IV. THE PATIENT AND HIS ILLNESS A. SCHEMATIC DIAGRAM ( BOOK CENTERED ) 1.

Book Centered

NON-MODIFIABLE RISK FACTORS: ~ AGE (ANY AGE GROUP) ~ RACE ~HEREDITY ~GENDER (Male)

MODIFIABLE RISK FACTORS: ~ MEDICAL CONDITIONS ~ AIR POLLUTION ~EXPOSURE TO ALLERGENS ~ INFECTION ~EXPOSURE TO IRRITANTS ON THE JOB ~ DIET ~COLDS AND FLU ~ SMOKING ~EXPOSURE TO TOBACCO SMOKE ~ STEROID THERAPY

ANTIGEN DEPOSITED ON MUCOSA

ENVIRONMENTAL CHANGES (local imbalance between the parasympathetic and sympathetic divisions of the ANS)

COATING DESTROYED BY LYSOZYMES AUTONOMIC NERVOUS SYSTEM RESPONSE IMMUNE ACTIVATION OR IMMUNOLOGIC RESPONSE

B-LYMPHOCYTES PRODUCE IMMUNOGLOBULIN E (IgE)

DIRECT STIMULATION OF PARASYMPATHETIC RECEPTORS/CHOLINERGIC EFFECT AND BLOCKAGE OF B-ADRENERGIC SYSTEM

IgE antibodies attach to mast cells (first type of cells on the scene in an inflammatory response because they are resident cells in the tissues) and basophils (largely responsible for prolonged allergic response) in the bronchial walls

Mast cell degeneration

Release of chemical mediators of inflammation stored in mast cell granules

CHYMASE; TRYPTASE

PROSTAGLAN DIN; SLOWREACTING SUBSTANCE OF ANAPHYLAXIS (SRS - A)

HISTAMINE; PLATELETACTIVATING FACTORS BRADYKINI N

EOSINOPHIL CHEMOTACTI C FACTORS OF ANAPHYLAXIS (ECF - A)

NEUTROPHIL CHEMOTACTI C FACTOR

BREAKDOWN OF COMPLEX PROTEASE

DEGRADES BRONCHOACTIV E PEPTIDES

H1 RECEPT ORS

H2 RECEPT ORS

EPITHELIAL DAMAGE

CONSTRICTIO N OF SMOOTH MUSCLES IN BRONCHIAL AIRWAY

STIMULATION OF MUCUS GLAND SECRETIONS

CAPILLARY DILATION

INCREASED VASCULAR PERMEABILITY

AIRWAY REMODELING

NARROWING OF AIRWAY

INCREASED MUCOSAL SECRETION PRODUCTION

LEAKAGE OF SERUM CHON TO PERMEABLE CAPPILARIES

FIBROSIS AND THICKENING

BRONCHOSPA SM

CONGESTION

DECREASED MUCOSAL PRODUCTION

DECREASED CHON

EDEMA/INFLA MMATION OF THE AIRWAY

CHEST TIGHTNESS

WHEEZES IRRITATES BRONCHIAL AND TRACHEAL WALL

PEAK FLO W VARI ABILI TY

DYSP NEA

SHOR TNES S OF BREA TH

WHEE ZING

IRRITATES VAGAL NERVE

COUGH REFLEX INITIATED

IRRITATES VAGAL NERVE

INCREASED EOSINOPHIL ACTIVATION

NON PRODUCTIVE COUGH

INCREASED NEUTROPHIL ACTIVATION

INCREASED RESISTANCE TO AIRWAY / AIRWAY OBSTRUCTION PRODUCTIVE COUGH

IMPAIRMENT IN THE ALVEOLAR CO2 O2 LEVEL PRODUCTIVE COUGH

INCREASED AIR TRAPPING IN THE LUNGS

HYPERINFLATION OF ALVEOLI

DECREASED OXYGEN SUPPLY

INCREASED WORK OF BREATHING PRODUCTIVE COUGH INCREASE IN RR

HYPOXEMIA

CYANOSIS

HYPERCAPNIA

RESPIRATOR Y FAILURE

FATIGUE

INCREASING DYSPNEA

EXCESSIVE ELIMINATIO N OF ACID IN RESPIRATOR Y ROUTE INCREASED PRODUCTIVE COUGH HEART RATE

INCREASED O2 INTAKE

DECREASED BF AND O2 SUPPLY TO HEART MUSCLES DEATH

ANAEROBIC RESPIRATION

COMPENSATI ON OF HEART

RESPIRATORY ALKALOSIS GAS EXCHANGE COMPROMISE D PRODUCTIO N OF LACTIC ACID INCREASED BP

IRRITATES HEART MUSCLES

CHEST PAIN

INCREASED RESISTANCE TO AIRWAY / AIRWAY OBSTRUCTIO N PRODUCTIVE COUGH