Pathophysiology revision - SECTION II - Respiratory Systems

The passage of air into the lungs is governed by pressure differences caused by changes in lung volume lung capacity lung residue lung resilience( lung volume, lung capacity, lung residue, lung resilience ). The thoracic diaphragm lumbar diaphram cervical diaphram adregeneric diaphragm( thoracic diaphragm, lumbar diaphram, cervical diaphram, adregeneric diaphragm ) is the principle muscle of respiration which is innervated by the phrenic nerves derived from the ventral rami of cervical segments 3 – 5.

When the diaphragm contracts relaxes inverts( contracts, relaxes, inverts ), the vertical diameter of the thoracic cavity increases and air moves into the lungs. This relationship between volume and pressure is represented in Boyle’s Law Charles' Law Henry's Law Starling's Law( Boyle’s Law, Charles' Law, Henry's Law, Starling's Law )

Muscles of inspiration Muscles of expiration Normal conditions( Muscles of inspiration, Muscles of expiration, Normal conditions ): external intercostals, sternocleidomasoids, scalei, anterior serrate, trapezius, posterior neck muscles.

Muscles of expiration Muscles of inspiration Normal conditions( Muscles of expiration, Muscles of inspiration, Normal conditions ): internal intercostals, posterior inferior serrate, abdominal muscles.

Normal conditions Muscles of inspiration Muscles of expiration( Normal conditions, Muscles of inspiration, Muscles of expiration ): diaphragm and intercostals

In a patient with a pneumothorax, the lung collapses when the intraplural space extraplural space intercostal space myocardial space( intraplural space, extraplural space, intercostal space, myocardial space ) is violated and the negative positive inerrant backforce( negative, positive, inerrant, backforce ) pressure between the lung and chest wall is no longer maintained

Patients with Asthma have narrowed air passages due to smooth muscle contraction, mucus plugging and inflammation. This leads to an increase decrease( increase, decrease ) in residual volume, a decrease increase( decrease, increase ) in vital capacity and a decrease increase( decrease, increase ) in expiratory reserve volume

In patients with emphysema, lung tissue is destroyed and weakened airway walls collapse during expiration inspiration( expiration, inspiration ). Because of chronic lung tissue inflammation and swelling, the airway walls have decreased recoil and elasticity. Thus, inspiritory capacity and expiratory reserve volume decease increase( decease, increase ) while reserve volume increases decreases remains the same( increases, decreases, remains the same )

According to La Place’s Boyle's Charles' Henry's Starling's( La Place’s, Boyle's, Charles', Henry's, Starling's ) Law, the surface tension of smaller alveoli is greater lesser the same( greater, lesser, the same ) than that of larger alveoli. Surfactant Lubriol Protasine Pluratol( Surfactant, Lubriol, Protasine, Pluratol ) is a substance produced by type II alveolar cells which decreases surface tension of the alveoli and is an important component to think about when dealing with pre-mature babies obese patients geriatrics teenagers( pre-mature babies, obese patients, geriatrics, teenagers )

Damage to the capillary membrane, heart failure and valvular disease can all lead to pulmonary odeama Emphysema Asthma Bronchitis( pulmonary odeama, Emphysema, Asthma, Bronchitis ). This is due to an imbalance in the normal forces at the alveolar capillary membrane, causing fluid to accumulate in the pulmonary interstitial space and alveoli. This is best illustrated by Starling’s Law Henry's Law Charles's Law La Place's Law( Starling’s Law, Henry's Law, Charles's Law, La Place's Law )

Excess fluid accumulating within the pulmonary interstitial space is usually taken up by the lymphatic system artieral system pulmonary system endocrine system( lymphatic system, artieral system, pulmonary system, endocrine system )

Airway diameter and secretions are primarily controlled by the autonomic nervous system cardiac receptor system somatic nervous system enteric system( autonomic nervous system, cardiac receptor system, somatic nervous system, enteric system ). Beta-2 Beta-1 Alfa-1 Alfa-2( Beta-2, Beta-1, Alfa-1, Alfa-2 ) receptors function to dilate the bronchioles when activated by adrenergic agonists such as epinephrine and norepinephrine. Stimulation of these receptors also decreases increases( decreases, increases ) the secretions of mucus and serous glands

Inspiration Expiration Respiratory syncope( Inspiration, Expiration, Respiratory syncope ) is controlled neurologically via the medullary respiratory centre which sends signals via the phrenic nerve. Expiration Inspiration Respiratory syncope( Expiration, Inspiration, Respiratory syncope ) is controlled via the ventral respiratory group and is usually only activated during exercise or with certain diseases (COPD) where where expiration inspiration respiratory syncope( expiration, inspiration, respiratory syncope ) becomes an active process.

