Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

1st Year Med > Respiratory Physiology > Flashcards

Respiratory Physiology Flashcards

(88 cards)

Start Studying
1
Q

what are the functions of the respiratory tract?

A

conduction of air (warms/himidifies)
respiration (gas exchange)
pathogen protection (mucous)

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

what is the main purpose of breathing?

A

maintains blood-gas homeostasis

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

what is partial pressure?

A

the sum of the partial pressures of a gas must equal to total pressure

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

what muscles are involved in breathing?

A

diaphragm (dome shaped skeletal)
other respiratory muscles in strenuous breathing

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

explain the mechanism of quiet breathing and the activity of inspiration and expiration

A

inspiration (active) - diaphragm contracts downwards pushing abdominal contents outwards
external intercostals pulll ribs outwards and upwards

expiration (passive) - elastic recoil

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

explain the inspiration mechanism of strenuous breathing

A

active - greater diaphragm and external intercostals contraction (10x more than quiet)
inspiration accessory muscles active

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

explain the expiration mechanism of strenuous breathing

A

active - abdominal muscles recruited
internal intercostal muscles oppose external intercostals pushing ribs down and inwards

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

what does the cough reflex do?

A

remove offending material from airway

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

what is the cough reflex triggered by and how is it activated?

A

rapidly adapting pulmonary stretch receptors (RARs) found in epithelium of respiratory tract

activated by dust, smoke, ammonia, oedema etc.

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

how does a cough reflex get signalled for?

A

RARs send signal to brain using vagus nerve

brain sends signal to diaphragm/external intercostals via phrenic nerve

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

explain the stages of a cough reflex

A

air rushes into lungs
abdominal muscles contract to induce expiration
glottis opens to forcefully release air and irritants

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

what are conducting airways?

A

bronchi containing cartilage and non-respiratory bronchioles
dont partake in gas exchange

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

what are respiratory airways?

A

bronchioles with alveoli where gas exchange occurs
(from terminal bronchioles to alveoli)

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

what is the function of bronchial circulation?

A

brongs oxygenated blood to lung parenchyma

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

what is the partial pressure of O2 inside and outside the body?

A

inside: 150mmHg
outside - 159mmHg

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

name the structures in alveolar-capillary networks

A

type 1 alveolar epithelial cells
capillary endothelial cells
BM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how is oxygen carried in the blood?

A

dissolved (proportional to PP in an arterial blood sample)
bound to haemoglobin

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

name the pressure of O2 and CO2 in:
- pulmonary artery
- capillaries
- pulmonary veins
- anatomic dead space

A

PA: O2 = 40, CO2 = 46
PV and capillaries: O2 102, CO2 = 40
anatomic dead space: O2 = 150, CO2 = 0

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

explain the structure of haemoglobin

A

4 heme groups (2 alpha and 2 beta polypeptide chains)
each group contains Fe++ (site of O2 binding)

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

describe O2 saturation and what is it measured with

A

amount of O2 bound to Hb relative to maximum (211ml/l) binding capacity

pulse oximeters measure O2 sats
measures ratio of red and infrared absorption by oxyhaemoglobin and deoxyhaemoglobin

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

what are the general resting tissue requirements/excretions for O2 and CO2?

A

O2: 250ml/min
CO2: 200ml/min

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

how is CO2 carried in blood?

A

7% dissolved
23% bound to Hb
70% converted into bicarbonate

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

how do capillaries expel CO2?

A

systemic capillaries expel CO2 produced by tissues into blood
pulmonary capillaries expel CO2 into alveoli

