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Medical Studies 1 > Module 6a > Flashcards

Module 6a Flashcards

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USMLE® Step 1 flashcards
1
Q

How many Australians have some form of lung disease?

A

1 in 10

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2
Q

What Australian population is 3x more likely to die of lung disease than any other?

A

Indigenous

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3
Q

What structures make up the upper airway?

A

Nasopharynx
Oropharynx
Laryngophaeynx
Larynx

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4
Q

What structures make up the lower airway?

A

Trachea
Bronchial tree
Alveoli
Lungs

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5
Q

What is the process of inspiration?

A
  • Contraction (flattening) of the diaphragm that increases the size of the thoracic cavity. (Intercostal muscles assist in times of increase demand)
  • The lungs expand increasing the anterior-posterior thorax dimensions
  • Pressure drops enhancing pressure gradient
  • Pressure drops enhancing pressure gradient
  • Atmospheric pressure is now greater than intrapulmonary pressure and atmospheric air moves into the lungs.
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6
Q

What are the accessory breathing muscles?

A
  • Sternocleidomastoid
  • Scalene
  • Pectoralis minor
  • Serratus (inspiration)
  • Abdominal muscles (expiration)
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7
Q

Define tidal volume (TV)

A

Air volume inspired in a normal breath (av. 500ml)

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8
Q

Define minute volume

A

Tidal Volume X respiratory rate over 1 minute

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9
Q

Define inspiratory reserve volume (IRS)

A

Maximum amount of air that can be forcibly inhaled in excess of normal inspiration (3000ml)

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10
Q

Expiratory reserve volume (ERV)

A

Maximum volume of air expired following a passive expiration (1100ml)

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11
Q

Define Residual Volume

A

Air remaining in lungs after forced expiration

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12
Q

Define Vital Capacity

A

Maximal amount of air expired following a maximal inspiration (4600ml)

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13
Q

Define total lung capacity

A

Volume in the lungs after maximal inspiration (5800ml)

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14
Q

What is ‘dead space’ in relation to the respiratory system?

A

Areas of the respiratory system that do not partake in gaseous exchange.
Anatomical - nasal passage, bronchi
Pathological - obstruction, collapse/disease of alveoli

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15
Q

What are the ventilation controls and what parts do they play?

A

Medulla Oblongata

  • sets basic rate & rhythm
  • fine coordination centre in Pons

Inspiratory Centre

  • phrenic: supplies diaphragm
  • intercostal: supplies intercostal muscles
Expiratory Centre (only in forced expiration) 
- usual expiration passive as inspiration stops
-
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16
Q

What factors influence ventilation control?

A
  • Drugs and medication
  • CNS depression
  • Stress and emotions
  • Stretch receptors of the lungs
  • Voluntary control - limited
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17
Q

What is the respiratory control cycle?

A
  • Holds breath
  • Increased Pco2 in blood and CSF
  • Stimulates central chemoreceptors in medulla
  • stimulates inspiratory muscles
  • Increases respiratory rates
  • Removes more CO2
  • Decreased Pco2
  • Decreased chemoreceptor stimulation
  • Slow respirations
  • Retain more CO2
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18
Q

What is pulmonary respiration?

A

The exchange of gases between the cells of the body and the outside environment is the essence of respiratory pathophysiology. Air must move freely in and out for this to occur.

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19
Q

What factors affect the pulmonary respiration?

A
  • Structure and function of the chest wall
  • Central nervous system control
  • Acid-base balances
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20
Q

What is a V-Q mismatch?

A

A defect which occurs in the lungs whereby ventilation (the
exchange of air between the lungs and the environment) and perfusion (the
passage of blood through the lungs) are not evenly matched

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21
Q

What is a high VQ mismatch?

A

The patient has an adequate ventilation but reduced perfusion. This leads to ‘dead space’ where the ventilation is essentially wasted. E.g. A pulmonary embolism - Ventilation wont be effected however perfusion will be as blood wont be able to travel pass the clot.

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22
Q

What is a low HQ mismatch?

A

The patient has reduced ventilation but has adequate perfusion. E.g. Asthma.

23
Q

Respiratory emergencies are the result of a disruption to …. ?

A
  • Ventilation to the lungs: Movement of air in and out of the lungs
  • Perfusion: Circulation of the blood through the capillary bed
  • Diffusion: Gas exchange between the alveoli and capillary bed
24
Q

What must be intact to ensure ventilation can occur?

A
  • Neurological control (to initiate ventilation)
  • Nerves between brain stem and muscles of
    respiration
  • Functional diaphragm and intercostal muscles
  • Patent upper airway
  • Functional lower airway
  • Alveoli that are functional and have not collapsed

Problems associated with ventilation:

  • Upper and lower airway obstruction
  • Chest wall impairment
  • Problems in neurological control
25
Q

What must be intact for diffusion to occur?

A

• Alveolar, capillary walls not thickened
• Interstitial space between alveoli and capillary wall not enlarged or
filled with fluid

Problems associated with diffusion:
• Inadequate O2
concentration in air
• Alveolar disorders
• Interstitial space disorders
• Capillary bed disorders
26
Q

What needs to be intact for perfusion to occur?

A

• Adequate blood volume
• Adequate haemoglobin in the blood
• Pulmonary capillaries that are not occluded
• Efficient pumping by heart provides a smooth
flow of blood through pulmonary capillary bed

Problems associated with perfusion:
• Inadequate blood volume/haemoglobin levels
(eg: hypovolaemia, anaemia)
• Impaired circulatory blood flow (eg: pulmonary
embolus)
• Capillary wall disorders

27
Q

What symptoms indicate respiratory disease?

A
  • Sneezing
  • Coughing
  • Sputum
  • Abnormal breathing patterns
28
Q

What are 5 types of sputum and what do they indicate?

A

– Yellowish-green, cloudy, thick mucus
• Often indication of a bacterial infection

– Rusty or dark-colored sputum
• Usually sign of pneumococcal pneumonia

– Very large amounts of purulent sputum with foul odor
• May be associated with bronchiectasis

– Thick, tenacious mucus
• Asthma or cystic fibrosis, blood-tinged sputum—may result from chronic cough; may also be sign of tumor or tuberculosis

– Haemoptysis
• Blood-tinged frothy sputum, usually associated with
pulmonary oedema

29
Q

What are signs of life threatening respiratory distress?

A
  • Alterations in mental status
  • Severe cyanosis
  • Audible respiratory sounds
  • Inability to speak one or two words without dyspnoea
  • Tachycardia
  • Pallor and diaphoresis
  • Retractions and/or the use of accessory muscles to assist breathing
30
Q

What is the general management of respiratory distress?

A

• Primary survey
• A to E with respiratory status assessment
• Cardiac monitoring
• Focused history using OPQRST
• Medication history
• Systematic treatment: high concentration O2, pharmacology
(bronchodilators, adrenaline, etc.), IV access, airway
management
• Rapid transport

31
Q

Chronic Airway Limitations (CAL) or Chronic Obstructive Pulmonary
Disease (COPD) is a group of chronic respiratory disorders including:

A
  • Chronic Bronchitis

* Emphysema

32
Q

What are the general mechanisms of CAL?

A
  • Distension and destruction of alveoli
  • Reduced surface area for gas exchange
  • Reduced elasticity of the lungs
  • Bronchial constriction
  • Chronic inflammation
  • Excessive mucous production
33
Q

How does adrenaline work in respiratory distress?

A

Stimulates the alpha and beta of the sympathetic nervous system.

34
Q

Breakdown of the alveolar wall results in …?

A
  • Loss of surface area for gas exchange
  • Loss of pulmonary capillaries
  • Loss of elastic fibers
  • Altered ventilation-perfusion (VQ) ratio
  • Decreased support for other structures
35
Q

Fibrosis in the lungs results in…?

A
  • Narrowed airways
  • Weakened walls
  • Interference with passive expiratory airflow
36
Q

As emphysema progresses, patients experience

increasing difficulty with…

A

Expiration

37
Q

Patients with advanced emphysema and loss of tissue experience…

A

• Adjacent damaged alveoli forming even larger air spaces.
• Pneumothorax (occurs when pleural membrane surrounding large blebs
ruptures)
• Hypercapnia becomes marked
• Hypoxia becomes driving force of respiration- “CO2 dependent”
• Frequent infections
• Pulmonary hypertension and cor pulmonale* may develop in late stage.

38
Q

What is a barrel chest an indicator of?

A

Progressive emphysema due to fixation of the ribs in a respiratory position.

39
Q

Signs and symptoms of emphysema?

A

• Dyspnoea and reduced exercise tolerance
• Hyperventilation with prolonged expiratory phase
• Anorexia and fatigue: including weight loss
• Clubbed fingers
• Sitting up – tripod position
• Noisy resps - usually with wheeze
• Use of accessory muscles / nasal flaring
• Barrel chest
• Productive cough
• Pursed lip breathing
• Confused and agitated
• Cyanosis (around lips and nail beds)
• Patients often develop bullae (thin-walled cystic lesions in lung) from destruction of alveolar walls; Blebs
(collection of air within visceral pleura) also develop
• Bullae and blebs can lead to pneumothorax

40
Q

What is the treatment of emphysema?

A
  • Primary survey
  • A to E with Respiratory status assessment
  • Vital signs: GCS, HR, RR, BP, SPO2, ECG
  • Focused history using OPQRST
  • Bronchodilators and oxygen therapy
41
Q

What is the long term management of emphysema?

A
  • Avoidance of respiratory irritants
  • Immunisation against influenza and pneumonia
  • Pulmonary rehabilitation
  • Appropriate breathing techniques
  • Adequate nutrition and hydration (improves energy levels, resistance to infection)
  • Lung reduction surgery
42
Q

What is chronic bronchitis?

A

A condition involving inflammatory
changes and excessive mucus production in the
bronchial tree

43
Q

What are the characteristics of chronic bronchitis?

A

• An increase in the number and size of mucus-producing glands: mucosa
are inflamed and swollen
• Hypertrophy and hyperplasia of mucous glands
• Fibrosis and thickening of bronchial wall
• Low oxygen levels
• Severe dyspnoea and fatigue
• Pulmonary hypertension
• Alveoli are not seriously affected and diffusion remains relatively normal…
• However patients have low oxygen pressure (Po2) because of changes in
ventilation–perfusion relationship

44
Q

Hypoventilation leads to …?

A
  • Hypercapnia (high levels of CO2)
  • Hypoxaemia (low levels of O2)
  • Increases in Pco2
45
Q

Signs and symptoms of chronic bronchitis?

A

• Constant productive cough
• Tachypnea and shortness of breath
• Frequent thick and purulent secretions
• Cough and rhonchi more severe in the morning
• Hypoxia, cyanosis, hypercapnia (all caused by airway
obstruction)
• Polycythaemia (over production of RBC), weight loss and signs of cor pulmonale
possible (as vascular damage and pulmonary hypertension
progresses)

46
Q

What is the short term management of chronic bronchitis?

A
  • Primary survey
  • A to E with Respiratory status assessment
  • Vital signs: GCS, HR, RR, BP, SPO2, ECG
  • Focused history using OPQRST
  • Bronchodilators and oxygen therapy
47
Q

What is the long term management of chronic bronchitis?

A
  • Cessation of smoking and reduction of exposure to irritants
  • Treatment of infection using AB’s
  • Vaccination for prophylaxis
  • Expectorants
  • Appropriate chest therapy (including postural drainage and percussion)
  • Low-flow oxygen
  • Nutritional supplements
48
Q

What are the three pathophysiological responses occurring in the lungs during an asthma attack?

A
  • Bronchial smooth muscle contraction
  • Hypersecretion of mucus, resulting in bronchial plugging
  • Inflammatory changes in bronchial walls
49
Q

What is asthma?

A

a disease characterised by recurrent attacks of breathlessness and wheezing due to inflammation and constriction of the air passages in the lungs.

During an attack, the lining of the airway swells causing narrowing and reduced flow of air in and out of the lungs.

50
Q

What is the pathophysiology of asthma?

A

Inflammation of mucosa, bronchoconstriction and excess mucus secretion
causes;
• Increased resistance to airflow and decreased flow rates
• Hyperinflation then occurs distal to obstructions, which results in…
• Altered breathing mechanics and increased work of breathing
• Oxygen consumption increases in respiratory muscles
• Increased intra pleural pressures are raised
• Decreased perfusion occurs at the alveoli
• Decreased ventilation also occurs
• This all leads to VQ mismatch
• …which eventually causes respiratory acidosis

51
Q

What is the typical presentation of a patient with asthma?

A 
• Cough
• Marked dyspnoea
• ‘Tight’ feeling in chest
• Wheeze
• Rapid and laboured breathing
• Expulsion of thick or sticky mucus
• Tachycardia: which might include
pulsus paradoxus
• Hypoxia
• ‘Silent’ chest
52
Q

What are the two types of asthma and how are they different?

A 
Intrinsic asthma:
• Non seasonal
• Non allergic
• First occurs later in life
• Chronic and persistent

Extrinsic asthma (allergic):
• Caused by exposure to inhaled airborne antigen
• Causes production of antibodies (IgE)
• Bind to mast cells in bronchial tree that release histamine
• Histamine release stimulates bronchospasm and increased oedema with
inflammation

53
Q

What are the signs and symptoms of asthma?

A

• Respiratory alkalosis: initially caused by
hyperventilation
• Respiratory acidosis: caused by air trapping
• Severe respiratory distress: hypoventilation leads to
hypoxaemia and respiratory acidosis.
• Respiratory failure: indicated by decreasing
responsiveness, cyanosis

Medical Studies 1 (11 decks)

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