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Medical Studies 1 > 6.3 Atopy, Anaphylaxis and the Immunology of Respiratory Disease > Flashcards

6.3 Atopy, Anaphylaxis and the Immunology of Respiratory Disease Flashcards

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USMLE® Step 1 flashcards
1
Q

Define Atopy

A

Genetic tendency to make allergic immune responses to common airborne allergens, and to develop allergic disease

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2
Q

Define “Allergy”

A

Adverse reaction to foreign substance (allergen) that is excessive/inappropriate and directed towards specific substances

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3
Q

Does an allergy require a previous encounter with the antigen?

A

Yes

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4
Q

Define sensitisation

A

Production of IgE antibodies in response to specific allergens

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5
Q

Is “allergy” the same as “sensitisation”?

A

No

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6
Q

At what point in someone’s life does atopy usually begin?

A

Infancy: dermatitis or eczema

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7
Q

List some environmental factors that are thought to have increased prevalence of allergic disease

A
  • Tobacco smoke
  • Air pollutants
  • Diet
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8
Q

Th1 vs Th2 immune responses

A

Th1: Important for cellular immune response to pathogens
Th2: Important for immunity against helminths, implicated in pathogenesis of allergic disease

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9
Q

Explain how Th2 skewing can predispose to allergic disease. How does this fit in with the hygiene hypothesis?

A
  • Th2 environment is skewed during gestation to promote tolerance of pregnancy
  • In atopic individuals, this Th2 skewing persists after birth
  • The hygiene hypothesis states that, due to increased sanitation, the environment remains Th2 skewed for longer, leading to more allergies
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10
Q

Cutaneous vs oral allergen exposure; which is more likely to cause allergy?

A
  • Oral exposure is more likely to promote tolerance
  • Cutaneous exposure is more likely to promote allergy
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11
Q

How early should allergens be introduced into food to prevent allergies?

A

Introduce allergenic foods by the age of 1

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12
Q

List some modern dietary changes that increase prevalence of allergic disease

A
  • Lower fibre
  • More omega 6 fats and less omega 3 fats
  • Less fresh foods
  • Higher saturated fats
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13
Q

Patient A takes folate during pregnancy to prevent neural tube defect. How can she make sure this is not likely to cause asthma and eczema in her unborn child?

A

Don’t take is in late pregnancy; only in early pregnancy

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14
Q

List three ways in which an infants microbiome can be influenced during pregnancy/birth

A
  • Use of antibiotics during pregnancy
  • Vaginal vs caesarian birth
  • Mother’s microbiome during pregnancy
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15
Q

What is the predicted impact of prebiotics on unborn child microbiome

A
  • Promotes growth of immunomodulatory microbiota
  • Effects last in infants and adults
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16
Q

A child has asthma, and his mother is pregnant. How much more likely is the next child to have asthma?

A

3-4x more likely than usual.

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17
Q

Is allergic predisposition monogenic?

A

Not usually; it is mostly influenced by multiple genes, and is quite complex. There are rare monogenic causes

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18
Q

Is allergic disease high or low in prevalence in australia? Is it increasing or decreasing?

A

It is high, and it’s getting higher.

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19
Q

List three common causes of anaphylaxis

A
  • Foods
  • Medications
  • Insects
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20
Q

List some uncommon causes of anaphylaxis

A
  • Latex
  • Cold temperature
  • Immunisations
  • Idiopathic
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21
Q

What substances are released during mast cell degranulation during an allergic reaction?

A
  • Histamine
  • Tryptase
  • Prostaglandins
  • Leukotrienes
  • Cytokines
  • Chemokines
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22
Q

List some consequences of an allergic reaction (i.e., what happens after mast cell degranulation?)

A
  • Vasodilation
  • Increased vascular permeability
  • Inflammatory cell recruitment
  • Mucus production
  • Bronchoconstriction
23
Q

Skin-based symptoms of anaphylaxis

A
  • Hives
  • Swelling
24
Q

GI symptoms of anaphylaxis

A
  • Vomiting
  • Abdo pain
25
Q

Respiratory symptoms of anaphylaxis

A
  • Difficult/noisy breathing
  • Swelling of tongue
  • Swelling tightness in throat
  • Difficulty talking and/or hoarse voice
  • Wheeze or persistent cough
26
Q

Cardiovascular symptoms of anaphylaxis

A
  • Low blood pressure
  • Persistent dizziness or collapse
  • Pale and floppy (in young children)
27
Q

Mild to moderate symptoms of allergic reactions

A
  • Swelling of lips, face, eyes
  • Hives or welts
  • Tingling mouth
  • Abdominal pain, vomiting
28
Q

Under what circumstances do vomiting and abdominal pain become severe symptoms of anaphylaxis?

A

When they are brought about by an insect sting

29
Q

Severe symptoms of anaphylaxis:

A
  • Swelling of tongue
  • Difficult/noisy breathing
  • Persistent cough or wheeze
  • Difficulty talking/hoarse voice
  • Presyncope/syncope
30
Q

What is urticaria?

A

Hives

31
Q

Do skin complications have to occur during anaphylaxis?

A

No

32
Q

In what age group do food-related anaphylaxis deaths almost always occur?

A

8-35 yrs

33
Q

What is the most common cause of anaphylaxis deaths (i.e. what triggers the reactions)?

A
  • Drugs (or probable drugs)
34
Q

What is systemic mastocytosis?

A

Increased number of mast cells

35
Q

List some risk factors for fatal anaphylaxis

A
  • No adrenaline administration
  • Upright posture during/after
  • Asthma
  • People with food allergy eating away from home/at restaurant
  • Initial misdiagnosis
  • Heart disease
  • Systemic mastocytosis
36
Q

Two most common causes of anaphylaxis (in order)

A
  1. Peanuts
  2. Treenuts
37
Q

Are hypersensitivity reactions just for allergic responses?

A
  • No
  • They apply to a diverse range of immune responses
  • They can be considered a framework to understand broader immune reactions
38
Q

What type of hypersensitivity reaction is anaphylaxis?

A

Type 1

39
Q

Describe type 1 hypersensitivity

A
  • Initial exposure, Th2 cell prompts plasma cell to produce IgE antibodies, which bind to mast cell
  • Upon secondary exposure, antigen cross links antibodies, leading to degranulation and hypersensitivity reaction
40
Q

What type of hypersensitivity reaction is allergic rhinitis?

A

Type 1

41
Q

What is cytopenia?

A

Low levels of RBCs

42
Q

Describe type 2 hypersensitivity

A
  • Antibodies bind to antigen on self cell (can be extrinsic or intrinsic)
  • Activates complement, either causing immune cells to come and kill the self cell, or creating the membrane attack complex and killing the cell that way
43
Q

Is type 1 hypersensitivity faster or slower than type 2?

A

Type 1 is faster; type 2 can take 2-7 days

44
Q

Explain type 3 hypersensitivity reactions

A
  • Antigen binds to antibody, forming immune complexes that are not large enough to trigger phagocytosis
  • Deposited in tissues, triggering complement system and leading to inflammation
  • Can damage blood vessels, and exacerbate local inflammatory response
45
Q

How long does type 3 hypersensitivity take?

A

2-14 days

46
Q

Describe typ2 4 hypersensitivity reactions

A

Immune reactions mediated by T cells (can be T helper cells or cytotoxic T cells)

47
Q

Describe type 5 hypersensitivity, and give an example

A
  • Antibody takes on the role of a messenger molecules
  • Example: graves disease, where Thryoid stimulating immunoglobulin does the role of TSH, causing unregulated thyroid hypertrophy
48
Q

List some atopic diseases

A
  • Eczema
  • Food allergy
  • Asthma
  • Allergic rhinitis
  • Eosinophilic oesophagitis
49
Q

Are all atopic disease driven through IgE mediated allergies?

A
  • No
  • For instance, eczema is not, but allergic rhinitis is
  • There is a spectrum of IgE mediation
50
Q

Allergic rhinitis mech

A
  • Classic t1 hypersensitivity
  • APC -> Th2 -> plasma cell -> IgE -> mast cell -> secondary exposure -> inflammation
51
Q

Eczema mech

A
  • Damage to skin
  • Release of alarmins
  • Dendritic cell activates T cell, which samples antigen from skin surface
  • Activates B cell -> mast cell
  • And activates eosinophil
    -> perpetuates (allergen is bystander, not primary driver)
52
Q

Name two treatment pathways for eczema. How do each of these work?

A
  • Topical corticosteroids (reduce inflammation)
  • Moisturisers (reduce initial damage)
53
Q

How does immune tolerance induction help with allergies at a cellular level?

A
  • Helps skew immune system back towards Th1 pathways, as well as Treg cell production that prevents overstimulation of the immune system
54
Q
A

Medical Studies 1 (90 decks)

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