40 markers Flashcards

1
Q

Describe the normal airway structure of respiratory tree from trachea to alveoli

A

Trachea - singular tube, C ring cartilage, trachealis muscle, pseudostratified ciliated columnar epithelium
Bronchi - Begin at carina, right is wider short and more vertical, decreased cartilage
Secondary bronchi - 3 on right, 2 on left, have cilia and goblet cells to produce mucous
Tertiary bronchi - less cartilage, more smooth muscle to allow for increased/ decreased airflow, similar epithelium to trachea
Bronchioles - no cartilage, completely smooth muscle
Terminal bronchioles/ alveoli - 1 cell thick walls made of type 1 squamous cells and type 2 surfactant secreting cells, no cilia or goblet cells, in place have alveolar macrophage cells to find and destroy debris

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2
Q

Factors affecting normal sputum clearance

A

Sol layer - if viscosity is altered, cilia can’t beat it, mucociliary escalator impaired and sputum will not be coughed/ cleared. Can be due to diet/ hydration levels
Gel layer - similarly affects, if too thick cilia can’t beat
Impaired cough - if coughin caused pain, patients are likely to avoid, so sputum won’t be expelled from the airways
Obstruction - any condition blocking airways such as dynamic airway compression can prevent sputum moving up through the respiratory tree

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3
Q

What is COPD

A

Long term condition, occurs over time, limited exhalation due to blocking of airways, can be chronic bronchitis or emphysema (floppy airways/ alveoli). continual change in body

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4
Q

Explain how pathological changed in COPD cause the clinical features

A

productive cough - In normal airways, the gel/sol layers have a good balance so mucus can travel up the mucociliary escalator effectively. In COPD, an irritant causes epithelial damage causing lymphocyte and macrophage release, causing goblet cell meta plasma and mucous hypersecresion, therefore there is excess phlegm

Wheeze - in normal structures the airways are maintained open so that air can pass through at an optimal pressure. In COPD, an airway irritant causes fibroblast release causing smooth muscle hypertrophy, narrowing the airways causing a wheeze on exhalation

Struggling to inhale fully - In patients with emphysema, alveoli can become floppy, this causes air to be trapped and cannot be exhaled. As a result there is less available volume for a deep breathe to be taken

Right sided heart failure - Reduced oxygen levels cause blood pressure increases in the heart

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5
Q

In lobar pneumonia, what are the changes from usual values for Sa02, Pa02, PaCO2, Hb, pH and what is the significant with relevance to pathological changes.

A

Sa02 usual value is 94% or above. In lobar pneumonia is will be lower due to excess fibrin and dying white/red blood cells in alveolar spaces creating less space for oxygen and less gas exchange.

Pa02 is lower than usual at 13.8 because there is less gas exchange leading to a lower pressure of oxygen.

PaCO2 is as expected at 5.4kPa because there are no issues with exhaling in lobar pneumonia.

Hb levels are normal at 150g/L because lobar pneumonia is a ventilation related issue rather than perfusion - so there is enough haemoglobin.

There is no pH change from 7.42 because there is no excess CO2 to alter the pH in the blood as there are no exhalation issues

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6
Q

Explain the likely signs, symptoms and clinical features of lobar pneumonia

A

Increased respiratory rate - less available area for gas exchange due to alveoli being affected, so lungs have to work harder to maintain a functional level, also sympathetic nervous system may intervene if it feels the body isn’t getting enough oxygen which may cause death, which would lead to increased RR.

Non- productive cough - hard fibrin and dead white/red blood cells caugh alveoli blockage, causing the need to cough to clear them, but non productive because because the hard material can’t be cough out until broken down

Reduced breathing sounds/ expansions - may be painful due to residue in alveoli, alveoli already filled with unwanted substances so may not be able to expand any further due to blockages, these reductions will be limited to the lobe affected

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7
Q

A patient has lung function tests taken during an asthma attack, the results are
FVC: predicted = 3L patients = 3L
FEV1: predicted = 2.5L patients = 1.3L
PEFR: predicted = 359L/min patients = 255L/min

explain the significance of these results with reference to the pathological changes in asthma

A

The FVC is as expected during the attack. this relates to asthma because as an obstructive disease rather than restrictive, asthma affects exhalation rather than inhalation, so the patient won’t have issues with taking a long deep breathe in. Asthma causes inflammation of the airways, narrowing them so that less air can be exhaled, but because of the pressure when inhaling, the airways will still be opened.

However the FEV1 is 52% of the predicted value, which is lower than 80% so it’s normal variation. This is because with the inflamed airways and narrowing of them, less air can pass through at any one time so in one second, less air will be exhaled.

Similarly, the PEFR is 71% of expected, so isn’t within the normal range. This is because due to the constriction of the airways, less air can be sharply exhaled in one go.

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8
Q

Explain the signs, symptoms and clinical features of asthma with reference to pathological changes of asthma

A

Wheeze on exhale: result of variable airflow obstruction, inflammation caused by allergic response, muscles tighten and thin airway, more mucus produced, therefore air will collide and be blocked and will be pushed at a higher pressure causing a wheezing sound

Breathlessness: Takes longer for CO2 to be exhaled due to thinner airways, causing attempted sharper breathes which means there will be even less exhalation and the person will lose control of their breathing, stress as they lose control will cause their heart rate and respiratory rate to increase.

Productive cough: Airway tightening causes excess mucus production causing the stimulation of cough receptors causing a cough to remove the mucus.

Chest tightness: irritant causes inflammation causing airway restriction causing tightness in the chest.

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9
Q

Explain signs, symptoms and clinical features of bronchiectasis

A

Haemoptysis: Cole’s viscous cycle, initial infection causes inflammation causing potential damage to airways leading to blood leakages into the airways, causing stimulation of cough receptors and a cough bringing up blood

Chronic, productive cough: Impaired mucociliary clearance due to inflammation, therefore mucus hypersecretion leading to airway obstruction. This causes stimulation of cough receptors and a cough bringing up mucus, this cough will persist until the mucus is reduced.

Urinary incontinence: as a result of the chronic cough, there is a lot of pressure put on the muscles around the bladder, so can causes incontinence during a coughing period

Wheezing: Excess mucus blocks airways so when exhaling, the air passes the mucus and is diverted or blocked causing a wheezing sound

Chronic chest infections: Widened airways with excess mucus become suitable ground for microbial colonies to breed, and these pathogens won’t be removed due to the break down of the mucociliary escalator

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10
Q

What are the normal sputum mechanisms of the lungs?

A

Mucociliary escalator
Cough reflex
Swallowing

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11
Q

Explain pathology of chronic bronchitis

A

Airway irritant -> epithelial cell damage -> fibroblast release -> smooth muscle hypertrophy -> airway narrowing

Airway irritant -> epithelial cell damage -> lymphocyte and macrophage release -> goblet cell metaplasia -> mucous hypersecretion

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12
Q

Explain pathology of emphysema

A

Airway irritant -> protease and elastase release -> alveolar destruction -> reduced gas exchange -> air trapping

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13
Q

Describe cole’s vicious cycle

A

Initial infection -> inflammation -> impaired mucociliary clearance -> airway mucus hypersecretion and obstruction -> microbial colonisation and infection -> bronchial dilation/ airway destruction

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