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

explain the bicarbonate reaction

A

reaction: HCO3 -> H2O + CO2
regulated H+ ions and maintains base balance in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
how are CO2, HCO3 and H+ concentrations linked?
stabilise pH through strong buffer reaction (due to HCO3 strength)
26
what is the V/Q ratio?
ventilation:blood flow defined by single alveolus (alveolar ventilation:capillary flow) defined by lung (total alveolar ventilation:CO)
27
what are the general values for alveolar ventilation, pulmonary blood flow and V/Q?
alveolar ventilation: 4-6l/min pulmonary blood flow: 5l/min V/Q - 0.8-1.2
28
describe the effects of PO2 on Hb saturation in the O2 dissociation curve
drop from 100-60 in PO2 has little effect 60 below has much larger effect (more sensetive to change)
29
what factors shift the O2 dissociation curve to the right?
decreased affinity: increased temp increased PCO2 decreased pH
30
what factors shift the O2 dissociation curve to the left?
increased affinity: decreased temp decreased PCO2 increased pH
31
what is the rule of H+ ions on pH?
changes in H+ of a factor of 2 lead to a pH change of 0.3
32
name systems affected by acid-base disorders
CVR metabolic renal GI neurological
33
what are some of the threats to acid base disorders?
CO2 generation (aerobic respiration) food metabolism generating acid or alkali incomplete respiration (anaerobic) loss of alkali in stool loss of acid in vomiting
34
what are the major components of acid base balance and how do they regulate?
buffering ventilation (CO2 control) renal regulation (HCO3/H+ secretion and reabsorption) regulate H+ concentration at the expense of other concentrations (HCO3/CO2)
35
what are buffers and how do they work?
weak acids partially dissociated in solution react poorly with water reacts with H+ (base) or OH- (weak acid)
36
explain how ventilation results in acid-base regulation
CO2 remains constant as it is easily diffusable and is exhaled H+ addition consumes HCO3 generating CO2 (exhaled) and H2O free H+ leads to HCO3 generation H+ maintenance = HCO3 maintenance
37
name buffers and describe what they buffer
haemoglobin (blood CO2) proteins (intracellular) bone (long term) PO4 (urinary/intracellular)
38
how do buffers and the kidneys work together to regulate acid-base composition
dietary acids and anaerobic respiration acids are fixed (cant convert to (CO2) buffering fixed acids consume HCO3 kidneys generate more HCO3 to remove H+ ions
39
what is the function of the kidneys in acid-base regulation and how do they do it?
reabsorb filtered HCO3 secrete fixed acid by titrating PO4 in urine and secreting NH4 done using selective permeability of luminal/basolateral cell membranes to match transport of H+ and HCO3 in opposite directions
40
explain the reabsorption of filtered HCO3
active process in mainly proximal tubule small contributions from DCT and ascending LoH cant be reabsorbed in state of metabolic acidosis
41
what is respiratory acidosis?
levels of CO2 being expelled from the lungs too much in blood = acidosis too little in blood = alkalosis
42
what is metabolic acidosis?
levels of HCO3 expelled in urine too much in blood = alkalosis too little in blood = acidosis
43
what is lactic acidosis and how is it buffered?
reduced hepatic clearance of lactic acid produced from glycolytic metabolism of pyruvate buffered by HCO3 to lactate then metabolised in liver
44
what do chemoreceptors and mechanoreceptors provide feedback on?
chemoreceptors - PO2, PCO2, pH levels in blood mechanoreceptors - mechanical lung status, chest wall, airways
45
what structures receive signals from the brain to maintain breathing?
diaphragm/intercostals (rhythmic breathing) upper airway muscles (laryngeal, pharyngeal, tongue) reflexes to keep airways pateny (cough, sneeze, gag)
46
what is O2 decrease and CO2 increase medically called?
O2 - hypoxia CO2 - hypercapnia
47
describe peripheral chemoreceptors
small, vascularised bodies in carotid sinus and aortic arch info sent to glossopharyngeal and vagus nerve to brainstem (NTS) restore blood gases e.g arterial PO2
48
describe central chemoreceptors
clusters of neurones in brainstem activated when PCO2 is increased or pH is decreased
49
explain the result of changes in PCO2
small changes have large effects on ventilation hypercapnic response originating from central chemoreceptora in brainstem
50
describe mechanoreceptors
sensory receptors detecting chnges in pressure, movement and touch (e.g lung inflation and chest movements during inspiration)
51
what is the course of an impulse from mechanoreceptors?
stimulus (lung inflation) neural signal goes through vagus nerve to NTS in brainstem to adjuct ventilation
52
what do mechanoreceptors integrate?
respiratory pattern with other movements such as posture or locomotion
53
how do mechanoreceptors terminate inspiration?
in airway smooth muscle detects stimulus of inflation/distension of airways
54
what do mechanoreceptors in the airway epithelium detect?
rapid lung inflation/deflation (or oedema) causes sigh or shortened expiration
55
explain the course of action from the NTS
NTS receives signals from mechanoreceptors and peripheral chemoreceptors info processes in brainstem by neuronal clusters breathing rhythm generated and sent to respiratory muscles
56
describe the respiratory rhythm generating neurons
bilateral clusters of neurons with rhythm generating properties produce a rhythmic resp output even when isolated
57
where do the rhythmic output signals go after the brainstem?
sent down spinal cord which sends signals to resp muscles such as diaphragm (phrenic nerve) or intercostal muscles (thoracic spinal cord nerves)
58
what areas of the brainstem are responsible for resp rhythm generation?
pontine group (pons) ventral group (pattern/rhythm generating neurons) dorsal resp group (NTS)
59
what types of higher centre modulation control breathing?
volitional and emotional
60
what is the neural basis for voluntary control attributed to?
motor cortex
61
explain the role of the corticospinal tract in breathing regulation
cortical breathing control occurs here volitional breath control has upper motor neurones in primary motor cortex they descent the corticospinal tract and synapse with lower motor neurones in anterior horn of C3-5 (phrenic nerve)
62
what are the physiological effects of asthma?
loss of airway epithelium thickening of BM hypertrophy of smooth muscle layer (including mast cells)
63
what is asthma?
inflammatory disease of medium sized airways hyper-responsiveness to normal triggers of contraction abnormal contraction in response to benign triggers
64
what can asthma cause in the airway?
increased force contraction twitchy smooth muscle variable airway calibre loss of relaxation after contraction
65
what are the symptoms of asthma?
triggered breathlessness wheezing diurnal variation (night/morning) coughing
66
how is asthma measured?
bronchial hyper-reactivity is induced exaggerated response to usually constricting stimuli (often histamine used) is seen
67
what does spirometry measure and how does it do it?
measures airflow velocity a narrowed/constricted airwa yrelaxes and dilates in response to salbutamol (adrenaline beta agonist)
68
what are the common triggers of asthma?
allergy infection exercise drugs (beta blockers/NSAIDs) cold air scents
69
describe the smooth muscle only stage of asthma
triggered by direct mediator (histamine) causes rare wheezing
70
describe the chronic inflammation stage of asthma
irritates smooth muscle and causes regular wheezing
71
describe the acute inflammation stage of asthma
caused by viral infection and results in clinical exacerbations
72
what are the inflammatory factors often associated with asthma?
cells (lymphocytes, eosinophils, mast cells) cytokines (Il-4, IL-5) prostanoids (PGE2, leukotriene D4) immunoglobulins (IgE)
73
explain the role of mast cell mediators
e.g histamine at H1 receptor, prostoglandin at PC2 receptor causes smooth muscle contraction, blood vessel formation and airway wall oedema
74
explain the role of beta 2 agonists in asthma
e.g salbutamol active adrenaline receptor activated G-protein on GPCR which activates cAMP resulting in smooth muscle relaxation
75
what do corticosteriods do in asthma?
block transcription factors causing an inflammatory response reduce muscle twitchiness reduce exhaled NO
76
what do anti-leukotrine receptor drugs do in asthma?
trats resistant inflammation targets onlt leukotrine D4 in airway effecting mast cells and smooth muscle
77
what is the 4D approach to prescribing inhalers?
diagnosis drug and device disease control device disposal
78
what is a preventer inhaler?
anti-inflammatory inhaler using inhaled corticosteroids (ICS)
79
what is a combination inhaler?
uses inhaled corticosteroids (ICS) and long acting beta agonist (LABA)
80
what is a reliever inhaler?
bronchodilating inhaler containing a short acting beta agonist (SABA) or a long acting beta agonist (LABA)
81
how can asthma and COPD be distinguished?
asthma patients will respond more to a bronchodilator and oral prednisolone peak flow will vary ~20% daily COPD isnt present if the FEV1/FVC ratio returns to normal with drugs
82
describe NO exhalation measurement
only valid in non-smokers normal results: <25ppb abnormal results: >50ppb indicates eosinophilic inflammation in airways
83
how does COPD develop?
inflammatory cells produce excess protease enzymes (neutrophil elastase) and insufficient antiprotease enzymes (a1 antitrypsin) imbalance causes lung tissue damage and COPD development
84
what are the effects of emphysema?
elastic support loss causing airway compression this causes airway obstruction (peripheral airway disease) ventilation maldistribution (poor gas exchange)
85
what are some common diseases associated with COPD?
asthma bacterial colonisations hypoxia reflux underlying bronchiectasis
86
explain the symptoms of bronchiectasis
purulent daily sputum 50% idiopathic recurrent infections lungs crackle on exam
87
what is bronchodilation and bronchoconstriction generally caused by?
bronchodilation - inhibitory nerves, circulating epinephrine bronchoconstriction - excitory nerves, vagus nerve
88
briefly explain what COPD is
largely irreversible airflow obstruction often including emphysema

1st Year Med (52 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions