2. CVID
  3. Selective IgA deficiency
  4. Wiskott Aldrich
132
Q

Congenital agammaglobulinemia - presentation, diagnosis, prognosis, tx?

A
133
Q

CVID - presentation, diagnosis, prognosis, tx?

A
134
Q

Selective IgA deficiency - basics

A
135
Q

wiskott-aldrich syndrome?

A
136
Q

patients with acquired humoral deficiencies are predisposed to what type of infections?

A

encapsulated organisms and giardiasis

137
Q

splenectomy and functional asplenia increases risk for what types of infection?

A

pneumococcal/encapsulated, malarial, babesial

138
Q

what are the 3 classic posttransplantation time periods and their associated infection risks?

A
139
Q

Digeorge syndrome?

A
140
Q

big highlights of inherited humoral deficiency?

A
141
Q

describe the CD markers on T-cells?

A
142
Q

Describe interleukins?

A
143
Q
A

int med exam 0828 (24 decks)

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