Chemoreceptors play an important role in the regulation of respiration. Central chemoreceptors in the medulla aorta cerebellum cerebrum( medulla, aorta, cerebellum, cerebrum ) are sensitive to PH of cerebrospinal fluid. When the PH level drops, the ventilary rate increases decreases( increases, decreases ). This would be due to an increase decrease( increase, decrease ) in C02 levels

Peripheral chemoreceptors exist in the carotid and aortic bodies medulla recticular respiratory zone pluralistic bodies( carotid and aortic bodies, medulla, recticular respiratory zone, pluralistic bodies ). These are sensitive to oxygen carbon dioxide hydrogen ions bicarbonate( oxygen, carbon dioxide, hydrogen ions, bicarbonate ) and hence, if levels fall to a very low rate (below 60 mmHg), these are activated to increase ventillary rate. Those who have this system consistently activated are said to have a hypoxic drive asthmatic tendancy ventilation to perfusion mismatch tachypnoeic altercation( hypoxic drive, asthmatic tendancy, ventilation to perfusion mismatch, tachypnoeic altercation )

Albuteral, bitolterol and salmeterol are all examples of Beta-2 Agonists anticholinergic agents Glucocorticoids Afla-1 Agonists( Beta-2 Agonists, anticholinergic agents, Glucocorticoids, Afla-1 Agonists ), used for treating Asthma and COPD. These work by inducing relaxation constriction spasm exitation( relaxation, constriction, spasm, exitation ) of the bronchial musculature. However, they can also have an effect on Beta-1 receptors causing increased heart rate reduced heart rate Atrial fibrillation Atrial flutter( increased heart rate, reduced heart rate, Atrial fibrillation, Atrial flutter )

Ipratopium bromide works to reverse overstimulation of the autonomic nervous system by blocking the parasympathetic sympathetic( parasympathetic, sympathetic ) neurotransmitters. They are hence known as anticholinergic agents Beta-2 agonists glucocorticoids Beta blockers( anticholinergic agents, Beta-2 agonists, glucocorticoids, Beta blockers )

Glucocorticoids also reffered to as corticosteroids are compounds synthesized from the zona recticulars fasciculars zona glomerulosa zona medullla( zona recticulars fasciculars, zona glomerulosa, zona medullla ) of the adrenal cortex. Methylprednisolone ibatropium albuterol salbutamol( Methylprednisolone, ibatropium, albuterol, salbutamol ) is an example of this steroid

The National Heart, Lung and Blood institute defines asthma as a chronic inflammatory disorder acute respiratory implication rare pathological damage pulmonary odemic complication( chronic inflammatory disorder, acute respiratory implication, rare pathological damage, pulmonary odemic complication ) of the airways

Extrinsic Intrinsic Excretory Excitory( Extrinsic, Intrinsic, Excretory, Excitory ) asthma is believed to be caused by an antibody-dependant (IgE) activation of cells that release inflammatory mediators. For that reason, it is also known as allergic asthma and is usually picked up in childhood adulthood teenagers geriatrics newborns( childhood, adulthood, teenagers, geriatrics, newborns )

Intrinsic Extrinsic Intubatory Allergic( Intrinsic, Extrinsic, Intubatory, Allergic ) asthma is more common in adults, is not related to antibody activation, tends to be more chronic, is severe and often controlled only with corticosteroids Beta-2 agonists anticholinergic agents Beta blockers( corticosteroids, Beta-2 agonists, anticholinergic agents, Beta blockers ). Triggers include exercise or infections rather than exposure to allergens

The late response after response by-response recurrent response( late response, after response, by-response, recurrent response ) represents the secondary phase of an asthma episode, typically occurring 4-12 24 1-2 6( 4-12, 24, 1-2, 6 ) hours after the initial allergen introduction. This is significant as the cycle primes patients for future episodes by exposing sensitive irritant receptors that can later be more easily activated

Fill in the blanks:

Step 1 (mild intermittent) : QUICK RELIEF Short acting bronchodilator No daily medication required Low dose inhaled corticosteroid Mast Cell Stabliser Leukotrine inhibitor Long acting bronchodilator( Short acting bronchodilator, No daily medication required, Low dose inhaled corticosteroid, Mast Cell Stabliser, Leukotrine inhibitor, Long acting bronchodilator ); LONG TERM CONTROL No daily medication required Long acting bronchodilator Short acting bronchodilator High dose inhaled corticosteroid( No daily medication required, Long acting bronchodilator, Short acting bronchodilator, High dose inhaled corticosteroid )

Step 2 (mild persistent): QUICK RELIEF Short acting bronchodilator No daily medication required Low dose inhaled corticosteroid mast cell stabilizer long acting bronchodilator( Short acting bronchodilator, No daily medication required, Low dose inhaled corticosteroid, mast cell stabilizer, long acting bronchodilator ) ; LONG TERM CONTROL Low dose inhaled corticosteroid No daily medications high dose inhaled corticosteroid long acting bronchodilator( Low dose inhaled corticosteroid, No daily medications, high dose inhaled corticosteroid, long acting bronchodilator ) OR Mast Cell Stabiliser corticosteroid tablets( Mast Cell Stabiliser, corticosteroid tablets ) OR Leukotrine inhibitor Mast cell activator long acting brocnhodilator( Leukotrine inhibitor, Mast cell activator, long acting brocnhodilator )

