Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHASE ONE > Respiratory system > Flashcards

Respiratory system Flashcards

1
Q

3 components of the upper respiratory tract

A

Nasal cavity
Pharynx
Larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Functions of nose

A
  • Temperature of inspired air
  • Humidity
  • Filter function
  • defence function; cilia take inhaled particulates backwards to be swallowed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

The anterior narea open into the enlarged…

A
  • Vestibule (skin lined, stiff hairs)

- Surface area of the nose (doubled by turbinates)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What do turbinates create?

A

Superior meatus
Middle meatus
Inferior meatus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Superior meatus

A

Olfactory epithelium
Cribiform plate
Sphenoid sinus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Middle meatus

A

Sinus openings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Inferior meatus

A

Nasolacrimal duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the paranasal sinuses?

A

Evagination of mucous membrane from the nasal cavity.

Pneumatised areas of the frontal sinus, maxillary sinus, ethmoid sinus and sphenoid bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are the paransal sinuses arranged?

A

In pairs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Frontal sinuses (location and nerve supply)

A

Frontal sinuses are found within frontal bone and midline septum over the orbit and across superciliary arch.
Nerve supply: opthalmic division of V nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Maxillary sinuses (location, shape, structure)

A

Located within the body of the maxilla.

Pyramidal shape.

Base is lateral wall of the nose, apex is zygomatic process of the maxilla, roof is the floor of the orbit, an floor is the alveolar process.

Open into the middle meatus, sinus drain into nasal cavity through the hiatus semilunaris.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ethmoid sinuses (location, features and nerve supply)

A

Between the eyes
Semilunar hiatus of the middle meatus

Labyrinth of air cells

Nerve supply - ophthalmic and maxillary V nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sphenoid sinuses

A

Medial to the cavernous sinus
Inferior to the optical canal + pituitary gland
Empties into the sphenoethmoidal recess, lateral to the attachment of the nasal septum.

Nerve supply - ophthalmic V.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the pharnynx?

A

Fibromuscular tube lined with epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which kind of epithelium lines the pharynx?

A

Squamous and columnar ciliated

with mucuous glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Nasopharynx is bounded by…

A 
Base of skull
Sphenoid rostrum
C-spine
Posterior nose (choana) 
Inferiorly at soft palate opens to oropharynx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Components of nasopharynx

A

Eustachian tube orifices (lateral wall) which supply air to middle ear and thus equalise pressure.

Pharyngeal tonsils on posterior wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Oropharynx components and their anatomical positions

A

Soft palate anteriorly.
Palatine tonsils on the lateral walls; tonsils in-between the palatoglossal walls and palatopharyngeal fold.
Inferior to hyoid bone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Function of larynx

A

Valvular functions: prevents lipids and foods from entering lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Structure of larynx

A

Rigid structure with 9 cartilages and multiple muscles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How are vocal chords changed?

A

Arytenoid cartilages rotate on the cricoid cartilage to change vocal chords.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What specifically prevents food going down into the lungs

A

Epiglottis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Main nerves of laryngeal innervation (more detail in further flashcards)

A

The vagus nerve (X cranial nerve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Divisions of vagus nerve in laryngeal innervation

A

Vagus divides into superior laryngeal nerve and recurrent laryngeal nerve.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Superior laryngeal nerve

  • source
  • where does it go to
A

Inferior ganglion

Lateral pharyngeal wall, which divides into interal (sensation) and external (cricothyroid muscle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Recurrent laryngeal nerve

  • function
  • divisions and the course of each division
A

Main motor function - all muscles except cricothyroid.

Left RLN: lateral to arch of aorta, loops under aorta, ascends between trachea and oesophagus.

Right LRN: Right subclavian artery, plane between trachea and oesophagus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

3 main components of the lower respiratory tract

A

1) trachea
2) primary bronchi
3) lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Thoracic cage (anatomical stuff)

A

Sternal angle at level of carina

Manubrium sternal joint = 2nd rib. In the second intercostal in midclavicular line you can stick chest drain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Trachea features

  • Where does it span to and from
  • What vertebral level is the division of main left and right bronchi
  • Epithelium
A

Spans down from larynx to the carina; the division oof the main left and right bronci (5th thoracic vertebra, T5)

Pseudostratified, ciliated, columnar epithelium with goblet cells

Semicircular cartilages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is the name of the division of main left and right bronchi?

A

Carina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Difference between left and right bronchi?

A

Right main bronchus is shorter and wider while the left bronchus is longer and narrower. The right bronchus is more vertical compared to the left bronchus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Lobar bronchi

A

Right - 3:

  1. Upper lobe
  2. Middle lobe
  3. Lower lobe

Left - 2:

  1. Upper lobe and lingular
  2. Lower lobe

Left is smaller due to accomodating the cardiac structures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Segmental branches/bronchi

A

Right:
upper lobe => apical, anterior, posterior

middle lobe => medial and lateral

Lower lobe => apical, anterior, posterior, medial, lateral

Left:
upper lobe => apico-posterior, anterior
lingular => superior and inferior
Lower => apical, anterior, posterior, lateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Acinus

A

The acinus is a small saclike cavity in a gland that is supplied with air from one of the terminal bronchioles. There are ducts (short tubes with multiple alveoli).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Interconnections between alveoli:

A

pores of Kohn.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Types of cells in alveoli

A

Type I pneumocytes

Type II pneumocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Type I pneumocytes

A

barrier across which gas exchange occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Type II pneumocytes

A

Surfactant produces.

Surfactant decreases surface tension and keep alveoli open. Regenerate and replace damaged cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Other components of alveoli:

A
  • Alveolar macrophages
  • Basement membrane
  • Interstitial tissue
  • Capillary endothelial cell
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What does lung innervation supply?

A

Controls many aspects of function => smooth muscle tone, mucus gland secretion, vascular permability, blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Sympathetic lung innervation results in …

A

Bronchodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Parasympathetic lung innervation result

A

Bronchoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Pleura of lungs

A

2 main layers of mesodermal origin;

  • Visceral
  • Parietal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Visceral layer

A

Applied to lung surface

Autonomic innervation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Parietal layer

A

Applied to internal chest wall

Pain sensation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Pulmonary circulation

A

Left and right pulmonary arteries run from the right ventricle.
There are 17 orders of branching.
Elastic and non elastic, muscular arteries. Arterioles and capillaries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How much gas is respiratory pump required to move?

