Brainscape's Knowledge GenomeTM

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


See full index

RESP 1 > Mumbo Jumbo > Flashcards

Mumbo Jumbo Flashcards

1
Q

what are the 4 Type I hypersensitivities

A 
Systemic anaphylaxis
Acute urticaria 
Seasonal rhinoconjuncivitis 
Asthma
Food allerg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are the symptoms of systemic anaphylaxis

Route of entry?

A 
edema
increased vascular permeability 
laryngeal edema 
Circulatory collapse 
Death

route is intravenous (either directly or following oral absorption into the blood)

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

what are the symptoms of urticaria and route of entry

A

Local increase in blood flow and vascular permeability

through skin

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

what are the symptoms and route of entry of seasonal rhinoconjunctivitis

A

edema of nasal mucosa
sneezing

inhalation

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

what are the symptoms and route of entry of asthma

A

bronchial constriction
increased mucous production
Airway inflammation

inhalation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what are the symptoms and route of entry of food allergy

A 
vomiting
diarrhea
pruitis (itching)
urticaria 
anaphylaxis (rarely)

oral

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

what are the TH2 cytokines

A

IL-4
IL-5
IL-9
IL-13

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

where are mast cells most prominent

A

skin and mucosa

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

what are the preformed proinflammatory mediators (from granules) in the mast cell (4)

A

histamine
serotonin
heparin
serine proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the newly formed lipid mediators (eicosanoids) of the mast cells

A

prostaglandin D2

leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what do prostaglandins and leukotrienes cause

A

smooth muscle contraction
increase vascular permeability
stimulate mucus secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what do histamine and heparin do?

A

toxic to parasites
increase vascular permeability
cause smooth muscle contraction

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

what cells are the major contributor to tissue damage

A

eosinophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the cause of chronic allergic inflammation

A

Eo’s in high numbers

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

what does major basic protein do?

A

toxic to parasites and mammaian cells

triggers histamine release from mast cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the leukotrienes

A

LTC4, LTD4, LTE4

LTB4 - pro-inflammatory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the function of leukotrienes

A

overlapping activities with histamine

BUT have a much slower onset and more powerful, and have a much longer duration than histamine in bronchoconstriction

cause an INCREASE in capillary permeability and mucus production

antagonists against these work much better in the treatment of allergies/asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the functions of IL-4

A

TH2 cell growth factor

Isotype switching to IgE

Increase VCAM-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

function of IL-13

A

Airway esoinophilia

Mucous gland hyperplasia increased production of mucous in asthma but too much is detrimental

Airway fibrosis & remodeling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the function of IL-5

A

regulator of Eo production and survival

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

what is the function of TNF

A

Recruitment & activation of inflammatory cells

Altered function & growth of airway smooth muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is the early phase allergic response mediated by

A

histamine and lipid mediators (after antigen has bound a mast cell sensitized with IgE)

so smooth muscle response and vascular effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is the late phase reaction of IgE mediated allergic responses

A

inflammation due to cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what occurs during the early phase (minutes- hour)

A

cross linking of IgE on mast cells with allergen

Degranulation of mast cells

sneezing, pruritis, rhinorrhea, congestion
(increased mucus secretion and smooth muscle contraction leading to airway obstruction)

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

what occurs during the late phase chronic allergic response

A

hours 4-12

influx and activation of eo’s neutrophils, basophils and lymphocytes (TH2)

TH2’s release cytokines

increase in mast cells in the area and increased expression of FCe receptors on mast cells

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

what are the systemic symptoms of the last phase response

A

fatigue, myalgias, asthma

27
Q

what do eosinophils do once recruited in the late phase response?

A

Proinflammatory mediators
Local tissue damage, sinus infections
Chronic Hyperplastic eosinophilic sinusitis (CHES)

28
Q

what are some of the systemic responses of mast cell activation

A

(Histamines)
vasodilation
vascular leak

Lipid mediators (PAF,PGD2,LTC4)
Bronchoconstriction
Intestinal hypermotility

cytokines
inflammation

enzymes
tissue damage

29
Q

what are some of the systemic response of Eo activation in allergic response

A

tissue damage

killing of parasites and host cells

30
Q

what is the hygiene hypothesis

A

the more non-hygeniec the less likely a person is to have atopic response

31
Q

what occurs with a high dose of intravenous allergen

A

general release of histamine

causes systemic anaphylaxis

32
Q

what occurs with low dose of subQ allergen

A

local release of histamine

causes wheal and flare reaction

33
Q

what occurs with low inhaled dose of allergen

A

allergic rhinitis (upper airway) caused by increased mucus production and nasal irritation

asthma (lower airway) due to contraction of bronchial smooth muscle and increased mucus secretion

34
Q

what occurs with ingestions of allergen

A

contraction of intestinal smooth muscle which induces vomiting

outflow of fluid into gut causes diarrhea

antigen diffuses into blood vessels and is widely disseminated causing urticaria (hives)
or anaphylaxis

35
Q

what is allergic rhinitis

A

Paroxysms of sneezing, rhinorrhea, nasal obstruction, and itching of the eyes, nose, and palate
Postnasal drip, cough, irritability, and fatigue

36
Q

what are allergic shiners

A

Both infraorbital edema and darkening due to subcutaneous venodilation and accentuated lines or folds below the lower lids (Dennie-Morgan lines) suggest allergic conjunctivitis.

37
Q

what is the difference between acute and chronic urticaria

A

Acute urticaria:
New onset urticaria that has been present for less than six weeks.

Chronic urticaria:
Recurrent urticaria occurring most days of the week for a period of more than six weeks.

38
Q

what is the cause and symptoms of acute urticaria

A

Mediated by cutaneous mast cells in the superficial dermis.

Release mediators upon activation, including histamine, which cause itching, and vasodilatory mediators, which cause localized swelling in the uppermost layers of the skin.

A typical urticarial lesion is an intensely pruritic, erythematous plaque. Individual lesions usually appear over the course of minutes, enlarge and coalesce with other lesions, and then disappear within a few hours. Urticaria is sometimes accompanied by angioedema, or swelling deeper in the skin.

39
Q

what are the mediators of the early phase?

what are the mediators of the late phase

A

early - mast cell mediators

late- influx of inflammatory celsl (T’s, Eo’s Basophils)

40
Q

what are the symptoms of asthma

A

Airway hyperresponsiveness
-intermittent wheezing cough and dyspnea

Contraction & relaxation of airway smooth muscle

Anywhere in tracheobronchial tree – varying degrees of obstruction

variable airflow limitations – reversible

41
Q

what is the early phase of asthma

A

Bronchoconstriction (minutes)
Due to Release of mast cell mediators
Contract smooth airway muscles, reflex neural pathways

42
Q

what is the late phase of asthma

A

Bronchoconstriction (several hours)
Influx of inflammatory cells (Ts, Eos, Baso)
Contract smooth airway muscles

43
Q

what are the treatments for asthma

A

corticosteroids to reduce inflammation

epinephrine to induce bronchial relaxation

leukotriene antagonists to inhibit bronchial constriction

44
Q

what are some of the symptoms of anaphylaxis (exposure by blood route)

A

Due to systemic mast cell activation:

Hypotension: Increased vascular permeability can produce a shift of 35% of vascular volume to the extravascular space within 10 minutes
Tachycardia
Urticaria
Flushing
Bronchoconstriction
Laryngeal edema
Diarrhea
Sense of “doom”
45
Q

what is the difference between anaphylactic and anaphylactoid ?

A

anaphylactic is allergy (IgE mediated)

anaphylactoid is direct, non immunological release of mediators

46
Q

what are some examples of anaphylactoid reactions

A

Aspirin
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Radiopaque contrast media Fluorescein
Dextran
Thiamine
Opiates
Complement components: Anaphylatoxins C3a, C4a, & C5a

47
Q

what is the timing of onset of symptoms to fatal cardiac arrests in food, drugs and venom

A

Food 5-35 minutes
Drugs 10-20 minutes
Venom 10-15 minutes

Early response

48
Q

what are the risk factors for anaphylactic shock

A

Atopy
Route and timing of administration of Ag
Asthma is a risk factor for fatal anaphylaxis
Delayed epinephrine is a risk factor for fatal outcomes

49
Q

what are some of the treatment methods for treating anaphylactic shock

A

induce T regulatory T cells to stop TH2 activation

block co-stimulation and inhibit TH2 cytokines in order to prevent activation of B cell to produce IgE

Inhibit effects of IgE binding to mast cell in order to prevent mast cell activation

inhibit effects of mediators and inhibit synthesis of mediators (by using antihistamine)

block IL-5 and CCR3 in order to block cytokine and chemokine receptors that mediate eosinophil recruitment and activation

50
Q

what are the effects of SIT (allergen specific immunotherapy) on immune parameters

A

increase ratio of TH1 to TH2 cytokines

Induce T regs

Class switching to IgA,IgG which compete with IgE for allegro binding thereby decreasing allergen capture and presenation that is facilitated by IgE in complex with the high-affinity receptor for IgE

decrease the number of mast cells and their ability to release mediators

decrease recruitment of neutrophils and eosinophils

51
Q

problems in conventional allergen-specific immunotherapy `

A

long term treatment is required for decrease in specific IgE levels

52
Q

what is allergen sensitization

A

repeated exposures

53
Q

the TH2 cytokines IL-4 and IL13 do what…

A

isotype switching to IgE prduction

54
Q

what are the environmental factors for developing type I hypersensitivity

A

pollution
diet
allergen burden
disease

55
Q

mast cells release what in what response

A

histamine in the early response

56
Q

eosinophils release what in what response

A

leukotrienes

57
Q

what do the pulmonary stretch receptors do?

A

slow and lie in the smooth muscle; reflex effect is a slowing of respiratory frequency due to increased expiratory time (Hering-Breuer inflation reflex); reflex is not evident in adult subjects unless the tidal volume exceeds 1 L.

if it is over 1 L they get stretched out and they slow down breathing rate

58
Q

what do irritant receptors do?

A

lie between airway epithelial cells; stimulated by noxious gases, cigarette smoke, inhaled dusts, and cold air; reflex can include bronchoconstriction and hyperpnea; rapid

59
Q

what do the j receptors do

A
  • ending of non-myelinated C fibers; believed to be located in the alveolar walls, close to capillaries; respond quickly to chemicals injected into the pulmonary circulation; induce rapid shallow breathing; receptors can be triggered by an increase in interstitial fluid volume (linked to respiratory sensation of difficulty in breathing associated with left heart failure and interstitial lung disease)
60
Q

what do bronchial c fibers do

A

like J receptors but sense changes in the bronchial circulation

61
Q

what are the 3 points in respiratory control that contribute to increased PaCO2 in acute on chronic respiratory failure

A

Loss of stimulation of the peripheral chemoreceptors leading to reduced ventilation b/c he was given 100% O2
–hypoxemia is partly responsible for driving respiratory rate

Worsening of ventilation-perfusion mismatch
loss of hypoxic vasoconstriction upon administration of 100% O2

Haldane effect
administration of 100% O2 results in a higher release of CO2 from hemoglobin and subsequently higher PaCO2 levels

62
Q

what is hypersensitivity pneumonitis

A

Group of lung diseases caused by inhalation of exogenous antigenic molecules (usually organic)

Transient fever, hypoxemia, myalgias, arthralgias, dyspnea, cough 2-9 hr after exposure

Symptoms resolve without treatment provided there is no re-exposure to antigen

Examples include bird fancier’s disease and pigeon breeder’s lung

63
Q

what is the immunology associated with hypersensitivty pneumonitis

A

Prior sensitization is necessary
Not associated with IgE or eosinophils
Higher prevalence in non-smokers (80-95%)
>40% lymphocytes suggestive of HP; higher percentage of neutrophils and degranulated macrophages
Cell-mediated immune process
TGF-β, IL-1, IL-12, TNF-α, IL-6
IL-2, IFN-γ
Disease can be transferred with CD4+ T cells
Tx with corticosteroids aids recovery initially, long-term outcome is unaffected

RESP 1 (2 decks)

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