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Patho Bros

on 29 October 2015

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Transcript of Asthma

Learning Objective 1:

What is Asthma?
What are its stages?
What are the effects of her usual asthma action plan?
Leaning Objective #4:

What lifestyle choices led to Susan's ultimate demise?
Leaning Objective 2:

What are the mechanisms linked to Susan's acute exacerbation?

Group 1 (Patho Bros): Justin Camacho, Jenna Cope, Erika Bove, Karelle Cote, Elias Gaoro, and Dara Brunette
Leaning Objective 3:

What were the additional management strategies used to treat Susan's acute exacerbation?
Psychosocial Factors
Behavioural Factors
Single Mother of a 2 year old child

Over controlling mother
Lack of Self Responsibility
Dust and Allergens
Not compliant to treatment
Possible bacterial infection
Yellow sputum
Sore throat
Nasal catarrh
Systemic glucocorticoids
Prednisolone (oral)
Hydrocortisone (IV)
Tapering of prednisolone

How do they get to the nucleus of the epithelial cell?
- transported via systemic circulation
- bind to glucocorticoid receptor in cytoplasm
- dimerize+ translocate to nucleus
In nucleus
binds to GRE
inc transcription of genes coding for anti-inf proteins :
- lipocortin-1
- interleukin-10
- interleukin-1
- endopeptidase
soluble compound of theophylline +ethylenediamine
Active ingredient

- solvent

Direct relaxation of smooth m. of bronchial airways + pulmonary vessels

Possible effect on diaphramatic contractility Work of breathing
possible mechanisms:
- inc phosphodiestarase= inc cAMP
- translocation of intracellular Ca2+
- prostaglandin antagonism
- stim catecholine endogenously
- dec cyclic guanasine monophosphate metabolism
- inhibition of adenosine receptor antagonism

Theophylline= also is anti-inflammatory at low therapeutic doses
60% Oxygen

respiratory distress=30 breath/min
-normal perfusion
-altered ventilation

Why administer oxygen?
O2 concentration
Alveolar ventilation
Nonuniform reversible increase in airway resistance
Asthma attack
Hyperinflation of the lung
Premature airway closure

Increased work of breathing

Decreased peak flow

Increased residual volume

Mismatch in V/Q
- Uneven ventilatory distribution

- Blood saturation irregularities

Changes in arterial blood gas pressures
PaC02 (54mmHg>35-45mmHg))
- Hypercapnia (increased PaC02)
- Hypoxemia (PaO2 <95mmHg)
- Respiratory Acidosis (pH<7.35)
Acute Respiratory Failure
Aerobic > anaerobic metablism

Lactate accumulation

Decreased pH

= Ventilation
Systemic routes of administration
- Oral
- IV
- Prevent acute adrenal insufficency
- life-threatening
return to normal function gradually of hypothalamus, anterior pituitary gland, adrenal cortex.
- Helps avoid exacerbation of inflammation
PaO2= not at a level that needs oxygen administration (aka 7.8kPa)
V/Q mismatch
Physiologic shunt
- Hyperactive immune system [Allergens and toxins e.g. Pollen spores, env. pollution, dust mites, smoke, animals, molds]
- Epi/Genetics [Childhood]
- Chronic Infections [Viral + Bacterial]
- Stress via immune sys.
- Bronchospasm [Transient Bronchoconstriction] via smooth muscle rings [CN X Vagus n. ACh]
- Airways inflammation response
- Mucus accumulation and edema
- Pulmonary plexus = Vagus + Sympathetic inn.
- Nore/Epinephrine = bronchodilators
* Both Para/Symp. sys.
can dilate and constrict airways [NTs]
Immunity of asthma and its signal transduction

Trigger = Antigen in air ways [Exogenous substance]
Th2 cells orchestrate the major inflammation cascades via interleukins [Immune sys. signaling proteins]
Abcam international inc. fluorescent proteins and antibodies lab
Dendritic cells [Antigen-presenting cell] signal Th2 cells via transmembranal proteins bound to the antigen [Cell-Cell recognition]
Eosinophiles and mast cells release inflammation biomarkers such as hitamine [h1 rec. Bronchocostriction],proteases, cytokines, leukotrienes [ Mucus] and prostaglandins [Regulator].
Thank you!
- immune reaction
inf processes
Full transcript