Common Respiratory Conditions Flashcards

1
Q

Dysphnoea

A

Difficulty breathing

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2
Q

Ventilation

A

Amount of air entering/ leaving the lungs

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3
Q

Perfusion

A

Amount of blood perfusing a capillary bed (alveolar or in tissue)

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4
Q

Hyperventilation

A

Excessive ventilation

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5
Q

Hypo ventilation

A

Decreased ventilation

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6
Q

Tachypnoea

A

Increased respiratory rate

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7
Q

Badypnoea

A

Decreased respiratory rate

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8
Q

Hypoxia

A

Reduced tissue oxygen

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9
Q

Hypoxaemia

A

Reduced oxygen levels in the blood
Under 60mm Hg or 8KPa

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10
Q

Hyper apnea

A

Increased carbon dioxide levels in the blood
Over 42mm or 5.6KPa

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11
Q

Cyanosis

A

Blood discolouration of skin

Mucous membranes associated with levels of oxygenation

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12
Q

Acidosis

A

Low blood pH <7.35

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13
Q

Alkalosis

A

High blood pH > 7.45

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14
Q

Pathophysiology

A

The physiology of abnormal states

The functional changes that accompany a particular syndrome or disease.

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15
Q

Parenchyma

A

Respiratory tissue of the lungs

Including respiratory surface and alveoli

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16
Q

Describe restrictive respiratory disease?

A

Eg. Interstitial lung disease and children’s interstitial lung disease
- Small volume of air flowing in
- Total lung capacity low
- Decreased lung compliance
- Restriction to airflow – difficult to inflate the lung
Intrinsic – changes inside the lung
Extrinsic – issues outside the lungs

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17
Q

What are two categories of restrictive respiratory diseases?

A

Intrinsic – changes inside the lung
Extrinsic – issues outside the lungs

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18
Q

What are obstructive respiratory diseases?

A

Eg. Emphysema or asthma
- Small volume of air flowing out
- Vital capacity low
- Increased lung compliance

Obstruction to air flow – difficult to expel air

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19
Q

Is cystic fibrosis an obstructive or restrictive disease?

A

Often termed obstructive disorder but some elements of restriction observed.

Reduced pulmonary volumes but also mucus production.

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20
Q

How are lung and pressure of the lungs effected by obstructive respiratory diseases?

A
  • high lung volume
  • low inspirations pressure
  • easy to fill the lungs
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21
Q

How is volume and pressure in the lungs effected by restrictive respiratory diseases?

A
  • Similar to a healthy person residual volume
  • decreased total lung volume
  • Decreased compliance
  • Lower volume
  • Higher pressure
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22
Q

What are the perceived causes of cystic fibrosis?

A
  • Genetic variant
  • CFTR gene (chromosome 7) (cystic fibrosis transmembrane conductance regulator)
  • Most common variant -ΔF508 – deletion mutation of one amino acid phenylaniline
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23
Q

How are Caucasians vs African and Asian ethnicities disproportionally effected by cystic fibrosis?

A
  • Caucasians 1 in 3500 (Irish 1 in 1400)
  • Africans and Asians < 1 in 15,000 births
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24
Q

What does the CFTR gene do when deficient?

A

Chloride ion transporter – multiple categories of variant defects

Main cellular defect caused by CFTR variants
1. Defects in protein production
2. Defects in function of the pump
3. Defects in regulation of the pump
4. Defects in protein processing (proteins do not pump chloride out of the cell so effect movement of sodium ions out the cell

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25
Q

What systems are effected by cystic fibrosis?

What are some symptoms of the disease?

A

-Recurrent pulmonary infection
- Lung abscess, chronic bronchitis, brochietasis, honeycomb lung
- cor Pulmonata
- chronic pancreatitis
- secondary Hilary cirrhosis
- malabsorption
- meconium ileus (newborn)
- obstructed vas deference (sterility)
- abnormal sweat electrolytes

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26
Q

What are some pathophysiological features of cystic fibrosis in the lungs?

