week 5 respiratory

Question 1

pleura

Answer 1

Thin, transparent, double-layered serous membrane lining thoracic cavity & encasing lungs
Parietal layer: lines pulmonary cavities & adheres to thoracic wall, mediastinum & diaphragm
Visceral layer: covers lung & adheres to all its surfaces

Question 2

conducting airway

Answer 2

Nasal passages, mouth & pharynx, larynx, trachea, bronchi & bronchioles

Question 3

mucociliary blanket

Answer 3

• Cilia are in constant motion to remove foreign materials

- Cilia are in constant motion to remove foreign materials

Question 4

Gas exchange within lungs depends on

Answer 4

Open airways
Expansion of lungs
Adequate surface area for gas diffusion
Blood flow through the pulmonary capillary bed.

Question 5

Acute Respiratory Failure - Hypoxemic

Answer 5

lack of O2 or insufficient amount

Question 6

Acute Respiratory Failure - Hypoxemic- Ventilation-Perfusion Mismatch

Answer 6

Ventilation-Perfusion Mismatch: areas of lung are ventilated but not perfused, or vice versa
Portion of lung is either being inadequately ventilated, or perfused
Results in carbon dioxide retention
CO2 is a stimulus for respiration, so respiratory rate (RR) increases to prevent hypercapnia (excessive carbon dioxide levels
Increased RR & work of breathing  extremely tired patient

Question 7

Acute Respiratory Failure - Hypoxemic- Impaired Diffusion

Answer 7

gas exchange between alveolar air & pulmonary blood impeded
Due to increased distance for diffusion OR decreased permeability of respiratory membranes
Gas exchange affected, often due to surface area issue (E.g. ARDS pulmonary oedema, pneumonia – all involve fluid within lung)

Question 8

Acute Respiratory Failure – Hypercapnic/Hypoxemic

Answer 8

-Ventilating insufficiently to clear CO2 & maintain normal O2 levels (hypoventilation)
-Causes increased PCO2 &, typically, hypoxemia
-results from Respiratory centre (CNS) depression (drug overdose, brain injury)
Diseases of nerves supplying respiratory centre (Guillain-Barre syndrome, spinal cord injury)
Disorders of respiratory muscles (muscular dystrophy)
Chronic lung disease (COPD)
Thoracic cage disorders (crushed chest)

Question 9

acid-base balance

Answer 9

If acidosis/alkalosis occur, respiratory system regulates respiratory rate to return normal pH
Chemoreceptors detect changes in pH & respond:
Acidaemia: increased respiratory rate & depth to eliminate CO2
Alkalaemia: decreased respiratory rate & depth to retain CO2

Question 10

solubility of CO2

Answer 10

CO2 is 20x more soluble in plasma than O2

Question 11

respiratory acidosis

Answer 11

Pulmonary ventilation decreases so CO2 rises
Retained CO2 combines with H2O  carbonic acid
Dissociates to release free hydrogen & bicarbonate ions
Stimulate increased respiratory drive to expel CO2

Question 12

respiratory alkosis

Answer 12

Pulmonary ventilation increases leading to excessive CO2 exhalation
-↓CO2 causes cerebral vessel constriction
Dizzy, light headed, tingling & numbness of fingers & toes
-Short periods of apnoea may occur as CO2 level short-term stimulus for respiration

Question 13

CORD – Emphysema

Answer 13

• caused by smoking and Inherited deficiency of α1-antitrypsin
• results from elastin & other alveolar component breakdown by protease enzymes this breakdown leads to increased airspace size, & loss of elasticity, alveolar wall, and cappilary bed destruction, impairing gas exchange
• leads to hyperinflation of lungs- barrel chest
• pink puffers

Question 14

AAT

Answer 14

-Protease enzymes damage healthy lung tissue while removing bacteria in acute respiratory dysfunction
-α1-antitrypsin (AAT): protease-inhibitor, protects lung
-Some individuals born without AAT; smokers have inadequate production & release of AAT
Cigarette smoke & other irritants stimulate inflammatory cells in lungs to increase protease enzymes, as part of an inflammatory response
-not enough anti-protease can be produced
-Elastic tissue destruction occurs, & cellular resources cannot counter this

Question 15

CORD – Bronchitis

Answer 15

• Major & small airway obstruction
• Chronic irritation from smoking & recurrent infections
• History of chronic productive cough for ≥3 consecutive months in ≥2 consecutive years
• Large airways: mucus hypersecretion, associated with hypertrophy of submucosal glands in trachea and bronchi
• Small airways: obstructed,Increased goblet cell numbers Mucus plugging of lumen,Inflammation, Fibrosis of bronchial wall

Question 16

COPD

Answer 16

both emphesema and bhronchitis

Question 17

main factors contibuting to CORD

Answer 17

Inflammation
Fibrosis of the bronchial wall
Excess mucus secretion
Obstruct airflow leading to VQ mismatch

Question 18

PE pulmonary embolism

Answer 18

Blood-borne substance lodges in a pulmonary artery branch, mechanically obstructing flow (obstructive shock)

• thrombus (blood clot), air, fat (occurring from fracture), or amniotic fluid (maternal waters break
• leads to bronchoconstriction in affected area, Wasted ventilation,Impaired gas exchange,Loss of alveolar surfactant
• right heart failure may develop due to massive vasoconstriction if embolism big enough

Question 19

pneumonia

Answer 19

Inflammation of parenchymal structures of the lung

Four stages of development:
Oedema: alveoli filled with fluid containing multiple organisms causing capillary congestion.
Red hepatisation: massive outpour of leukocytes and red blood cells.
Grey hepatisation: (2+++ days) arrival of macrophages, phagocytose fragmented bacterial cells, red blood cells, cellular debris.
Congestion diminished but lung still firm
Resolution: alveolar exudate removed, lung slowly returns to normal
2 types
-bacterial
-viral

Question 20

plerisy

Answer 20

Inflammation of pleura

Common in infectious processes, especially pneumonia

Question 21

pleural effusion

Answer 21

Abnormal collection of fluid in pleural cavity
either excess rate of formation or decreased lymphatic clearance.
-fluid can be pus, blood, intravascular oe extravascular.
-Fluid enters pleural space from capillaries in parietal pleura, & removed by lymphatics

Question 22

pleural effusion-hydrothorax

Answer 22

accumulation of serous transudate; unilateral or bilateral

Typically caused by congestive heart failure; also renal failure, nephrosis, liver failure or malignancy

Question 23

pleural effusion= Chylothorax

Answer 23

lymph effusion from GI tract

Trauma, inflammation, or malignant infiltration obstructing chyle transport

Question 24

pnemothorax

Answer 24

Presence of air in pleural space, causing partial or complete collapse of affected lung
May be spontaneous or traumatic.

Question 25

Primary Spontaneous pneumothorax:

Answer 25

occur in healthy people
Tall boys/men aged 10 – 30 years
Smoking, family history of pneumothorax

Question 26

Secondary Spontaneous pneumothorax

Answer 26

Occur in people with lung disease
Associated with conditions causing gas-trapping & lung tissue destruction
Life threatening due to underlying issue & poor compensatory mechanisms

Question 27

Catamenial pneumothorax

Answer 27

Occurrence associated with menstrual cycle, usually recurrent; unknown cause
Women 30 – 40 years with history of endometriosis
Usually right lung
Develops within 72 hrs of menses onset

Question 28

tension pneumothorax

Answer 28

• Most likely to occur in traumatic pneumothorax,
• life-threatening; intrapleural pressure exceeds atmospheric pressure.
• Permits air entry, but no air exit
• Rapid increase in pressure within chest, causing compression atelectasis of UNaffected lung

Question 29

Haemothorax

Answer 29

• Type of pleural effusion- accumulation of blood in pleural cavity
• Blunt or penetrating trauma or medical issue
• ≥250ml blood in pleural cavity
• Lung may collapse as pressure of blood disallows lung expansion
• Mediastinal shift may occur, where pressure causes heart & great vessels to be affected

Question 30

Parenchymal:

Answer 30

portion of lung involved in gas transfer (alveoli, alveolar ducts, respiratory bronchioles)