A

5L/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Which parts are always involved in the respiratory pump

A 
Bones
muscles
pleural 
peripheral nerve
airways
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Respiratory pump and pressure

A

Negative intra-alveolar pressure has to be generated to allow inspiration of air. Diaphragm contracts in inspiration, becoming flat and increasing the tidal volume of lung.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Bony thorax function

A

Bony structure supports respiratory muscles and protects lungs. Helps support rib movement.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Describe the process of inspiration

A
  1. The diaphragm contracts causing its dome to move downards thereby enlarging the thorax and increasing its volume
  2. Simultaneously, activation of the motor neurones in the intercostal nerves to the EXTERNAL intercostal muscles causes them to contract, resulting in an upward and outward movement of the ribs and a further increase in thoracic volume
  3. As the thorax expands the intrapleural pressure is being lowered and the transpulmonary pressure becomes more POSITIVE, resulting in lung expansion since the force acting to expand the lungs (i.e. transpulmonary pressure) is becoming greater than that of the elastic recoil exerted by the lungs
  4. The lung expansion results in the alveolar pressure becoming negative which results in an inward airflow
  5. At the end of inspiration, the chest wall is no longer expanding but has yet to start passive recoil, since lung size is not changing and the glottis is open at this point.
    • Alveolar pressure = atmospheric pressure, since the elastic recoil of the lungs has been balanced by the transpulmonary pressure - resulting in no airflow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the process of expiration

A
  1. At the end of inspiration, the motor neurones to the diaphragm and external intercostal muscles decrease their firing so these muscles can relax; the diaphragm ascends thereby decreasing thoracic volume
  2. As they relax, the lungs and chest walls start to passively collapse due to elastic recoil - this is because the muscle relaxation causes the intrapleural pressure to increase, thereby decreasing the transpulmonary pressure so it becomes more negative.
  3. As the lungs become smaller, air in the alveoli becomes temporarily compressed resulting in an increase in alveolar pressure i.e it becomes more positive and exceeds atmospheric pressure resulting in air flowing outwards
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Muscles of inspiration

A

Diaphragm = 70% of volume change

External intercostals = lift ribs 2-12 and widen thoracic cavity

Scalenes lift ribs 1-2

Pectoralis major lifts ribs 3-5

Sternocleidomastoid elevates the sternum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Nerves involved with the lungs

A

MOTOR
Diaphragm C3, 4, 5
Thoraco-lumbar nerve roots

SENSORY

  • Sensory receptors assessing flow, stretch etc.
  • Afferent via vagus (X cranial nerve)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Static lungs

A

Both chest wall and lungs have elastic properties and a resting unstressed volume.
Changing this volume requires force, and release of this force leads to a return to the resting volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What do terminal bronchioles lead to?

A

Respiratory bronchioles (at the centre of acinus), alveolar ducts and alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Dead space definition

A

volume of air not contributing to gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pre-inspiration/end expiration volume of air

A

500mls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

How much of 500mls go to blood (in ml)

A

350

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How is alveolar dead space increased?

A

Very rapid breaths increase DS and under ventilates the alveoli.
Vice versa - big breath hyperventilate and over ventilate alveoli.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How many capillaries per alveolus?

A 
1000 
Each RBC (erythrocyte) can come into contact with multiple alveoli.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

At what point is Hb fully saturated

A

At rest 25% of the way through the capillary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What does perfusion of capillaries depend on

A

Pulmonary artery pressure
Pulmonary venous pressure
Alveolar pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Pulmonary vascular resistance

A

Certain pulmonary arteries have smooth muscle within their walls
Hypoxic pulmonary constriction (which is the opposite from systemic circulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Hypoxic pulmonary vasoconstriction

A

Blood vessels divert blood to the more oxygenated parts of the lungs away from [low O2] areas, or areas with collapsed airways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

PaCO2 definition

A

arterial CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

PACO2 definition

A

alveolar CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

PaO2 definition

A

arterial O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

PAO2 definition

A

alveolar O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

PIO2

A

Pressure of inspired oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

V’A

A

Alveolar ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

V’CO2

A

CO2 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

HCO3-

A

bicarbonate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Why are O2/Hb dissociation curves non-linear

A

More binding of O2 and Hb facilitates further binding due to changes in Hb binding sites.
=> sigmoidal S shape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Alveolar gas equation

A

PAO2 = PiO2 - PaCO2/R

R = respiratory quotient

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Why is the alveolar gas equation important?

A

Important for patients in the ICU to know how much oxygen to give them.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the pressure of inspired O2

A

21 kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the atmospheric pressure of O2

A

100kPa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Causes of hypoxeamia (low blood O2)

A

Alveolar hypoventilation
Reduced PIO2
V/Q mismatch
Diffusion abnormality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

CO2 equation

A

PaCO2 = k V’CO2/V’A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What shape is CO2/Hb dissociation curve?

A

Linear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

3 ways CO2 is carried

A
  1. bound to Hb (approx 23% of CO2)
  2. dissolved in plasma
  3. As HCO3- (bicarbonate)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is PaCO2 directly proportional to? What is it inversely proportional to?

A

Directly p to amount of CO2 produced

Inversely p to alveolar ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Physiological causes of high [CO2]

A

V’A reduced
Increased dead space by rapid shallow breathing
Increased dead space by V/Q mismatching
Increased CO2 production

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Why is acid-base balance controlled carefully?

A

Normally body acids and bases are regulated to ensure the pH of the extracellular fluid is within a narrow range to ensure optimal function (e.g. of enzymes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Normal range of [H+]

A

34-44nmol/L

optimal = 40nmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Is HCO3- a strong or weak base

A

weak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Is H2CO3 a strong or weak acid?

A

Weak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Which is a particularly important buffer in the blood?