A

1.Dyregulated / reduced chloride secretion
2. Increased sodium reorption into epithelial cells
3. Water follows the sodium and is absorbed into the epithelium
4. Mucus becomes thickened more sticky and dehydrated
5. Mucus more adherent
6. PH lowered in bronchial epithelial
7. PH change – defects in anti microbial deference

Secretion of chloride ions by mucus secreting epithelial cells controls the parallel secretion of fluid and thus the viscosity of the mucus.

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27
Q

What are some respiratory pathological features of cystic fibrosis?

A

1.Chronic sinusitis – bacterial infection
2. Hyperinflation of lungs – obstructive characteristic
3.Bronchiectsis - airway widening
4. Peribronchial cuffing – bronchial wall thickens
5. Chronic pulmonary inflammation
6. Atelectasis – collapsed alveoli
7. Lung abscess – painful collection of pus normally following bacterial infection

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28
Q

What is bronchictasis?

A

The widening of the airway
-Widened airway, scarred and thickened airway wall and mucus
- reduces elastic recoil – difficult to empty lungs

29
Q

What is the vicious cycle theory of bronchiectasis?

A
  1. Abnormal mucus clearance
  2. bacterial infection
  3. colonisation
  4. neutrophil inflammation
  5. airway destruction and distortion.

repeating

30
Q

What is the effect of cystic fibrosis on bronchiectasis (the immune response)?

A
  • Production of elastase
  • Production of ROS (oxygen)
  • Increased superoxide or hydrogen peroxide
  • Loss of elasticity in airways
  • Loss of smooth muscle
31
Q

WHat are pathophysiological complications of cystic fibrosis?

A

1.Chronic airway infection in occluded areas
2. Pneumothorax
3. Fragile, distended blood vessels – often bursting
4. Widespread tissue destruction
5/ Pulmonary fibrosis (restrictive) and pulmonary hypertension
6.Ventilation-perfusion mismatching occurs
7. Chronic respiratory failure. Hypercapnia, hypoxia or both

32
Q

What are risk factors of chronic obstructive pulmonary disease?

A
  • Mostly associated with adult behaviours eg. 98% smoking
  • Indoor air pollution (biomass fuel used in cooking and heating)
  • Outdoor air pollution
  • Occupational dusts and chemicals – vapours irritants and fumes
33
Q

What are risk factors of chronic obstructive pulmonary disease? Childhood?

A
  • Maternal asthma
  • Paternal asthma
  • Childhood asthma
  • Severe respiratory infections before 5 years old
  • Maternal smoking
34
Q

What is COPD?

Chronic obstructive pulmonary disease

A

Airflow obstruction
- Flat diaphragm
- Hyper inflated lungs

Reduction of expiratory flow rate

35
Q

What is chronic bronchitis?

A

– Inflammation of the bronchiole
– change to lining epithelial of the bronchi
– overgrowth submucosa and mucus glands
– disorganised and dysfunctional bronchus cells

36
Q

What is emphysema?

A
  • LoosE parenchyma of lung
    – less surface
    – no where for oxygen to cling too
    – fewer larger alveoli
37
Q

What are the causes of Chronic Obstructive pulmonary disease in lumen? COPD?

A

-In lumen
- Over production of mucus, development of pus, neutrophils overactive (produce pus)

38
Q

What are the causes of Chronic Obstructive pulmonary disease in the wall? COPD?

A
  • Causes in the wall
  • Inflammation and oedema, hypertrophy, bronchi constrictions
39
Q

What are the causes of Chronic Obstructive pulmonary disease outside the airways? COPD?

A

Loss of arancyma
– loss parenchyma of lung
- loss of elastase
- loss of radial traction (smaller radius)
- less elastic recall

40
Q

What is emphysema?

A

Example of obstructive lung disorder

-Permanent Restruction and enlargement of alveolar airspace’s
- Enlargement of the alveolar airspaces with loss of elastic recoil and reduced alveolar gas exchange surfaces area.
- Loss of radial traction
- Removal of elastic tissue

41
Q

What the process of acquiring emphysema?

Smoking example

A

1.Smoke particles and chemicals inhaled
2. Macrophages/neutrophils phagocytose
3. Serine elastase released
4. Elastin destroyed
5. Smoke and ROS inactive alpha1 - antitrypsin – elastase inhibitor – when inactive uncontrollable loss of elastic tissue

42
Q

What’s the genetic predisposition of getting emphysema?