Step 3 (moderate persistent) : QUICK RELIEF short acting bronchodilator no daily tablets mast cell stablisers luekotrine inhibitors( short acting bronchodilator, no daily tablets, mast cell stablisers, luekotrine inhibitors ); LONG TERM CONTROL Medium dose inhaled corticosteroid Low dose inhaled corticosteroid High dose corticosteroid Mast cell activator( Medium dose inhaled corticosteroid, Low dose inhaled corticosteroid, High dose corticosteroid, Mast cell activator ) AND long acting bronchodilator short acting bronchodilator corticosteroid tablets Leukotrine inhibitor( long acting bronchodilator, short acting bronchodilator, corticosteroid tablets, Leukotrine inhibitor )

Step 4 (severe persistent): QUICK RELIEF short acting bronchodilator long acting bronchodilator Mast cell stabilizer No quick relief( short acting bronchodilator, long acting bronchodilator, Mast cell stabilizer, No quick relief ) ; LONG TERM CONTROL high dose inhaled corticosteroid medium dose inhaled corticosteroid low dose inhaled corticosteroid Leukotrine inhibitor( high dose inhaled corticosteroid, medium dose inhaled corticosteroid, low dose inhaled corticosteroid, Leukotrine inhibitor ) AND long acting bronchodilator short acting bronchodilator( long acting bronchodilator, short acting bronchodilator ) AND corticosteroid tablets corticosteroid injections corticosteroid inhibitors( corticosteroid tablets, corticosteroid injections, corticosteroid inhibitors )

Several risk factors for COPD have been identified, but by far the primary cause is related to tobacco smoke exposure obesity cardiac failure excessive exercise( tobacco smoke exposure, obesity, cardiac failure, excessive exercise )

Someone who is known to be a “pink puffer” will be likely to have what characteristics?

Age: >50 Young (50s)( >50, Young (50s) )
Disease process: Emphysema Bronchitis( Emphysema, Bronchitis )
Cough: Mild Chronic( Mild, Chronic )
Weight Changes: weight loss weight gain( weight loss, weight gain )
Sputum: Scant Copious( Scant, Copious )
Degree of hypoxia: Mild Severe( Mild, Severe )
Response to bronchodilators: Mild improvement Great improvement( Mild improvement, Great improvement )
Cough type: Dyspneic Tussive( Dyspneic, Tussive )
Accessory Muscle Use: Yes No( Yes, No )
Hyperventillation: Yes No( Yes, No )

Someone who is known to be a “blue bloater” will be likely to have what characteristics?

Age: Young (50s) >50( Young (50s), >50 )
Disease process: Bronchitis Emphysema( Bronchitis, Emphysema )
Cough: Chronic Mild( Chronic, Mild )
Weight Changes: weight gain weight loss( weight gain, weight loss )
Sputum: copious scant( copious, scant )
Degree of hypoxia: Can be severe Mild( Can be severe, Mild )
Response to bronchodilators: great improvement mild improvement( great improvement, mild improvement )
Cough: Tussive Dyspneic( Tussive, Dyspneic )
Accessory muscle use: No Yes( No, Yes )
Hyperventilation: No Yes( No, Yes )

Match the following clinical characteristics to the most appropriate type of COPD patient:

- A 66 y/o woman with dyspnoea, mild hypoxia and a history of weight loss – EMPHYSEMA (pink puffer) BRONCHITIS (blue bloater) NEITHER( EMPHYSEMA (pink puffer), BRONCHITIS (blue bloater), NEITHER )

- A 55 y/o morbidly obese smoker with dyspnoea who improves significantly after two treatments of nebulised albuterol – BRONCHITIS (blue bloater) EMPHYSEMA (pink puffer) NEITHER( BRONCHITIS (blue bloater), EMPHYSEMA (pink puffer), NEITHER )

- A 72 y/o male smoker with accessory muscle use, hyperventilation and a barrel chest – EMPHYSEMA (pink puffer) BRONCHITIS (blue bloater) NEITHER( EMPHYSEMA (pink puffer), BRONCHITIS (blue bloater), NEITHER )

- A 50 y/o female with a history of chronic occupational smoke exposure who presents with copious sputum, chronic cough and severe hypoxia – BRONCHITIS (blue bloater) EMPHYSEMA (pink puffer) NEITHER( BRONCHITIS (blue bloater), EMPHYSEMA (pink puffer), NEITHER )

- An 8 y/o female with a history of wheezing after exposure to a new pet – NEITHER BRONCHITIS (blue bloater) EMPHYSEMA (pink puffer)( NEITHER, BRONCHITIS (blue bloater), EMPHYSEMA (pink puffer) )

Venostsis; vessel wall inflammation and/or endothelial injury; hypercoagulability all relate to Virchow’s triad Cushing's triad Beck's triad Dieulafoy's triad( Virchow’s triad, Cushing's triad, Beck's triad, Dieulafoy's triad ) for pulmonary embolism.

With few exceptions, almost all emboli arise within the large deep veins of the pelvis humerus sternum ulna ribcage spine( pelvis, humerus, sternum, ulna, ribcage, spine ) and lower extremities upper extremities mid auxiliary components( lower extremities, upper extremities, mid auxiliary components ).