A

Carbonic acid/bicarbonate buffer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

CO2 is under predominant ??? control

A

respiratory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

HCO3- is under predominant ??? control

A

renal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

pH of bodily fluids is regulated by three main buffering systems:

A
  1. intracellular and extracellular buffers
  2. the lungs eliminating CO2
  3. renal HCO3- reabsorption and H+ elimination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Acid continually produced by …

A

metabolic processes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Carbonic acid equilibrium

A

CO2 + H2O <=> H2CO3 <=> H+ and HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Hendersson-Hasselbach equation

A

pH = 6.1 + log 10 [[HCO3-]/[0.03*PCO2]]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

4 main acid-base disorders are:

A
  1. Respiratory acidosis
  2. Respiratory alkalosis
  3. Metabolic acidosis
  4. Metabolic alkalosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Respiratory acidosis

A

Increased PaCO2
decreased pH
mild increased HCO3-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Respiratory alkalosis

A

Decreased PaCO2
increased pH
mild decrease HCO3-

can be caused by hyperventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Metabolic acidosis

A

reduced bicarbonate

decreased pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Metabolic alkalosis

A

increased bicarbonate

increased pH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

acidotic

A

not enough CO2 removed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Acute inflammation

A
  • Vasodilation leads to excretion of plasma, including antibodies.
  • Activation of biochemical cascades e.g. complement and coagulation cascades
  • Migration of blood leukocytes into the tissues; mainly neutrophils but also some monocytes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Double edged sword of inflammation

A

Inflammation is the body’s defence against infection and a hostile environment. But many of us die of causes caused by inflammatory processes (e.g. pneumonia).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Inflammation-mediated tissue damage in the lung (examples)

A

COPD (chronic obstructive pulmonary disease).

Acute Respiratory Distress Syndrome.

Brionciesctasis

Interstitial lung disease

Asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

COPD

A

Caused by cigarette smoking and fossil fuels.
Casued by the action of neutrophils on the lung: leads to destruction of the alveolar membrane.
Proteases degrade elastase and cause collapse of airways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Acute respiratory distress syndrome

A

Respiratory failure

Water and neutrophils fill the alveoli causing lungs to appear more grey on an X-ray.

Any condition that causes inadequate tissue oxygenation may precipitate ARDS e.g. trauma, lung infetion, sepsis, surgery etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Pathophysiology of ARDS

A
  • Endothelial leak (leaking to extravasatation of protein and fluid)
  • Lungs - reduced compliance makes lungs stuff, increasing shunting.
  • Heart - pulmonary hypertension, reduced cardiac output
  • Hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Where is acute inflammation initiated

A

Initiated in the tissues by epithelial production of hydrogen peroxide when it is damaged. Hydrogen peroxide is natural bleach and attracts neutrophils (haemotaxic effect).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

How is the acute inflammation initial response amplified?

A

Initial response amplified by specialist macrophages.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Specialist macrophages in the acute inflammation response

A
  • Kupffer cells (liver)
  • Alveolar macrophages (lungs)
  • Histiocytes (skin, bone)
  • Dendritic cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

(acute inflammation) Response to pathogens or tissue injury involves the recognitio of:

A
  1. PAMPs (pathogen-associated molecular patterns) which recognise pathogens
  2. DAMPs (damage-associated molecular patterns) which recognise damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What are pattern recognition receptors (PRRs)

A

These receptors recognise new pathogens and are involved in signalling and endocytosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Examples of Pattern Recognition Receptors (PRRs)

A

Toll-like Receptors which recognise endogenous mediators of inflammation

Nod-like receptors (NLRs)

Endocytic PRRs
=> mannose receptors
=> glucan receptors
=> scavenger receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

What are alveolar macrophages similar to cytochemically and morphologically

A

mature tissue macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Where do alveolar macrophages arise from?

A

monocytes

foetal macrophages populate lungs to form alveolar macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

3 types of macrophages and their function

A

M1 - host defence; produce Th-cells and NK cells

M2a - tissue repair; stimulating fibroblasts

M2b - resolution - healing, sending away immune cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Brief overview of neutrophil functions

A 
Identification
Activation
Adhesion
Migration/chemotaxis
Phagocytosis
Bacterial killing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Neutrophils + activation

A

Stimulus-response coupling; matching immune response to stimulus.
Allowing phagocytosis of bacteria.
Signal transduction pathway including calcium, protein kinases, phospholipases, G proteins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Neutrophils and migration

A

They are able to detect a concentration gradient of bacterial products or chemokines and move along it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Neutrophils + bacterial killing

A

Lysosomal enzymes in granules (cathepsins, elastase)

Reactive oxygen species

ROS generated by a membrane enzyme complex - the NADPH oxidase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Pack-year

A

1 pack year = smoking 20 cigarettes per day for 1 year

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What is spirometry

A

A test used to assess how well your lungs work by measuring how much air you inhale, how much you exhale and how quickly you exhale

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What is ACOS

A

Asthma and COPD overlap syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Regulation of airwys smooth muscle tone

A

Airway smooth muscle is regulated, contracting and relaxing to regulate airway diameter. This is important in diseases such as COPD and asthma.
It is regulated by inflammation and the autonomic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Regulation of airwys smooth muscle tone

A

Airway smooth muscle is regulated, contracting and relaxing to regulate airway diameter. This is important in diseases such as COPD and asthma.
It is regulated by inflammation and the parasympathetic NS.
Contractile signals cause increase in intracellular calcium in smooth muscle, which activates actin-myosin contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Parasympathetic bronchoconstriction

A

Vagus nerve neurons terminate in the parasympathetic ganglia in the airway wall. Short post-synaptic nerve fibres reach the muscle and release acetylcholine, which acts on muscarinic receptors of the M3 subtype on the muscle cells. This stimulates airway smooth muscle constriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Excessive bronchoconstriction

A

EB narrows the airway in asthma and in COPD (and other like bronchiectasis).
Therefore, inhibition of the parasympathetic nervous system will be beneficial.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Drug action to inhibit parasympathetic nervous system to prevent excessive bronchoconstriction

A

Drugs block the M3 rceptor, and are called ANTI-CHOLINERGICS or ANTI-MUSCARINICS.

Short acting: ipratropium bromide (atrovent).

Long acting: LAMAs such as tiotropium, glycopyrrhonium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Anti-cholinergics

A

SAMA (short acting muscarinic antagonist)

LAMA (long acting muscarinic antagonist)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Short acting muscarinic antagonists (SAMAs)

A

Ipratropium bromide exists as an inhaler and can be used as inhaled treatment to relax airways in asthma and COPD.

Its not that effective, and is much less used since LAMAs were invented.

It is still used in high dose in nebulisers as part of acute management of severe asthma and COPD.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Long acting muscarinic antagonists (LAMAs)

A

Have a long duration of action (many hours), often given once a day.
Increase bronchodilation and relieves breathlessness in asthma and COPD.
Seem to reduce acute attacks as well.

132
Q

SABAs and LABAs

A

Short-acting (salbultamol) and long-acting (formoterol, salmeterol)

Acute rescue of bronchoconstriction
Prevention of bronchoconstriction
Reduction in rates of exacerbations

Given with steroids in asthma, often without steroids in COPD.