A

– alpha 1 antitrypsin deficiency

  • link to severe emphysema in younger people
43
Q

What is ROS?

A

Restricted oxygen species

44
Q

What are the symptoms of COPD?

Chronic obstructive pulmonary disorder
Chronic bronchitis

A

-Hypertrophy of mucus glands in larger bronchi (Overgrowth of gland cells so excessive amounts of mucus)
- Excessive mucous production
- Excessive expectoration
-Chronic inflammatory changes in smaller bronchi

45
Q

What is the chronic bronchitis pathology?

A

1.Submucous contains submucousal glands
2. Basal cell meta plasma – cells divide to make more cells – grow disorganised so thicker basement membrane – fibroblasts disorganised
3. Squamous cell metaplasia – not ciliated – loose ciliated lined – so can’t clean out mucus – mucoscilary escalator that’s typical of goblet cells
4. Overgrowth of mucus gland hyperplasia – excessive mucus and pitting of mucus in can’t move the mucus as cilia has been lost
5. Lymphocyte recruitment – thickening and stiffening of walls of airways
6. Fibroblasts – recruitment lay down collagen fibres to thicken within the cell

46
Q

What is the reid index?

Related to chronic bronchitis

A

Given handle of state of chronic bronchitis - how severe
- Ratio of thickness of mucus gland tissue and thickness of submucosa
- Normal < 0.4
- Severe > 0.7
- To measure is they have lung problems removing are from lungs - FEV1:FVC (forced vital capacity) – blow into meter and register how much of vital capacity you can blow out in first second. Normal 80%, Obstructive 42%

47
Q

What are some ethologic factors of asthma?

A

Obstructive lung condition

1.Character of air being breathed (allergens, cold air, insect/pet, smoking, pollutants, exercise and food)
2. Acid reflux
3. Post nasal drip
4. Stress and anxiety
5. Genetic linkage
6. Drug induces (NSAIDs)

48
Q

What does etiologic mean?

A

Causes and contributing factors for the development of disease and condition

49
Q

What is the delayed response pathophysiology of asthma?

A

1.Eosinophils release transmitters (disrupts Mucocilary escalator) – Inhibtates epithelial damage
2. Damage stimulates free never ending - activated by inflammatory mediators in wall of bronchiole 0 send emergency message to CNS about damage to walls – activated the parasympathetic nervous system
3. Autonomic (parasympathetic) discharge initiated - - also efferent a gal nerve discharge
4. Music secret or and smooth muscle respond – in positive feedback loop to reinforce the response. To further bronchi constrictions and mucus secretion – this amplifies the attack

50
Q

What is the pathophysiology of asthma with its effect on small diameter airways?

Long term effect of asthma

A
  • Smooth muscle hypertrophy
  • Mucus gland hypertrophy
  • Inflammatory cell infiltration
  • Oedema of bronchial wall
  • Scarring
  • Sub epithelial fibrosis
  • Structural remodelling
51
Q

What are the acute or reversible effects of asthma?

A
  • Narrowed irregular lumen
  • Sticky mucus
  • Epithelial damage
  • Increased vagaries tone
  • Reduced airflow
  • Wheezing
52
Q

What is diffuse pulmonary fibrosis?

A

A restrictive disorder
Type of interstitial lung disease

  • A lot of connective tissue to enhance the radial traction – restriction within the parenchyma as low elastic
53
Q

What’s the pathology of diffuse pulmonary fibrosis?

A

A restrictive disorder - type of interstitial lung disease

  • Interstitial space
    – reduces the size/ availability of space
    – fibrosis (collagen reduces elasticity of lung), fibroblast foci (lay down the collagen and form the scar tissue)
  • formation of scar tissue
  • A lot of connective tissue to enhance the radial traction
  • restriction within the parenchyma as low elastic
54
Q

What are the aetiology feature of diffuse pulmonary fibrosis?

A

1.immunological – arthritis
2. Genetic linkage – surfactant production – Mucus genes to produce mucus are effected
3. Viral pathology – repeated infections so recruit infection cells (macrophages and neutrophils) – inflammatory response lay down collagen fibres excessively

55
Q

What are the symptoms of diffuse pulmonary fibrosis?

