TH2 release the ff causing: 1. IL-5 2. IL-4, IL-13

1. IL-5: eosinophilic inflammation 2. IL-4, IL-13: increases IgE formation

Asthma Flashcards by Jem de la Cruz

Peak age of asthma

3 years

How well did you know this?

Not at all

Perfectly

Responsible for decreased mortality in patients with persistent asthma

ICS

How well did you know this?

Not at all

Perfectly

Major risk factors for asthma deaths (3)

poorly controlled disease with frequent use of bronchodilator inhalers
lack of or poor compliance with ICS therapy
previous admissions to hospital with near-fatal asthma.

How well did you know this?

Not at all

Perfectly

Major risk factor for asthma

Atopy

How well did you know this?

Not at all

Perfectly

Genetic predisposition in asthma

polymorphisms of genes on chromosome 5q, including the TH2 cells interleukin (IL)-4, IL-5, IL-9, and IL-13,
which are associated with atopy

How well did you know this?

Not at all

Perfectly

Novel genes in asthma (3)

ADAM 33
DPP-10
ORMDL3

How well did you know this?

Not at all

Perfectly

lack of infections in early childhood preserves the Th2 cell bias at birth, whereas exposure to infections and endotoxin results in a shift toward a predominant protective Th1 immune response.

Hygiene hypothesis

How well did you know this?

Not at all

Perfectly

More severe, persistent asthma

Intrinsic asthma

How well did you know this?

Not at all

Perfectly

Characteristics of intrinsic asthma

Adult onset
Non-atopic
Concomitant nasa polyps
Aspirin-sensitive
More severe, persistent asthma

How well did you know this?

Not at all

Perfectly

Most common allergens to trigger asthma

Dermatophagoides spp

How well did you know this?

Not at all

Perfectly

Common triggers of ACUTE SEVERE EXACERBATIONS

Rhinovirus
RSV
Coronavirus

How well did you know this?

Not at all

Perfectly

Mechanism is linked to hyperventilation

Exercise-induced asthma

increased osmolality in airway lining fluid and triggers mast cell mediator release, resulting in bronchoconstriction

How well did you know this?

Not at all

Perfectly

Physiologic abnormality of asthma

Airway hyperresponsiveness

How well did you know this?

Not at all

Perfectly

Important in initiating the acute bronchoconstrictor responses to allergens

Mast cells

How well did you know this?

Not at all

Perfectly

Activated by allergens via low-affinity IgE receptors (FcεRII)

Macrophages

How well did you know this?

Not at all

Perfectly

T helper phenotype

in asthmatics
In normal

2. TH1

How well did you know this?

Not at all

Perfectly

TH2 release the ff causing:

IL-5
IL-4, IL-13

IL-5: eosinophilic inflammation

2. IL-4, IL-13: increases IgE formation

How well did you know this?

Not at all

Perfectly

Major target cells for ICS

Epithelial cells

How well did you know this?

Not at all

Perfectly

Mast cell-derived mediators that contract airway smooth muscle, increase microvascular leakage, increase airway mucus secretion, and attract other inflammatory cells

histamine
prostaglandin D2
cysteinyl-leukotrienes

How well did you know this?

Not at all

Perfectly

Cytokines that amplify the inflammatory response

TNF-α and IL-1β

How well did you know this?

Not at all

Perfectly

Anti-inflammatory cytokines deficient in asthma

IL-10, IL-12

How well did you know this?

Not at all

Perfectly

Used in diagnosis and monitoring of asthmatic inflammation

FeNO

How well did you know this?

Not at all

Perfectly

Airway nerves release this neurotransmitter which may have inflammatory effects

substance P

How well did you know this?

Not at all

Perfectly

True in asthma, except:
A. reduction in FEV1
B. Reduction in FEV1/FBC ratio
C. Increased peak expiratory flow (PEF)
D. increase in airway resistance.

Should be Reduced PEF

How well did you know this?

Not at all

Perfectly

Characteristic symptoms of asthma

Wheezing Dyspnea Coughing

Reversibility in lung function test is demonstrated by

>12% and 200-mL increase in FEV 15 min 1. after an inhaled SABA; such as inhaled albuterol 400 μg OR 2. Oral corticosteroids (prednisone or prednisolone 30–40 mg daily)

Treatment: increases intracellular cyclic adenosine monophosphate (AMP), which relaxes smooth muscle cells and inhibits certain inflammatory cells, particularly mast cells

B2 agonist

Actions of B2-agonists, except: A. reversing and preventing contraction of airway smooth muscle cells B. inhibition of mast cell mediator release C. Increase in plasma exudation D. inhibition of sensory nerve activation

C. Should be reduction in plasma exudation

SABA duration of action

3-6 hours

LABA duration of action

12 hours Given BID (salmeterol, formoterol) Given OD (indacaterol, olodaterol, vilanterol)

Most common side effects of B2-agonists

Muscle tremor | Palpitations

prevent cholinergic nerve-induced bronchoconstriction and mucus secretion

Muscarinic receptor antagonists

Most common side effects of anticholinergics

Dry mouth

inhibition of phosphodiesterases in airway smooth-muscle cells, which increases cyclic AMP

Theophylline

Activated by theophylline which is a critical mechanism for switching off activated inflammatory genes and may therefore reduce corticosteroid insensitivity in severe asthma.

histone deacetylase-2 (HDAC2)

Used in patients with severe exacerbation that are refractory to SABA

Aminophylline

Most common side effects of theophylline

Nausea Vomiting Headaches *due to phosphodiesterase inhibition

Most effective controllers for asthma

ICS

Effect/Action of ICS

switch off the transcription of multiple activated genes that encode inflammatory proteins such as cytokines, chemokines, adhesion molecules, and inflammatory enzymes.

Timing of ICS

BID

First line for persistent asthma

ICS

Oral corticosteroids dosing for acute exacerbations

Prednisone or prednisolone 30-45 mg OD x 5-10 days

are potent bronchoconstrictors; cause microvascular leakage and increase eosinophilic inflammation through the activation of cys-LT1-receptors.

Cysteinyl-leukotrienes

effective in blocking trigger-induced asthma such as EIA and allergen- and sulfur dioxide-induced symptom

Cromones

blocking antibody that neutralizes circulating IgE without binding to cell-bound IgE and, thus, inhibits IgE-mediated reactions

Omalizumab

Anti-IL 5 used in asthma

Direct: Mepolizumab, resilizumab Receptor: Benralizumab

Treatment of Choi’s for all patients

ICS BID

Clinical features of acute severe asthma

Increased ventilation Hyperinflation Tachycardia

Mainstay of treatment in acute severe asthma

SABA via nebulizer or MDI with spacer

Target SpO2 in acute severe asthma

>90%

Impending respiratory failure in acute severe asthma

PCO2 is normal or rises *prophylactic intubation is indicated

two major patterns of difficult asthma

1. persistent symptoms and poor lung function, despite appropriate therapy 2. normal or near normal lung function but intermittent, severe (sometimes life-threatening) exacerbations

most common reason for poor control of asthma is poor adherence with medication

ICS

Treatment: Severe premenstrual worsening of asthma unresponsive to corticosteroids

progesterone OR gonadotropin-releasing factors

Persistent pattern of variability and may require OCS, or at times, continuous infusion of B2-agonists

Type 1 brittle asthma

normal or near-normal lung function but precipitous, unpredictable falls in lung function that may result in death

type 2 brittle asthma

Most effective therapy in brittle asthma

Subcutaneous epinephrine

Treatment safe in pregnancy

SABA ICS Theophylline

Improves lung function and reduces steroid resistance

Smoking cessation

Results from an allergic pulmonary reaction to inhaled spores of Aspergillus fumigatus

Bronchopulmonary Aspergillosis

Treatment for BPA that is beneficial in preventing exacerbations

Oral antifungal itraconazole

Treatment for ACO

Triple therapy with ICS, LABA, LAMA

Brainscape's Knowledge GenomeTM

Asthma Flashcards

Brainscape's Knowledge Genome^TM