Pathophysiology revision - SECTION II - Respiratory Systems

Label the areas of the respiratory CONDUCTING zones as appropriate:

The passage of air into the lungs is governed by pressure differences caused by changes in [blank_start]lung volume[blank_end]. The [blank_start]thoracic diaphragm[blank_end] 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 [blank_start]contracts[blank_end], the vertical diameter of the thoracic cavity increases and air moves into the lungs. This relationship between volume and pressure is represented in [blank_start]Boyle’s Law[blank_end]

[blank_start]Muscles of inspiration[blank_end]: external intercostals, sternocleidomasoids, scalei, anterior serrate, trapezius, posterior neck muscles. [blank_start]Muscles of expiration[blank_end]: internal intercostals, posterior inferior serrate, abdominal muscles. [blank_start]Normal conditions[blank_end]: diaphragm and intercostals

In a patient with a pneumothorax, the lung collapses when the [blank_start]intraplural space[blank_end] is violated and the [blank_start]negative[blank_end] pressure between the lung and chest wall is no longer maintained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 [blank_start]increase[blank_end] in residual volume, a [blank_start]decrease[blank_end] in vital capacity and a [blank_start]decrease[blank_end] in expiratory reserve volume

In patients with emphysema, lung tissue is destroyed and weakened airway walls collapse during [blank_start]expiration[blank_end]. Because of chronic lung tissue inflammation and swelling, the airway walls have decreased recoil and elasticity. Thus, inspiritory capacity and expiratory reserve volume [blank_start]decease[blank_end] while reserve volume [blank_start]increases[blank_end]

According to [blank_start]La Place’s[blank_end] Law, the surface tension of smaller alveoli is [blank_start]greater[blank_end] than that of larger alveoli. [blank_start]Surfactant[blank_end] 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 [blank_start]pre-mature babies[blank_end]

Damage to the capillary membrane, heart failure and valvular disease can all lead to [blank_start]pulmonary odeama[blank_end]. 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 [blank_start]Starling’s Law[blank_end]

Excess fluid accumulating within the pulmonary interstitial space is usually taken up by the [blank_start]lymphatic system[blank_end]

Airway diameter and secretions are primarily controlled by the [blank_start]autonomic nervous system[blank_end]. [blank_start]Beta-2[blank_end] receptors function to dilate the bronchioles when activated by adrenergic agonists such as epinephrine and norepinephrine. Stimulation of these receptors also [blank_start]decreases[blank_end] the secretions of mucus and serous glands

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

Chemoreceptors play an important role in the regulation of respiration. Central chemoreceptors in the [blank_start]medulla[blank_end] are sensitive to PH of cerebrospinal fluid. When the PH level drops, the ventilary rate [blank_start]increases[blank_end]. This would be due to an [blank_start]increase[blank_end] in C02 levels

Why would a hyperventilating patient lose consciousness?

Peripheral chemoreceptors exist in the [blank_start]carotid and aortic bodies[blank_end]. These are sensitive to [blank_start]oxygen[blank_end] 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 [blank_start]hypoxic drive[blank_end]

Albuteral, bitolterol and salmeterol are all examples of [blank_start]Beta-2 Agonists[blank_end], used for treating Asthma and COPD. These work by inducing [blank_start]relaxation[blank_end] of the bronchial musculature. However, they can also have an effect on Beta-1 receptors causing [blank_start]increased heart rate[blank_end]

Ipratopium bromide works to reverse overstimulation of the autonomic nervous system by blocking the [blank_start]parasympathetic[blank_end] neurotransmitters. They are hence known as [blank_start]anticholinergic agents[blank_end]

Glucocorticoids also reffered to as corticosteroids are compounds synthesized from the [blank_start]zona recticulars fasciculars[blank_end] of the adrenal cortex. [blank_start]Methylprednisolone[blank_end] is an example of this steroid

Your unit is called to the scene of a 33-year old asthmatic complaining of severe shortness of breath. Lung sounds are decreased with diffuse wheezing and a prolonged expiratory component. All of the following are muscles of expiration, EXCEPT:

What would pulmonary function testing be likely to show in a patient experiencing a severe asthma attack?

Patients with COPD are expected to have which of the following?

Neonatal respiratory distress syndrome occurs in certain infants as a result of:

The mechanism of beta-2 agonists in asthma is:

A patient is hyperventilating and loses consciousness – what is the pathologic mechanism responsible for this?

A 69-year old with emphysema becomes less responsive with decreased respirations while on 4 lpm of oxygen during a prolonged inter-facility transport. What is the likely mechanism for these findings?

The National Heart, Lung and Blood institute defines asthma as a [blank_start]chronic inflammatory disorder[blank_end] of the airways

[blank_start]Extrinsic[blank_end] 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 [blank_start]childhood[blank_end]

[blank_start]Intrinsic[blank_end] asthma is more common in adults, is not related to antibody activation, tends to be more chronic, is severe and often controlled only with [blank_start]corticosteroids[blank_end]. Triggers include exercise or infections rather than exposure to allergens

When mast cells are stimulated by IgE antibodies, numerous mediators (i.e. cytokines) are released, contributing to what is known as a generalised state of bronchial hyperresponsiveness. This causes:

The [blank_start]late response[blank_end] represents the secondary phase of an asthma episode, typically occurring [blank_start]4-12[blank_end] 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

People who have symptom free intervals between episodes are said to have:

Match these signs with their main symptoms: Airways narrowing due to smooth muscle contraction / Inflammation of the airways – [blank_start]wheeze[blank_end] Hyperinflation from trapped air in the distal airways – [blank_start]dyspnoea and tachyponea[blank_end] Airway narrowing and hypersecretion – [blank_start]cough and chest tightness[blank_end] A fall of more than 10 mmHg in systolic pressure during inspiration as a consequence of lung hyperinflation which compresses the left ventricle (right ventricular end systolic pressure increases, compressing the intraventricular septum) – [blank_start]pulsus paradoxus[blank_end] Increased ventilation-perfusion mismatching due to airway obstruction – [blank_start]hypoxaemia[blank_end]

Match the clinical features with the asthma classification: [blank_start]Mild Intermittent[blank_end] (Step 1) – symptoms <2x/wk, brief exacerbations, PEF >80% [blank_start]Mild Persistent[blank_end] (Step 2) - symptoms >2x/wk, night symptoms >2x/mo, exacerbations effect activity, PEF >80% [blank_start]Moderate Persistent[blank_end] (Step 3) – symptoms daily, daily use of albuterol, excaserbations greater than 2x/week, night symptoms >1x/wk, PEF >60 - <80% [blank_start]Severe Persistant[blank_end] (Step 4) – symptoms continuous, liminted physical activity, frequent night symptoms, PEF ,60%

Fill in the blanks: Step 1 (mild intermittent) : QUICK RELIEF [blank_start]Short acting bronchodilator[blank_end]; LONG TERM CONTROL [blank_start]No daily medication required[blank_end] Step 2 (mild persistent): QUICK RELIEF [blank_start]Short acting bronchodilator[blank_end] ; LONG TERM CONTROL [blank_start]Low dose inhaled corticosteroid[blank_end] OR [blank_start]Mast Cell Stabiliser[blank_end] OR [blank_start]Leukotrine inhibitor[blank_end] Step 3 (moderate persistent) : QUICK RELIEF [blank_start]short acting bronchodilator[blank_end]; LONG TERM CONTROL [blank_start]Medium dose inhaled corticosteroid[blank_end] AND [blank_start]long acting bronchodilator[blank_end] Step 4 (severe persistent): QUICK RELIEF [blank_start]short acting bronchodilator[blank_end] ; LONG TERM CONTROL [blank_start]high dose inhaled corticosteroid[blank_end] AND [blank_start]long acting bronchodilator[blank_end] AND [blank_start]corticosteroid tablets[blank_end]

Match the drug to the action: Relaxes smooth muscle while also decreasing the release of mediators from mast cells and basophils – DRUG TYPE [blank_start]Beta-adrenergic agonist[blank_end] – EXAMPLE [blank_start]albuterol, epinephrine[blank_end] Inhibitory effect on bronchoconstricting leutrienes and prostaglandins by stopping phospholipid A2 – DRUG TYPE [blank_start]anti-inflamitory agent (corticosteroids)[blank_end], EXAMPLE [blank_start]prednisolone[blank_end] Inhibition of the parasympathetic nervous system by selectively binding and blocking the neurotransmitter acetylcholine to its receptor in nerve cells – DRUG TYPE [blank_start]anticholinergic[blank_end], EXAMPLE [blank_start]Ipatropium[blank_end]

Several risk factors for COPD have been identified, but by far the primary cause is related to [blank_start]tobacco smoke exposure[blank_end]

The four main actions of tobacco smoke are:

Someone who is known to be a “pink puffer” will be likely to have what characteristics? Age: [blank_start]>50[blank_end] Disease process: [blank_start]Emphysema[blank_end] Cough: [blank_start]Mild[blank_end] Weight Changes: [blank_start]weight loss[blank_end] Sputum: [blank_start]Scant[blank_end] Degree of hypoxia: [blank_start]Mild[blank_end] Response to bronchodilators: [blank_start]Mild improvement[blank_end] Cough type: [blank_start]Dyspneic[blank_end] Accessory Muscle Use: [blank_start]Yes[blank_end] Hyperventillation: [blank_start]Yes[blank_end]

Someone who is known to be a “blue bloater” will be likely to have what characteristics? Age: [blank_start]Young (50s)[blank_end] Disease process: [blank_start]Bronchitis[blank_end] Cough: [blank_start]Chronic[blank_end] Weight Changes: [blank_start]weight gain[blank_end] Sputum: [blank_start]copious[blank_end] Degree of hypoxia: [blank_start]Can be severe[blank_end] Response to bronchodilators: [blank_start]great improvement[blank_end] Cough: [blank_start]Tussive[blank_end] Accessory muscle use: [blank_start]No[blank_end] Hyperventilation: [blank_start]No[blank_end]

You are called to a 60 y/o patient who is sat in the tripod position on arrival. Respiratory inspection reveals use of excessory muscles to breathe, mild hypoxia and a mild cough producing little sputum. Pt is found to have a prolonged expiratory component with a wheeze on exhalation. Without any further history taking, what disease process could this patient have?

Permanent destruction of elastic segments of the alveoli by mechanical, chemical, or other factors is the pathogenetic hallmark of:

You are called to a 49 y/o patient with a chronic cough producing copious amounts of sputum. You notice the patient is overweight and on examination find them to be hypoxic but with only a small, insignificant rise in RR. The patient tells you that his breathing symptoms are part of a chronic condition and this is not acute.

Irritation of the mucosa by smoke, chemicals and other irritants leading to the hyperplasia of mucus glands and disruption of the normal function of cilia in the respiratory tissue lining the airways describes:

What pathologic changes are thought o be responsible for the development of the barrel chest of emphysema?

All of the following classes of medications can be used in the acute COPD exacerbations, EXCEPT:

While all of these are a risk factor for COPD, which is the most likely to cause it?

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 – [blank_start]EMPHYSEMA (pink puffer)[blank_end] - A 55 y/o morbidly obese smoker with dyspnoea who improves significantly after two treatments of nebulised albuterol – [blank_start]BRONCHITIS (blue bloater)[blank_end] - A 72 y/o male smoker with accessory muscle use, hyperventilation and a barrel chest – [blank_start]EMPHYSEMA (pink puffer)[blank_end] - A 50 y/o female with a history of chronic occupational smoke exposure who presents with copious sputum, chronic cough and severe hypoxia – [blank_start]BRONCHITIS (blue bloater)[blank_end] - An 8 y/o female with a history of wheezing after exposure to a new pet – [blank_start]NEITHER[blank_end]

Venostsis; vessel wall inflammation and/or endothelial injury; hypercoagulability all relate to [blank_start]Virchow’s triad[blank_end] for pulmonary embolism.

While all of these are a risk factor for PE, which is the most likely to cause it?

With few exceptions, almost all emboli arise within the large deep veins of the [blank_start]pelvis[blank_end] and [blank_start]lower extremities[blank_end].

Thrombus almost always starts in the veins of the calf (saphenous vein) and propagates to veins above the knee. Over 90% of emboli arise from the following viens (TICK THREE):

Signs and symptoms of a PE include:

All of the following are risk factors for developing a PE, EXCEPT:

While all of these are signs and symptoms of a PE, which are the most sensitive indications?

All of the following are acceptable actions during pre-hospital transport of a patient with suspected pulmonary embolism, EXCEPT:

Match the situation with the type of emboli risk: Fracture of a long bone (tibula/fibula) – [blank_start]FAT EMBOLI[blank_end] At the end of the first stage of labour – [blank_start]AMNIOTIC FLUID EMBOLI[blank_end] During placement of central cannulated lines – [blank_start]AIR EMBOLI[blank_end] Prolonged immobilisation – [blank_start]BLOOD CLOT EMBOLI[blank_end]