A

-Dyspnoea
- Dry, unproductive, cough
- Rapid shallow breathing
- Reduced chest movement
- lung crepitations
- reduced exercise capacity
- low FEV1 (possibly normal) and FVC
- clubbing if fingernails – reduced oxygen

56
Q

What are the pathological effect symptoms of diffuse pulmonary fibrosis?

A

segmental airway expanded

honeycombing

57
Q

What is the pathology of interstitial lung disease?

A

1.Reactive interstitial inflammation from injury in parenchyma of the lung
2. As this develops and persists – the inflammatory mediator fibroblasts lay down collagen fibres
3. Can invade the alveoli and amputate sections of alveoli
4. Ingrowth of bronchiole epithelium
These all reduce availability of alveoli
5.This leads to the issue of - Collapsed or distal airways, dense fibrosis and bronchiole epithelium stops lung tissue expansion

58
Q

What’s the FEV1 to FVC ratio for restrictive disorders like Diffuse pulmonary fibrosis ?

A

90% of oxygen expelled

This ratio however is high as there is less oxygen exhaled as they lungs are so restricted and so naturally smaller volume of air

59
Q

Whats the restriction and partial pressure of oxygen and carbon dioxide for restrictive disorders?
How does exercise/ non-exercise effect restrictive disorders?

A

Diffusion capacity is low

Flicks law of diffusion means there’s a low partial pressure of oxygen

  • less active = compensation and less symptoms - normal reserve capacity compensate for that lost and reduced availability at rest.
  • reduced exercise capacity as fewer reserves of O2.
60
Q

Give some examples of extrinsic restrictive disorders

A
  • Pneumothorax (collapsed lungs)
  • Ankylosis Spondylitis (Autoimmune disease causing skeleton to fuse and inflation of chest is restricted)
  • Scoliosis/kyphosis (spinal curves to compromise chest as can’t inflate lungs)
    Obesity hypoventilation syndrome (Mechanical interference with breathing, particularly changes in respiratory drive in response to hypercapnia)
61
Q

How do lungs get more of less acidic? acid-base balance?

A

-constant CO2 production in respiring tissues
- Buffering system can donate or accept protons but the elimination of excess clearing carbon dioxide important
- More protons means more acidic less protons means more alkali blood

  • Kidneys handle 100mEq per day and lungs handle 10,000 mEq per day
  • This means the lung needs to get rid of or gain hydrogen to keep a balance
62
Q

What is acidosis? What causes acidosis?

A

– pH <7.35 (low more acidic)
– hypoventilation, lung disease, opiate driven hypoventilation

63
Q

What is alkalosis? What causes alkalosis in lungs?

A

– pH >7.45 (high more alkaline)

– hyperventilation, anxiety and high altitude.

64
Q

What are acidosis and alkalosis?

A

Changes in blood pH due to respiring tissues.

Normally pH 7.4

Acidosis <7.35 and alkalosis >7.45

65
Q

What are symptoms of acidosis?

A

Acidic lungs

-headaches, sleepiness, confusion, loss of consciousness and coma
- Shortness in breath, coughing
- Arrhythmia, increased heart rate
- Nausea and vomiting
- diarrhoea
- Seizures and weakness

66
Q

What are symptoms of alkalosis?

A

Alkaline

-Confusion, light headedness, coma
-Peripheral tingling, pain, reduced calcium, reduced potassium
- reduced output of heart
- Muscular spasms
- Nausea and vomiting

67
Q

What are the effects of aging on the respiratory system?

A
  • Decreased respiratory surface area
  • Increased alveolar size
  • Increased bronchiole diameter
  • Reduced elasticity of lung tissue
  • Dysregulation of fibroblast function
  • Decreased thoracic compliance
68
Q

WHat epigenetic factors linked to aging and the respiratory system?

A

-Altered proteostasis
- Mitochondrial dysfunction
- Increased apoptosis
- altered nutrient sensing
- Stability of extracellular matrix
- changed to inflammatory response in the lung
- reduced antibody responses in the lung