LABA often given with LAMA in COPD.

133
Q

Mechanism of action of Beta 2-agonists

A

B2-aginist attaches to Beta-2 receptors on airway muscle. This has an affect on the G-protein and stimulates adenylyl cyclase which converts ATP into cAMP. Protein kinase is converted to pLA. This all causes RELAXATION of airway smooth muscles.

134
Q

Adverse effects of B2-agonists

A
  • Raising cAMP may activate Na/K exchange pump driving cellular influx of potassium
  • Tachycardia - increased HR
  • Hyperglycaemia: loss of insulin sensitivity, increased liver glucose release, OD of salbutamol
  • If patients have acute asthma exacerbations give salbutamol nebulisers. Blood test should show low K levels since salbutamol drives potassium into cells. High K - renal failure.
135
Q

Relieving inflammation may involve ???
Treating infection may involv ???
Preventing excess mucus may involve ???

A
  1. steroids
  2. antibiotics
  3. LAMAs
136
Q

Immediate Treatment of an Asthma attack

A

O2 up to 60% (CO2 retention is not usually a problem)
Salbutamol nebuliser 5mg
Prednisolone 30-60mg
Magnesium or aminophylline IV

137
Q

Non-respiratory functions of the lungs

A

Synthesis, activation and inactivation of vasoactive substances, hormones, neuropeptides.

138
Q

2 types of host lung defence

A
  • intrinsic

- innate

139
Q

intrinsic host defence

A 
always present 
Physical and chemical barriers
- Apoptosis
- Autophagy (removal of cells) 
- RNA silencing
- antiviral proteins
140
Q

innate host defence

A

Induced by infection

  • interferon
  • cytokines
  • macrophages
  • NK cells
141
Q

Adaptive immunity

A

Tailored to a specific pathogen (T cell, B cell)

142
Q

Molecules secreted from the epithelium during host defence:

A
  • Antiproteinases
  • Anti-fungal peptides
  • Anti-microbial peptides
  • Surfactant -A and -D
143
Q

What do Surfactant A and D do

A

Opsonise pathogens for enhanced phagocytosis (bind to the pathogen and make it more visible for immune response)

144
Q

Cellular physical barrier

A

Airway epithelium

145
Q

What do epithelial cells do in the upper respiratory tract?

A

Epithelial cells secrete granules from secretory cells into the pericellular lining fluid. A mucin layer forms on the apical surface. The secretory components also come from the submucosal gland and move through the duct to the pericellular fluid. Within the specific cell types, specific genes and proteins are produced.

146
Q

Two types of peripheral lung tissue in the lower tract

A

Type I: biosynthetic, thin, next to capillaries and allows for gas exchange

Type II: secrete host defence and surfactant which coats the lungs (helps to keep the lungs open due to surface tension)

147
Q

What kind of epithelium is in bronchus? What other components are there?

A 
Pseudostratified ciliated epithelium 
Basal cells
Goblet cells
Submucosal gland and duct
Inflammatory cells
148
Q

What kind of epithelium is in bronchiolus?

A

Cuboidal ciliated epithelial

149
Q

Cells in alveoli

A

Thin layer of tube cells

Type I and II pneumocytes

150
Q

Type I pneumocytes

A

Allow for air diffusion by forming the barrier across which gas exchange occurs
thin squamous cells

151
Q

Type II pneumocytes

A

innate defence cells and secrete protective molecules - important for surfactant production

152
Q

What does airway mucus contain?

A

Airway mucus is a viscoelastic gel containing water, carbohydrates, proteins and lipids

153
Q

What secretes mucus?

A

Submucosal glands and the goblet cells of the airway surface epithelium

154
Q

Two different pathways of a cough as a defence reflex (nerves)

A

Afferent and efferent
Afferent limb - induces receptors within the sensory distribution of the trigeminal, glossopharyngeal, superior laryngeal and vagus nerves => go TOWARDS the CNS.

Efferent limb - includes the recurrent laryngeal nerve and the spinal nerves => goes AWAY from the CNS.

155
Q

Infecctions targeting specific airway epithelial cells

A

Virus target expression of specific proteins. Recovery phase occurs as cell dies as a result. The epithelium can effect a complete repair after injury. The epithelium exhibits a level of functional plasticity. Cells can change phenotypes.

156
Q

What happens when mucociliary transport is impaired?

A

Pulmonary diseases

Mucus plug/inflammation =severe disease
Blocking the airway in a patient with severe cystic fibrosis.

157
Q

Residual volume

A

The volume of air that remains in the lungs after forced expiration

158
Q

Total Lung Capacity

A

Total amount of air in thorax at full inspiration including the air you can’t get rid of at at max expiration
TLC= VC + RV

159
Q

Inspiratory capacity

A

Maximum volume of air that can be inhaled following a resting state
IC = IRV + TV

160
Q

Tidal volume

A

Amount of air that can be inhaled/exhaled during one respiratory cycle

161
Q

Inspiratory reserve volume

A

Amount of air that can be forcibly inhaled after a normal tidal volume.

162
Q

Expiratory reserve volume

A

The volume of air that can be exhaled forcibly after exhalation of normal tidal volume.

163
Q

Vital capacity

A

The amount of hair exhaled after maximum inhalation

VC = TV + IRV + ERV

164
Q

Function residual capacity

A

The amount of air in the lungs at the end of a normal exhalation

165
Q

FEV1

A

Forced expiratory volume in 1 second

166
Q

FVC

A

Forced vital capacity (total amount of air forced out)

167
Q

FEF25

A

Flow at point when 25% of total volume to be exhaled has been exhaled

168
Q

Peak expiratory flow (rate) - PEF

A

Single measure of highest flow during expiration. (L/min)
Effort dependent
Measured over time, giving a patient a PEF meter and chart.

169
Q

Gas Dilution method

A

Measures of all air in lungs that communicates with the airways including residual.
Does not measure air in non-communicable bullae.

Gas dilution techniques use either:

  • close-circuit helium dilution
  • open-circuit nitrogen washout.

Usually the patient is connected at the end-tidal position of the spirometer, measuring FRC.

170
Q

Total body plethysmography

A

Alternative method of measuring lung volume (Boyle’s Law) including gas trapped in bullae. From theFRC,patient “pants” with an open glottis against a closed shutter to produce changes in the box pressure proportionate to the volume of air in the chest. The volume measured (TGV) represents the lung volume at which the shutter was closed.

171
Q

DL CO

A

diffusion capacity of lung for carbon monoxide

172
Q

Causes of Low DL CO

A

COPD and emphysema

173
Q

DLCO is an overall measure of the interaction of …

A

Alveolar surface area
Alveolar capillary pressure
Physical properties of the alveolar capillary interface
Capillary volume
Hb concentration and the reaction rate of CO and Hb.

174
Q

COPD is a ? condition

A

progressive

175
Q

Symptoms of COPD

A

Wheeze and shortness of breath on exercise

176
Q

What is reduced during COPD?

A

Mid expiratory flows

177
Q

3 overall phases of embryological development of the respiratory tract

A
  1. Conducting airways
  2. Units for gas exchange
  3. Blood supply
178
Q

Stages of pulmonary development

A 
Embryonic
Pseudo glandular
Canalcular
Sacular
Alveolar
179
Q

Order the components of the respiratory system are developed

A 
Bronchi
Bronchioles
Terminal bronchioles
Respiratory broncioles
Alveolar ducts
Alveolar sac
180
Q

Development of respiratory diverticulum

A

By the 5th week the lung buds enlarge to form right and left main bronchi. The oesophagotracheal septum develops and separates the trachea from oesophagus.

181
Q

Where does the lung bud develop from

A

the foregut

182
Q

How does separation of the two lung buds come about?

A

The fusion of esophagotracheal ridges to form the eosophagotracheal septum.

183
Q

When the embryo is 5 weeks old, what is identifiable? What do these structures go on to form?

A

two primary lung buds. The lung buds go on to form their first subdivisions, with 3 lobar buds developing in the right lung bud and 2 lobal buds developing in the left.

184
Q

What are the lung buds forerunners of?

A

The right upper, middle and lower lobes and the left upper and lower lobes.

185
Q

What happens in the 8 week old embryo?

A

Development progresses as the lobar buds subdivide and form the bronchopulmonary segments.

186
Q

What are lung buds lined by? How does it develop?

A

endodermally derived epithelium

187
Q

What is the innervation of the lungs derived from?

A

Ectoderm

188
Q

Which parts of the lungs is the mesoderm an origin

A

blood vessels
smooth muscle
cartilage
other connective tissue

189
Q

week 5/6-17

A

pseudoglandular stage

190
Q

What is formed during PG stage

A

Conductive airways are formed by progressive branching. Eventually 16-25 generations of primitive airways are formed.

191
Q

Under what conditions do endodermal lung bugs undergo branching?

A

Only if they are exposed to bronchial mesoderm.

192
Q

What is the rate and extent of branching of endodermal lung buds directly proportional to?

A

the amount of mesenchyme present

193
Q

By how many weeks are all bronchial airways formed? What happens after this time in terms of further growth?

A

16

Further growth occurs by elongation and widening of existing airways

194
Q

What happens by 13th week in terms of differentiation of the lung epithelium

A

cilia appear in the promixal airways

195
Q

What is necessary for epithelial differentiation to occur?

A

Mesenchyme

196
Q

week 16-25

A

Canalicular phase

197
Q

What has already happened by the canalicular stage?

A

The gas exchange portion of the lung is formed and vascularised.

198
Q

By week 20 there is differentiation of the …

A

type I pneumocyte

199
Q

Capillaries begin to grow in close proximity to ..?

A

The distal surface of the alveolar cells

200
Q

There is the appearance of ??? in type II alveolar cells.

What is the function of them?

A

lamellar bodies AKA inclusion bodies

Lamellar body is site of surfactant storage, prior to its release into the alveolar space.

201
Q

What encompasses the period from 26 weeks til term?

A

The saccular stage / terminal sac

202
Q

Saccular stage

A

There is a decrease in interstitial tissue and a thinning of the alveolar walls. As this stage progresses, there are recognizable Type I and Type II cells.

203
Q

What does the stability of the lung at birth correlate to?

A

The number of lamellar bodies present

204
Q

What happens if there is absence of surfactant?

A

The body can only maintain alveoli in an open state for a very short time.

205
Q

Features of foetal lungs?

A

Shunting of blood from right to left
High pulmonary vascular resistance
Tissue resistance
Low systemic resistance

206
Q

Where does blood travel to to get O2 instead of lungs

A

placenta

207
Q

Foetal circulation

A

1 umbilical vein with oxygenated blood
2 umbilical arteries with deoxygenated blood
3 fetal shunts

208
Q

3 foetal shunts

A

Ductus venosus
Foramen ovale
Ductus arteriosus

209
Q

Ductus venosus

A

hepatic system

within liver - oxygenated blood from placenta moves through liver to inferior vena cava

210
Q

Foramen ovale

A

between right and left atrium

Supplies developing brain, heart and rest of body

211
Q

Ducus arteriosus

A

vein connects pulmonary artery to descending aorta

Since blood doesn’t need to go to lungs, some shunts across back into systemic circulation.

212
Q

What happens with systemic circulation once cord is cut

A

The pressure in the systematic circulation increases and forms more pressure on the left side, thus closing the shunts in the liver and heart.

213
Q

What can go wrong with foetal lungs/circulation

A

Persistant foetal flow circulation/persistent pulmonary hypertension of new born
Right to left shunt => hypoxia => pulmonary hypertension

214
Q

What does hypoxia in newborn babies lead to?

A

Blue baby
blood doesnt attract enough oxygen into lungs; high pressure in lungs means there is less oxygenation and baby continues to be blue until intervened.

215
Q

Fetal airways are distended with …

A

lung fluid

216
Q

At the time of birth, what changes with lung fluid

A

Due to hormones and stress, the lung channels change from mainly secretory to mainly absorptive, so lung fluid is removed.

217
Q

What is surface tension a measure of?

A

The force acting to pull a liquids surface molecules together at an air-liquid interface.

218
Q

Why is surfactant useful for alveoli?

A

Alveoli are lined with fluid, which theoretically should cause them to collapse, but this doesn’t happen due to surfactant. Surfactant removes surface tension, allowing alveoli to expand. Surfactant allows homogenous aeration and maintenance of functional residual capacity.

219
Q

Which cells produce surfactant?

A

Type 2 pneumocytes from 34 weeks gestation, dramatically increase in 2 weeks prior to birth

220
Q

The first breath

A

Fluid is squeezed out of lungs by birth process (where lung channels change from secretory to absorptive). Adrenaline and stress cause increased surfactant release. Air is inhaled, and oxygen vasodilates pulmonary arteries, increasing pulmonary blood blow and decreasing resistance. Umbilical arteries constrict and ductus arteriosus constricts.

221
Q

Antibodies

A

IgM - tetramers made at beginning of infection. Not specific.
IgGs - very specific. Target single epitopes.
IgE - involved in allergic response and parasites.
IgA - in mucous membrane.

222
Q

Type 1 IgE hypersensitivty reaction

A
  • Acute Anaphylaxis
  • Hayfever
  • Asthma
  • Immune memory to something causing an allergic response
  • Atopy
223
Q

Definition and examples of atopy

A

inherited tendency to exaggerate IgE response

e.g. hayfever, eczema, asthma

224
Q

What are Type 1 reactions driven by?

A

Histamine; mast cell mediators which release cytokines and tryptase

225
Q

Which test can show is someone is having an IgE/anaphylaxis reaction

A

Tryptase test

226
Q

Different types of reactions within type 1

A

Local e.g. wheezing

Systemic e.g. anaphylaxis

227
Q

Diagnosis of Type 1

A

Skin prick test
Radioallergosorbent test RAST
ImmunoCAP

228
Q

Type 1 treatment

A

Prevent exposure
Anti-histamines
Steroids - reducing local inflammation
Desensitisation

229
Q

Type 2 hypersensitivty reactions

A

IgG reaction; Ig bound to cell surface antigens

  • Transfusion reactions
  • Autoimmune disease
230
Q

Examples of Type 2 hypersensitivity reactions (Goodpasture’s syndrome)

A

Goodpasture’s syndrome
- follow viral infection
- pulmonary haemorrhage in lung and glomeurulonephritis (renal inflammation of glomeruli)
Treatment: remove antibodies using steroids, cyclophosphamide, plasma exchange

231
Q

Examples of Type 2 hypersensitivity reactions (Mycoplasma pneumonia)

A

Mycoplasma pneumonia
- cross reacting immune epitopes; protein on mycoplasma looks like protein on haemoglobin
= Antibodies react with antigen on red blood cells causing agglutination and haemolytic anaemia.

232
Q

Type 3 hypersensitivity reactions

A

immune complex disease, activation of complement-IG bound to antigen

Lumps of antibody + target get deposited in the skin, lung, kidneys ect + activate immunity -> tissue damage
(do not get cleared away )

example: farmer’s lung, SLE, Post-streptococcal GN

233
Q

Type 4 hypersensitivity

A

T-cell mediated delayed type hypersensitivity
Examples:
- Tuberculosis
- contact dermatitis

  • Formation of granulomas of T cells and macrophages (Slow) keeping inflammation away from other tissue.
  • Dependent upon activation of T cells
  • Widespread granulomas and inflammation affect many organs (lung, eyes, skin, nervous system)
234
Q

Hypersensitivity drug induced reactions (examples)

A

Injury, hypersensitivity, haptenization
Breathlessness, cough, fever, chest pain
Respiratory failure

Types of drugs:
Amiodarone - lung fibrosis
Bleomycin - direct pneumotoxicity 
Methotrexate
NSAIDs
235
Q

Pathophysiology - cycle

A
  1. Respiratory tract infection due to microbial insults/defect in host defence
  2. Bronchial inflammation
  3. Respiratory tract damage -> progressive lung disease
236
Q

Normal vs abnormal CFTR protein

A

Normal: transports protein on membrane of epithelial cells and moves Cl- ions out of cells

Abnormal: lead to disregulated epithelial fluid transport; does not move Cl- ions out causing mucus to build up outside of cell

237
Q

Cystic Fibrosis diagnosis

A
  • genetic profile (heel prick test at birth)
  • Clinical symptoms (frequent infection, malabsorption, failure to thrive)
  • Abnormal salt/Cl- exchange; raised skin salt
  • Late diagnosed vs infertility services
238
Q

Cystic fibrosis symptoms (Respiratory)

A
  • Persistent cough with thick mucus
  • Wheezing
  • SOB
  • Frequent chest infections
  • Sinusitis, nasal polyps
239
Q

Cystic fibrosis symptoms (Digestive)

A

Bowel disturbances
Weight loss
Obstruction
Constipation

240
Q

Cystic fiborsis complications

A

Sinusitis and nasal polyps
Airway obstruction, bronchiectasis, pneumothorax, haemoptysis
Obstructive billiary tract disease
Enzyme insufficiency leading to diabetes
Distal intestinal obstruction syndrome, rectal prolapse
Infertility

241
Q

CF Treatment

A

Rescue antibiotics - IV antibiotics

CF Prevention management:
Segregation
Surveillance - review every 3 months
Airway clearance - physio + exercise (remove mucus)
Nutrition
Psychosocial support

Drugs:
Suppression of chronic infections - antibiotic nebs
Bronchodilation - salbutamol nebs
Anti inflammatory - azithromycin, steroids
Diabetes - insulin
Vaccinations - influenza, pneumococcal
Personalised medicine:
Individual tailored target medicine
Stratified based on predicted response or risk of disease
Genetic information major factor
Allows each patient to benefit from treatment

242
Q

What does AATD stand for? What is it?

A

Alpha-1 antitrypsin deficiency

Autosomal recessive genetic disorder with 80 different mutations of the SERPINEA1 gene on C14 chromosome.

243
Q

Consequences of AATD

A

Early onset emphysema/bronchiectasis because of unopposed action of neutrophil elastase in lung due to not enough alpha-1 antitrypsin.

244
Q

Normal blood gas ranges for PaO2, PaCO2 and pH

A

PaO2 - 10.5-13.5kPa
PaCO2 - 4.5-6.0kPa
pH - 7.36-7.44

245
Q

Altitude blood gases

A

PaO 2 - 7 kPa
PaCO 2 - 3 kPa
pH - 7.44

246
Q

Determinants of PaCO2

A

PaCO2 directly proportional to 1/alveolar ventilation

PaCO2 = k V’CO2/V’A

247
Q

Alveolar gas equation

A

PAO2 = PiO2 - PaCO2/R*

PiO2 = pressure of inspired O2 
R = respiratory quotient
A = Alveolar
a = arterial
248
Q

Calculating PaO2

A
  1. PiGas = Patm x Fi Gas
  2. PAO 2 = PiO 2 - PaCO 2 / R
  3. PaO 2 = PAO 2 - (A-aDO 2 )
249
Q

Why are alveolar and arterial oxygen pp not equal?

A

Not all of the oxygen enters the blood from the alveoli

250
Q

Normal response of lungs at altitude? (6)

A

Hypoxia leads to hyperventilation, which allows for better oxygen absorption at altitude. CO2 levels drop leading to a smaller difference between alveolar and arterial oxygen.
More oxygen is retained.
Minute ventilation is increased, leading to a lowered PaCO2.
Alkalosis intitially
Tachycardia.

251
Q

What compensates for alkalosis caused by high altitude?

A

Renal bicarbonate excretion

252
Q

What is Boyle’s law?

A

At constant temperature, the absolute pressure of a fixed mass of gas is inversely proportional to its volume.
P1V1 = P2V2

253
Q

What is Henry’s Law? What is the significance to do w lungs and depth

A

The amount of gas dissolved in a liquid is directly proprtional to the partial pressure of the gas.
As a result, more gas dissolves into tissues at DEPTH. If ascending rate exceeds the body’s capacity to clear this excess gas; inert bubbles form in the tissues -> decompression illness.

254
Q

What is Dalton’s Law? What is its significance?

A

Individual gas pressures add up to total air pressure.
PO2 increases as you descend.
Due to this law, O2/N2 toxicity can occur.

255
Q

What is ATA? How much is 1 ATA?

A

atmosphere absolute
1ATA = 100kPa
Every 10m you descend, ATA increases by +1

256
Q

Pulmonary oxygen toxicity (ATA)

A

PiO2 > 0.5 ATA

257
Q

What is inert gas narcosis?

A

Nitrogen toxicity. N2 is forced into tissue, lung and brain. It worsens with increased pressure. Influencing factory include cold, anxiety, fatigue and drugs.

258
Q

What is decompression illness?

A

Delayed ‘dived’ symptoms.
N2 in body tissues and moves into CNS and brain.
Type I - cutaneous
Type II - neurologic

259
Q

What is an arterial gas embolism (AGE)

A

If an inexperienced diver takes a deep breath in gas expands rapidly, causing chest to expand and pulmonary veins rip. Air moves to the head and gas enters circulation via torn pulmonary veins.AGE can cause death.

260
Q

Pulmonary barotrauma

A 
Air leaks into chest
Air leaks from burst alveoli: 
- pneumothorax
- pneumomediastinum 
- subcutaneous emphysema
261
Q

Asthma

A

Common chronic inflammatory disease
Characterised by variable and recurring symptoms, reversible airflow obstruction and bronchospasm.
Common symptoms include wheezing, coughing, tight chest and shortness of breath.

262
Q

Environmental influences (asthma)

A
  • Pollens, fungi, pets, air pollution
  • Infectious agents and micro-organisms
  • Aero allergen exposure occurs after birth
  • Pets
  • Air pollution (aggravating lung disease; response to pollutants can be analogous to vieal respones). Air pollution can aggravate pre-existing lung diseases such as COPD.
263
Q

What is hypersensitivity pneumonitis?

A

Inflammation of the alveoli caused by hypersensitivity to inhaled dusts. Lungs become inflamed.
Immune complex related disease, where an antigen reacts with an antibody, causing a mornal IgG response.

264
Q

Different forms of hypersensitivity pneumonitis?

A

Acute
Sub acute
Chronic

265
Q

Influences causing hypersensitivity pneumonitis?

A

Farmers lung
Bird fanciers lung
Metal working gluids

266
Q

Characteristics of COPD

A

Chronically poor airflow
Worsens over time
Slow progressive lung disease

267
Q

FEV1/FVC ratio of COPD

A

FEV1:FVC < 0.7

268
Q

Breathing is autonomic. What does this mean?

A

It is a non-conscious effort. The rate and depth of breathing depends upon cyclical excitation and control of muscles in the upper and lower airway, diaphragm and chest wall.

269
Q

Overnight breathing

A

Hypopneic (slow breathing)

6 breaths a minute

270
Q

Which neurons form the respiratory control centre?

A

groups of neurons in the PONS and MEDULLA

271
Q

Respiratory control centre neurons send impulses to the primary respiratory muscles via which 2 nerves?

A

phrenic

intercostal

272
Q

Which respiratory group controls expiration

A

ventral

273
Q

Which respiratory group controls inspiration

A

dorsal

274
Q

Which respiratory group controls the rate and pattern of breathing

A

pontine

275
Q

Where are peripheral chemoreceptors found?

A

Carotid body

Aortic body

276
Q

What do peripheral chemoreceptors detect large changes in?

A

pO2

277
Q

When low levels of oxygen are detected, what happens?

A

Afferent impulses travel via the glossopharyngeal and vagus nerves to the medulla oblongata and the pons in the brainstem.

278
Q

Which actions then happen to increase the pO2

A

The respiratory rate and tidal volume are increased to allow more oxygen to enter the lungs and subsequetly diffuse into the blood. Blood flow is directed towards the kidneys and the brain (as these organs are the most sensitive to hypoxia). Cardiac output is increased in order to maintain blood flow, and therefore oxygen supply to the body’s tissues.

279
Q

Where are central chemoreceptors?

A

Central chemoreceptors are located in the medulla oblongata of the brainstem.

280
Q

What do central chemoreceptors detect?

A

They detect changes in the arterial partial pressure of carbon dioxide.

281
Q

When changes are detected, what happens?

central chemo

A

The receptors send impulses to the respiratory centres in the brainstem that initiate changes in ventilation to restore normal pCO2.

282
Q

What does the body do restore CO2 levels.

A

Detection of an increase in pCO2 leads to an increase in ventilation. More CO2 is exhaled so the pCO2 decreases and returns to normal. Detection of a decrease in pCO2 leads to a decrease in ventilation.

283
Q

What ratio establishes the pH of the CSF

A

pCO2: [HCO3-]

284
Q

Which levels remain relatively constant and which change?

A

HCO3- levels remain relatively constant whereas CO2 freely diffuses across the blood-brain barrier.

285
Q

What constitutes the blood-brain barrier?

A

arterial blood supply and the cerebrospinal fluid

286
Q

When CO2 reacts with H2O what does it produce? What effect does this have on the pH?

A

Carbonic acid

Lowers the pH

287
Q

Does a small decrease in pCO2 lead to an increase or decrease in the pH of the CSF?

A

Increase in the pH, and vice versa is there is a small increase in pCO2, which decreases the pH.

288
Q

When the pH of the CSF changes, what are the respiratory centres stimulated to do for either an increase or decrease?

A

Increase in pH = decrease ventilation

Decrease in pH = increase ventilation

289
Q

What happens if pCO2 levels stay abnormal for a longer period of time? Which disease is this relevant in?

A

Choroid plexus cells within the blood brain barrier allow HCO3- ions to enter the CSF. Movement of HCO3- ions alters the pH which in turn resets the pCO2 to a different value.

COPD

290
Q

Centres in the pons and their function

A

Pneumotaxic centre: reduces respiration rate

Apneustic centre: moderates effect of pneumotaxic centre i.e. moderating amount of lung stretch. Prevents over inflation of lungs.

291
Q

What does the pons moderate?

A

natural breathing patterns

292
Q

Groups in the medulla oblongata? When is each one active?

A

Dorsal Respiratory Group - predominantly active during inspiration.

Ventral (front) respiratory group - active during both inspiration and expiration.

293
Q

What do both groups have in common?

A

Each are bilateral and project into the bulbo-spinal motor neurone pools and interconnect

294
Q

What is the medulla oblongata in charge of?

A

Phasic discharge of action potentials

295
Q

What is the Central Pattern Generator?

A

Neural network of interneurons.

296
Q

Where is the CPG located?

A

Located with in the dorsal and ventral respiratory groups

297
Q

CPG function

A

generate repetitive patterns of motor behaviour independent of any sensory input or feedback.

298
Q

Inspiration (nerves)

A

Progressive increase in inspiratory muscle activation. DRG + VRG both involved. Lungs fill at a constant rate until the tidal volume is reached. At the end of inspiration, there is a rapid decrease in excitation of the respiratory muscles due to the medulla and pons.

299
Q

Expiration (nerves)

A

First part of expiration; active slowing with some inspiratory muscle activity (breaking between late expieration and early inspiration). Increased demand leads to further muscle activity being recruited. Can become active with additional abdominal wall muscle activity.

300
Q

Afferents of carotid and aortic bodies individually

A 
Carotid = glossopharyngeal nerve
Aortic = vagal
301
Q

Neurotransmitter secretion of peripheral chemoreceptors

A

When exposed to hypoxia, type I cells release stored neurotransmitters that stimulate the cuplike endings of the carotid sinus nerve. Neurotransmitter secretion during hypoxia sends afference to DRG/VRG Pons to increase ventilation.

302
Q

3 Lung receptors

A

Stretch
J
Irritant

303
Q

Afferent nerves of lung receptors

A

Vagus nerve

304
Q

Stretch receptors: location, function and speed

A

In smooth muscle of conducting airways.
They sense lung volume.
Slow adapting and rapid adapting.

305
Q

Irritant receptors: location, function and speed

A

Larynx and pharynx and larger conducting airways.
Receptors for inhaled particles.
Rapidly acting: cough, gasp

306
Q

J (juxtapulmonary capillary) receptors

A

Pulmonary + bronchial C fibres

307
Q

What is the definition of hypoxia?

A

a deficiency of oxygen at tissue level

308
Q

What is the most common type of hypoxia?

A

Hypoxic hypoxia

Hypoxemia - in which the arterial partial pressure of O2 is reduced

309
Q

What are the most common causes of hypoxia?

A
  1. Hypoventilation
  2. Diffusion impairment
  3. Shunting
  4. Ventilation/Perfusion mismatch
310
Q

What does hypoventilation result in and why does it happen?

A

Hypoventilation results in an increased arterial partial CO2 pressure. This is because the alveoli fail to ventilate adequately.
Causes:
- muscular weakness (motor neurone disease)
- obesity
- loss of respiratory drive (E.g. if you prevent the brain from accessing the lungs due to morphine for example)

311
Q

What does diffusion impairment result from? What is it caused by?

A

Results from thickening of the alveolar membranes or a decrease in their surface area which causes the partial pressure of O2 to decrease and alveolar partial pressure to fail to equilibrate.

Caused by pulmonary oedema, anaemia and interstitial fibrosis between alveoli and capillaries.

312
Q

What is shunting? Where can it occur?

A

anatomical abnormality of the cardiovascular system that causes mixed venous blood to bypass ventilated alveoli in passing from the right side of the heart to the left side. This can occur when there is a ventricular septal defect.

It can also be a result of an intrapulmonary defect in which mixed venous blood perfuses unventilated alveoli. This can occur in bronchial arteries.

313
Q

What is ventilation-perfusion mismatch? What can it be caused by?

A

Occurs in COPD and many other lung diseases where arterial partial CO2 pressure may be normal or increased, depending on how much ventilation is reflexively stimulated.

Causes:

  • pulmonary embolus (blockage of artery in the lung)
  • asthma
  • pneumonia
  • pulmonary oedema
314
Q

What is hypercapnia

A

Carbon dioxide retention and an increased arterial partial pressure of CO2.

315
Q

What is hypercapnia caused by?

A

hypoventilation (main)

or V/Q mismatch

316
Q

Oxygen, CO2 and HCO3- in Type 1 respiratory failure

A

low pO2
low or normal pCO2
normal HCO3-

317
Q

What are the causes of type 1 respiratory failure? Which is the most common?

A 
pulmonary embolism = most common
COPD
pneumonia
asthma
pulmonary oedema
high altitude
318
Q

Oxygen, CO2 and HCO3- in Type 2 respiratory failure?

A

low pO2
high pCO2
normal HCO3- **

319
Q

What are causes of type 2 respiratory failure?

A 
hypoventilation 
opiate overdose
severe asthma
COPD
hypothyroidism
muscle disorders
drowning
320
Q

What is different when type 2 is chronic?

A

high HCO3- because the kidneys make more to buffer the increase in H+

321
Q

When does type 1 resp failure progress to type 2?

A

when patient becomes fatigued and respiratory rate decreases, no longer blowing off CO2

322
Q

Why can you not give high flow O2 to COPD patients?

A

As their central chemoreceptors will have reset to accommodate increase PaCO2 - oxygen will then cause further reduction as peripheral chemoreceptors are inhibited by increased O2, leading to death from acidosis caused by hypercapnia.

323
Q

Anaemic hypoxia

A

not enough Hb to carry O2

324
Q

Stagnant hypoxia

A

blood flow to the tissue is too slow

325
Q

Histotoxic hypoxia

A

toxic agents prevents cell from using O2

PHASE ONE (19 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions