transition block Flashcards
respiratory centres receive stimuli from?
central chemoreceptors (CO2 i.e. [H+] from CSF) peripheral chemoreceptors (oxygen and [H+] in blood) higher brain centres stretch receptors in bronchi + bronchioles i.e. Hering-Bruer reflex (protects against hyperinflation) J(uxtapulmonary) receptors Joint receptors - stimulated by joint movement i.e. exercise baroreceptors - increased ventilation in response to decreased BP
J receptor fucntion? Stimulated by?
cause rapid shallow breathing * pulmonary oedema! * pulmonary emboli
factors that increase ventilation rate?
hypoxia hypercapnia acidosis central arousal e.g. anxiety increased body temp pain joint movements during exercise drugs e.g. amphetamines
where are peripheral chemoreceptors? central chemoreceptors?
peripheral = carotid bodies + aortic bodies central = near medulla of brainstem (respond to [H+] of CSF i.e CO2)
what is most potent stimulant of respiration in normal poeple?
arterial pCO2 acting through central chemoreceptors ([H+] in CSF)
how does hypoxia cause hyperventilation? Stimulated when….
stimulates peripheral chemoreceptors stimulated only when PO2 falls <8.0 kPa
how does H+ cause hyperventilation? Role?
peripheral chemoreceptors major role in adjusting for ACIDOSIS e.g. lactic acid during exercise, DKA
how does pneumothorax cause SOB?
loss of transmural pressure gradient
(collapsed lung also does this)
major muscles of inspiration + innervation
diaphragm - increases vertical volume of thorax (C3, 4, 5 - phrenic)
external intercostal muscles - lift ribs and move out sternum “bucke thandle mechanism”
respiratory muscles
3 pressures important in ventilation
what happens during inspiration? expiration?
atmospheric pressure - 760
intra-alveolar pressure - 760
intrapleural pressure - 756
inspiration = intralveolar pressure + intrapleural pressure decreases
expiration = increases
opposing forces in the lung
forces keeping alvoeli open = transmural pressure gradient, pulmonary surfactant, alveolar interdependence
forces promoting alveolar collapse = elastic recoil, alveolar surface tension
parasympathetic effect on airways?
sympathetic?
parasym = bronchoconstriction
sympathetic = bronchodilation
how do asthma + COPD cause SOB?
increased airway resistance (expiration more difficult than inspiration)
dynamic airway compression?
causes no problems in normal people
causes problems in asthma + COPD (made worse by lack of elastic recoil e.g. emphysema)
why does pulmonary fibrosis cause SOB?
decreased compliance
rate of tranfer influenced by
(+ examples)
increases as partial pressure gradient increases (oxygen more than CO2)
increases as surface area increases
inreases as diffusion coefficient increases (CO2)
decreases as thickness increases
emphysema + lung collapse = decreased SA
pulmonary fibrosis, pulm oedema + pneumonia = increased thickness
pulmonary embolism = decreased perfusion
CO?
equation?
normal value
CO = volume of blood pumped by each ventricle per minute
CO = SV x HR
resting CO = ~5 litres/min
(can reach 25 L/min during exercise)
stroke volume?
equation
SV = volume of blood ejected by each ventricle per heartbeat
SV = EDV - ESV
Intrinsic control of stroke volume?
Extrinsic?
Intrinsic = Starling’s Law (the greater the end diastolic volume, the greater the stroke volume)
extrinsic = nervous + hormonal control
EDV determines?
venous return to heart determines?
effect of heart failure on frank starling curve?
EDV dtermines PRELOAD
venosu return to heart determines EDV
heart failure = shifts Frank Starling curve to the right (decreased SV)
left vs right sided heart failure?
left = pulmonary oedema (SOB)
right = pitting oedema, raised JVP
primary factor in determining %Hb saturation with O2?
PO2 (oxygen concentration in blood i.e. dissolved oxygen i.e. partial pressure)
normal PO2
13 kPa
mechanism for SOB in anaemia?
impairs O2 carrying capacity (tissue hypoxia and increased [H+])
PO2 (sensed by peripheral chemoreceptors) is NORMAL
lung volumes and capacities
spirometry used to determine?
FVC, FEV1 and thus FEV1/FVC ratio
(reduced in asthma + COPD)
GOLD classification COPD
GOLD 1 (mild) = FEV1 >80%
GOLD 2 (mod) = FEV1 50-79%
GOLD 3 (severe) = FEV1 30-49%
GOLD 4 (very severe) = FEV1 <30%
answer = D
A is wrong because would DECREASE in obese subjects
B is wrong because FVC and FEV1 is measured with spirometry
C is wrong becuse it is INCREASED in COPD
E is just wrong
answer = E
answer = C
answer = B
answer = A
answer = A
B is wrong because its supplied by broncho-circulation NOT pulmonary circulation (gas exchange)
answer = D
answer = B
answer = C
answer = C (obstructive shock)
answer = D
kPA is normally 13 (98%)
at 8 kPa it will be around 90%
answer = B
PO2 saturation will be normal even if Hb is low
A
C
B
reduces preload on heart via dilation of peripheral vessels
D
A
A
A
B
C
C
D
Farmer’s lung
D
D
classical rare genetic disorders vs common
rare
phenotype = genotype (single mutation) + environment
Common
phenotype = genotype + environment
monogenic/mendelian inheritance examples
autosomal dominant
autosomal recessive
X-linked
C - 3 billion
C - 3 million
array comparative hybridisation (aCGH) is preferable to karyotyping because?
it has higher resolution
12 year old girl has learning difficulties. Deletion of single base identified in 3rd exon on DEAF1 gene (a gene that cause slearnign difficulties). This is not found in either parent. How would you classify this genetic variant?
Definetely pathogenic
