Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

ICM > Allergies > Flashcards

Allergies Flashcards

1
Q

FOOD ALLERGY

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Examples of IgE immunologic mediated responses.

A

IgE-Mediated

  • Oral allergy syndrome
  • Anaphylaxis
  • Urticaria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Examples of Non-IgE immunologic mediated responses to food?

A

Examples of Non-IgE mediated:

  • Protein-induced enterocolitis/enteropathy
  • Eosinophilic proctitis
  • Dermatitis herpetiformis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Examples of foods that cause a toxic, non-immunologic, response?

A

Toxic non-immunologic:

  • Scromboid fish poisoning
  • Bacterial food poisoning
  • Caffiene
  • Alcohol
  • Histamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Examples of nontoxic (intolerance) non-immunologic reactions to food?

A

Non-toxic, non-immunlogic, reactions:

  • Lactose intolerance
  • Galactosemia
  • Pancreastic insufficiency
  • GB/Liver disease
  • Hiatal hernia
  • Anorexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Top 3 Foods children are allergic to? Overal prevalence?

A

Children:

  • Milk (2.5%)
  • Egg (1.3%)
  • Peanuts (0.8%)

Overal - 6%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What food is most likely to cause allergy in adults?

Overall Allergy in Adults?

A

Adults

  • Shellfish (2%)
  • Peanuts (0.6%)

Overall: 3.7%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is largest antigenic load the body processes?

A

Food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Antigen Absorption:

  • What decreases absorption?
  • What increases absorption?
A

Antigen Absorption?

  • Decreases: presence of other food and increase stomach acidity
  • Increases: presence of alcohol and decrease in stomach acidity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Type I IgE reactions vs. Type II vs. Type IV?

A
  • Type I IgE
    • Sensitization in mast cells of gut
    • Degranulation (mucous secretion, smooth muscle contraction, mucosal edema, and increased absorption of foreign antigens)
  • Type II reactions
    • Ab-dependent thrombocytopenia secondary to milk
  • Type IV
    • Supports role in atopic dermatitis, EGID
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical manifestations of IgE?

A
  • Skin
    • 84% of pts: urticaria, angioedema, atopic dermatitis
  • GI
    • 52%: edema, pruritis of lips/palate/pharynx, N/V
  • Respiratory
    • 32%: rhinitis, dyspnea, wheezing, cought
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

When should anaphylaxis be considered?

Most common reason cited for fatal reaction?

A

Anaphylaxis: 2+ organ systems involved

Fatal reaction: delay in administration of epinepherine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the highest risk foods resulting in anaphylaxis?

A

Anaphylaxis foods:

  • Peanuts
  • Tree nuts
  • Seafood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Fatal food anaphylaxis risks?

Often lack what symptoms?

A

Risks:

  • underlying asthma
  • symptom denial
  • previous severe reaction
  • delayed use of epinepherine

Often lack cutaneous symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Oral allergy syndrome:

  1. Usually due to?
  2. What occurs?
  3. Cause?
A

Oral allergy syndrome:

  1. Fresh fruits and veggies
  2. Oral pruritis, rapid onset, IgE-mediated
  3. Cause - cross reactive proteins with pollen/food
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Interpretation of Lab Tests?

A

Lab tests:

  • Positive prick/RAST
    • Presence of IgE ab NOT clinical reactivity (50% FP)
  • Negative prick/RAST
    • Excludes IgE ab (>95%)
  • ID skin test with food
    • Risk of systemic reaction and not predictive
  • Unproven (useless)
    • Neutralization, cytotoxic tests, applied kinesiology, hair analysis, IgG4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Absolute diagnosis?

A

Absolute diagnosis:

  • Elimination diets
    • Specific IgE ab negative - reintroduce food
    • Specific IgE ab positive - eliminate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Substitutes for infant formulas?

A

Formula substitution:

  • Soy
    • <15% soy allergy among IgE-cows milk allergy
  • Cow’s milk protein hydrolysates
    • >90% tolerance in IgE-CMA
  • Partial hydrolysates
    • Not hypoallergenic
  • Elemental amino acid-based formulas
    • DOESNT CAUSE ALLERGY
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Food allergy prevention is aimed at?

Best way to prevent?

A

Prevention is aimed at “high risk” newborn with FMHx:

Delay introduction of solid foods >6 months:

  • Milk/dairy: 6-12 months
  • Egg: 12-24 months
  • Peanut/tree nut/ seafood: >24-48 months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Eosinophilic GI Disorders (EGID)?

A

Primary eosinophilic GI disorders taht affect the GIT with eosinophil rich inflammation in the absence of known causes for eosinophilia (eg. drug reactions, parasites, malignancy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Different types of EGID?

A

EGID: Eosionophilic….

  • Esophagitis
  • Gastritis
  • Gastroenteritis
  • Enteritis
  • Colitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

EGID signs and symptoms?

A

EGID S/S:

  • Failure to thrive
  • Ab pain
  • Irritability
  • Gastric dysmotility
  • N/V/D
  • Dysphagia
  • Reflux
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

EGID:

  1. How can severity be reversed?
  2. Most common foods?
  3. What is found in tissues?
A

EGID:

  1. Reverse severity with allergen free diet
  2. Most common foods: milk, egg, wheat, soy, nuts, and seafood
  3. Mast cell degranulation found in tissue specimens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

EGID is a cross of what mediated disorders?

What is histologically characteristic?

A

EGID is a cross of Type I IgE and CMI disorders

Histologically characteristic: >24 eiosinophils/high power field

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

ALLERGIC RHINITIS

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is allergic rhinitis?

Risk factors?

A

IgE mediated inflammation of nasal mucous membranes

Risk factors:

  • +Family history
  • Ethnicity other than white
  • Birth in a pollen season
    • inhalant skin tests
  • Early introduction of foods/formula
  • Sedentary lifestyle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

3 most common complications/comorbidities of Allergic rhinitis?

A

Complications/Comorbidities of AR:

  • Chronic sinusitis (40-80%)
  • Asthma (38%)
  • Serous otitis media (21% in kids)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Signs and symptoms of AR?

Most common symptom of chronic allergic rhinitis

A

AR S/S:

  • nasal pruritis and sneezing
  • clear rhinorrhea with post nasal drip
  • Watery, itchy eyes
  • Fatigue, irritability, HA
  • Disrupted sleep and declines in cognitive processing

Chronic allergic rhinitis: Nasal obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Pathophysiology:

How does sensitization occur?

A

Sensitization:

  • Macrophages present Ag to T/B cells
  • B cells mature into a plasma cell that produces an Ag specific strain of IgE
  • Plasma cells secrete this IgE and it binds to mast cell Fc receptors –> NOW SENSITIZED
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the acute (early) phase response?

A

Acute phase response:

  • Re-exposure to Ag results in cross bridging to two IgE molecules and trigger degranulation
  • Vascular leakage, mucous secretion, and vasodilation
  • LTs/Acute Phase Proteins: function as chemotactic factors for immune cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is the Late Phase Response (LPR)?

A

LPR:

  • Activation of leukocytes 2-12 hrs after acute phase
  • Hallmark is the activated eosinophil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Review:

  1. APCs present by what class to T cell receptor?
  2. What type of T cells are activated?
A

Review:

  1. APCs present by MHC II
  2. Activation of specific CD4+ helper T cells of Th2 phenotype and secretion of cytokines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Diagnoses:

What establishes a pattern?

Examples of seasonal allergies?

A

Diagnosis:

History establishes a pattern

Seasonal allergens:

  • Ragweed (August and Sept)
  • Tree (March-May)
  • Grass (May and June)
  • Molds (Spring-Fall)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Perennial allergens (long lasting) examples?

A

Perennial allergens:

  • Dust mites
  • Insects
  • Animal dander
  • Indoor molds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Phyical diagnosis of allergic rhinitis?

A

Physical diagnosis:

  • Pale/boggy/enlarged turbinades
    • Clear secretions
  • Dark puffy lower eyelids
    • Allergic shiners
  • Mouth breathing
    • Allergic Gape
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Allergy testing?

A

Testing:

  • Immunoassays - RAST/ELISA
    • Detects presence of Ag-specific IgE
    • Useful in those that cant be skin tested
  • Non-specific tests
    • Nasal smear for eosinophils
    • Serum total IgE
    • Peripheral blood eosinophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

HYMENOPTERA ALLERGY

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

3 classes of Hymenoptera and insects included?

A
  • Apids
    • Honey/Bumble/Sweat Bee
  • Vespids
    • Yellow Jacket, hornets, wasps
  • Formicids
    • Fire ants and hervester ants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What do most venoms contain?

A

Venoms:

  • Vasoactive amines
    • Histamine, dopamine, and NE
  • ACh
  • Kinins
  • Hyaluronidase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Major allergen in the honeybee?

Major allergen in vespids?

A

Honeybee: phospholipase A

Vespids: Antigen - 5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

3 types of common venom induced reactions and symptoms?

A
  • Normal
    • Local pain/erythema/mild swelling
  • Large local
    • Extended swelling/erythema
  • Anaphylaxis: onset 15-20 min
    • Cutaneous: urticaria/flushing/angioedema
    • Respiratory: dyspnea
    • CV: hypotension/dizziness/loss of consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Large local reaction:

  1. Most represent what phase? Devolpment time?
  2. How long to subside?
A

Large local reaction:

  1. LATE phase IgE; Develops over 12-24 hrs
  2. 5-10 days to subside
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What type of reactions can occur to a large number of stings?

What specific reaction may happen with a large amount of fire ant stings?

A

Many stings:

  • Acute RF
  • Rhabdomyolysis
  • Hemolysis
  • ARDS
  • DIC

Fire ants: seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Name some reactions of unknown mechanisms?

A

Reactions of unkown mechanisms:

  • Serum sickness
  • Encephalitis
  • Peripheral/cranial neuropathy
  • Glomerulonephritis
  • Myocarditis
  • Guillan-Barre syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Primary evidence of allergic reactivity?

A

History is the primary evidence of allergic reactivity

46
Q

Skin testing for hymenoptera:

  1. When?
  2. Cross reactivity?
A

Skin testing:

  1. Performed 4-6 weeks after a sting
  2. Very high cross reactivity among vespids
47
Q

Skin testing:

  1. Reactivity correlation with severity of sting reaction?
  2. Largest reactions in what patients?
A

Skin testing:

  1. Degree of skin test reactivity does not correlate with severity of the sting reaction
  2. Largest reactions are often in patients with large local reactions
48
Q

What can large local reactions be mistaken for?

A

Large local reactions can be mistaken for cellulitis (unlikely if reaction appears 24-48 hrs after a sting)

49
Q

ANAPHYLAXIS

A
50
Q

Anaphylaxis definition?

A

A life-threatening, multiorgan, IgE mediated disorder characterized by signs and symptoms of histamine release and other mediators released from mast cells and basophils

51
Q

Risk factors for anaphylaxis?

A

Risk factors:

  • Atopy
  • Gender/Age
  • Route/constancy of administration
  • Time since last reactions
  • Economic status
52
Q

What things are NOT risk factors?

A

NOT risk factors:

  • Race
  • Geography
  • Chronobiology
  • Occupation
53
Q

Gender differences?

A

Females>Males for:

  • Latex
  • Muscle relaxants
  • Aspirin (ASA)
  • Idiopathic and OVERALL
54
Q

Risk factors in the role of Atopy in anaphylaxis?

A

Atopic Risk Factors:

  • Latex
  • Oral administration
  • Exercise
  • Radiocontrast media (RCM)
55
Q

Non-Risk factors in the role of Atopy in anaphylaxis?

A

Non-risk factors of Atopy:

  • Parenteral administration
  • Penicillin/Insulin
  • Hymenoptera
  • Muscle relaxants
56
Q

4 Mechanisms of anaphylaxis?

A
  • Immunologic
    • IgE-dependent
  • Non-IgE immunologic
    • C3a, C5a, and bradykinin
  • Nonimmunologic
    • Degranulation from physical factors (cold/exercise)
    • Degranulation from certain medications
  • Idiopathic
57
Q

IgE- Mediated Haptens?

(hapten is a small molecule that can elicit an immune response only when attached to a large carrier such as a protein)

A

IgE Mediated Haptens:

  • ABX
    • Penicillin/Cephalosporins/Sulfa
  • Other theraputic agents
    • Folic acid
    • General anesthetics
58
Q

IgE Mediated complete antigens?

A

IgE Mediated complete antigens:

  • Animal/Human proteins
    • Egg vaccines/stinging insects/animal dander
  • Hormones
    • Insulin/progesterone
  • Enzymes
  • Foods
  • Latex
  • Allergenic extracts
    • Skin testing/immunotherapy
59
Q

Non-IgE Immunologic

Due to activation of?

Examples?

A

Non-IgE Immunologic:

Due to activation of compliment anaphylatoxins and bradykinin from the contact system

Examples:

  • RCM
  • Dextran
  • Oversulfated chondroitin sulfate
60
Q

Examples of nonimmunologic agents that can cause anaphylaxis?

A

Non-immunologic Anaphylaxis

  • Drugs
    • Aspirin and NSAIDs
    • Opiates and Ethanol
  • Physical
    • Exercise
    • Cold/Hot (air/water)
    • UV radiation
61
Q

Key to all forms of anaphylaxis/anaphylactoid reactions?

What is the rule of 2’s?

A

Mast cell/basophil degranulation is the key

Rule of 2’s: signs and symptoms occur within 2 minutes to 2 hours after exposure

62
Q

Degranulation preformed mediators?

Degranulation newly generated mediators?

A

Preformed

  • Histamine
  • Tryptase and carboxypeptidase A
  • Proteoglycans (heparin)

Newly generated

  • PGD2 and LTD4
  • PAF
  • Kinins
63
Q

Pathophysiology:

Mediators result in an abrupt increase in?

A

Increase in

  • Vascular permeability
  • Vasodilation
  • Bronchoconstriction
  • Mucous secretion
64
Q

Most common organs involved?

A

Cutaneous (>90%)

Respiratory (55-60%)

Cardiovascular (30-35%)

Shock (30%)

65
Q

Anaphylaxis gross pathology?

A

Gross pathology:

  • Pulmonary hyperinflation
  • Laryngeal edema
  • RT edema
66
Q

Anaphylaxis histology?

A

Histology:

  • Increased bronchial secretions
  • Eosinophilic infiltration
    • Of RT, spleen, and liver sinusoids
67
Q

Anaphylaxis serologic indications?

A

Serology:

  • Elevated:
    • Histamine (rises in 5 min; only lasts up to 1 hr)
    • Tryptase (Lasts up to 5 hrs)
    • Carboxypeptidase A3
      • May be the better marker
    • Urinary histamine metabolites may remain elevated for up to 24 hours
68
Q

Anaphylaxis evaluation:

_____ is the key.

What supports the diagnosis?

A

Anaphylaxis eval:

History is the ky

Physical exam supports the diagnosis

69
Q

I know it says we dont need to know treatment buttt….

What position should a patient be in for the treatment of anaphylaxis and why?

A

Patient should lie flat bc those sitting up may be subject to an “empty heart” and sudden death

70
Q

ASTHMA

A
71
Q

Asthma definition?

Inflammation is associated with?

A

Asthma - is a chronic inflammatory disorder of the airways (doesnt matter what severity)

Inflammation is associated with hyperresponsiveness and airflow limitations

72
Q

What is the strongest predisposing factor for the development of asthma?

A

Atopy, the genetic predisposition for IgE mediated responses, is the strongest predisposing factor

73
Q

Asthma complications/comorbidities?

A

Asthma complications/comorbidities:

  • 80% of allergic asthmatics also have AR
  • 40% of all patients with AR experience asthma at some point
74
Q

Exercise induced bronchospasm:

General population versus patients with AR?

Asthmatics?

A

Exercise induced bronchospasm:

  • 10% of general population
  • 40% of individuals with AR
  • ALL Asthmatics
    • For some, this will be the only asthmatic manifestation
75
Q

Cluster 1 phenotype?

A

Cluseter 1 (15%)

  • Younger with child hood onset
  • Mostly female
  • Minimal meds
  • Atopic with normal lung function
76
Q

Cluster 2 phenotype?

A

Cluster 2 (44%)

  • Occurs in 30’s with childhood onset/atopic
  • 2/3 female
  • 2/3 have normal lung function
  • 30% use >3 meds
77
Q

Cluster 3 phenotype?

A

Cluster 3 (8%)

  • Obese older females
  • Late onset
  • NON atopic asthma
  • Moderate reduction in lung function
  • Frequent OCS for exacerbations

(OCS = oral corticosteroids)

78
Q

Cluster 4/5 phenotypes?

A

Clusters 4/5 phenotypes (33%)

  • Severe airflow obstruction
  • Variability in age of onset
  • Atopic status
  • Use of OCS
79
Q

Aspirin Sensitive Asthma:

Percent? Atopy?

Classic cases presentation?

A

Aspirin Sensitive Asthma:

  • 5-10% of asthmatics will worsen with Aspirin/NSAIDs
  • 2/3 of these are NOT atopic
  • Classic presentation
    • Nasal polyps with chronic sinusitis
    • Asthma with peripheral eiosinophilia
    • ASA/NSAID sensitivity

(often have high levels of LTs)

80
Q

Diagnosis:

50% of asthmatics will have?

A

Diagnosis

50% of asthmatics will have NORMAL PFT (pulmonary functions?) at rest

81
Q

IMMUNODEFICIENCY

A
82
Q

Main categories of primary immunodeficiency?

A
  • Complement deficiency
  • Immunoglobulin (B cell) deficiency
  • Lymphocyte defects (T cell)
  • Phagocyte Defects
83
Q

Acquired immunodeficiencies?

A

Acquired ID:

  • Malnutrition
  • AIDS
  • Chemotherapy
  • Organ transplant
84
Q

What does Compliment normally regulate?

A

Complement regulates:

  • Mast cell degranulation
  • Smooth muscle contraction
  • Chemotaxis of leukocytes
  • Phagocytosis
85
Q

Compliment deficiencies result:

Classic pathway?

C3 deficiency?

Late components?

A

Classic Pathway (C1/2/4)

  • Recurrent GP infections and high autoimmune incidence

C3 deficiency

  • Recurrent pyogenic infections with GP and GN

Late Components (C5-9)

  • Recurrent neisserial infections
86
Q

Complement Deficiency - Hereditary Angioedema:

Signs and Symptoms?

A

Hereditary Angioedema S/S:

  • Nonpitting edema of skin, GI, and respiratory tract
    • Skin = asymmetric; no pruritis or hives
    • Bowel wall edema = cramping and diarrhea
    • Laryngeal edema = most common cause of death
87
Q

Hereditary angioedema:

Deficiency?

Genetics?

Mediator responsible for the angioedema?

A

Hereditary Angioedema:

  • Deficiency of C1 esterase inhibitor
  • Genetics: AD inheritance
  • Mediator: Bradykinin (degradation slowed in absence of the enzyme)
88
Q

Hereditary angioedema:

Levels of C4?

Levels of C2?

Levels of C1 INH?

A

Hereditary angioedema:

  • C4: low or absent all the time
  • C2: drops during attacks only
  • C1 INH: low/absent OR nonfunctional
89
Q

Symptoms of Antibody deficiency?

A

Ab Deficiency S/S:

  • Recurrent OM/Sinusitis/pneumonia
  • Cellulitis
  • osteomyelitis
  • meningitis
  • Enteric infections
90
Q

X Linked Agammaglobulinemia:

Also known as?

What is abnormal? Linked to what part of X?

A

X Linked Agammaglobulinemia:

  • AKA Bruton’s
  • Abnormal Tyrosine kinase
  • Linked to q22
91
Q

X Linked Agammaglobulinemia:

What kind of infections?

Due to what bugs?

A

X Linked Agammaglobulinemia:

Recurrent Sinopulmonary pyogenic infections due to:

  • H. influenzae
  • Staph
  • Strep
  • Pneumococci
  • Meningococci
92
Q

X Linked Agammaglobulinemia:

Other infections? What do they lead to?

A

X Linked Agammaglobulinemia:

  • Sinusitis, pneumonia, abscesses, meningitis, septiciemia

Infections lead to:

  • bronchiectasis
  • Pulmonary insufficiency
93
Q

X Linked Agammaglobulinemia:

Resistance to fungi/viruses/GN – intact or no? Why?

A

X Linked Agammaglobulinemia:

Resistance to fungi/viruses/GN:

  • Intact
    • Normal T cell number and function
94
Q

X Linked Agammaglobulinemia:

Diagnosis:

Levels of Immunoglobulins and B lymphocytes?

A

X Linked Agammaglobulinemia:

Diagnosis:

Low to absent levels of all Ig, B lymphocytes, and circulating plasma cells

95
Q

Common variable immunodeficiency:

Suceptible to same infections as? But also?

Increased incidence of what cancer?

A

Common variable immunodeficiency:

Suceptible to same infections as Brutons and also Giardia

Increased incidence of lymphomas

96
Q

Common variable immunodeficiency:

Signs/Symptoms?

A

Common variable immunodeficiency S/S:

  • Lymphadenopathy
  • Splenomegaly
  • Lymphoid hyperplasia of the gut
97
Q

Common variable immunodeficiency:

B cell and T cell levels and functions?

A

Common variable immunodeficiency:

  • B cell
    • Present but abnormal function
  • T cell
    • Levels usually normal
    • Function may not be normal
98
Q

Most common primary immunodeficiency?

A

IgA deficiency

99
Q

IgA deficiency:

What types of recurrent infections?

May have anti-IgA abs that can cause what?

A

IgA:

  • Recurrent sinopulmonary infections
  • Anti-IgA antibodies
    • Anaphylaxis when given blood products
100
Q

T cell ID:

Often occur when? And how does it present?

What can occur with live viral vaccines?

A

T cell ID:

Often occur in infancy

Present as failure to thrive with diarrhea

Live viral vaccines can result in severe illness

101
Q

T Cell ID:

What is Hyper-IgM syndrome linked to?

What occurs in DiGeorge?

A

T Cell ID:

  • Hyper IgM syndrome
    • CD40 ligand
  • DiGeorge
    • Thymic dysplasia/aplasia
    • Facial clefts, hypocalcemia, cardiac defect
102
Q

T cell ID

What is reticular dysgenesis?

What is Ommen syndrome?

A

T Cell ID:

  • Reticular dysgenesis
    • Early defect in hematopoesis
  • Ommen syndrome
    • Hypereosinophila
    • High IgE
    • Hymphocytosis
    • Hepatomegaly
    • Rashes from birth
103
Q

T Cell ID:

What occurs in Wiskott Aldrich syndrome?

A

Wiskott Aldrich Syndrome:

  • Small platelets
  • Petechiae
  • Eczema
  • Early sinopulmonary infections
  • Atopy
104
Q

T Cell ID:

What is Ataxia Telangectasia?

What serum levels are increased?

A

T Cell ID:

  • Ataxia Telangectasia:
    • Loss of motor milestones in early childhood
    • Telangectasias appear later
    • Increased alpha fetal protein in serum
105
Q

Phagocyte Defects:

Average number of neutrophils?

What is neutropenia?

A

Phagocyte Defects:

  • Neutrophils: 5000/mcl
  • Neutropenia: <1000/mcl
106
Q

Phagocyte Defects:

Chronic granulomatous disease:

Presents?

Infections with what bugs?

A

Chronic Granulomatous disease:

Presents with lymphadenopathy

Infections with:

  • Staph aureus
  • Aspergillus
  • Nocardia
107
Q

Phagocyte Defects:

Chronic granulomatous disease:

Defect is in?

Bacteria/fungi and what enzyme cause recurrent life threatening infections?

A

Chronic Granulomatous Disease:

Defect: Oxidative killing of ingested microorganisms

Bacteria/Fungi + catalase = life threatening

108
Q

Phagocyte Defects:

Chronic granulomatous disease:

Organs affected?

A

Chronic granulomatous disease:

Organs:

  • Lungs
  • Liver
  • Lymph nodes
  • Skin
  • Bone
109
Q

Phagocyte Defects:

Leukocyte adhesion deficiency:

What is this?

How is it clinically characterized?

Mutation in?

A

Leukocyte adhesion deficiency:

  • Neutrophils fail to mobilize and migrate
  • Characterized by:
    • Delayed separation of umbilical cord
    • Gingivitis
    • Severe scarring skin infections
  • Mutation in CD18
110
Q

Phagocyte Defects:

Chediak-Higashi syndrome:

Inheritance?

Infections?

Signs/symptoms?

A

Chediak-Higashi syndrome:

  • Autosomal Recessive
  • Recurrent cutaneous and sinopulmonary pyogenic inf.
    • Dont respond well to abx
  • Signs:
    • Partial oculo-cutaneous albinism
    • mental retardation
    • neuropathy (late)
    • Weird hair sheen
111
Q

In the lab what does the presence of isohemagglutinins indicate?

A

Isohemagglutinins:

Presence indicates IgM antibodies to blood groups

ICM (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions