Physiology Flashcards
(147 cards)
Anatomic and physiological dead space
Anatomical dead space: conducting zones of the lung - ventilation and no blood flow ~150mls, increases with large inspirations because of
the traction or pull exerted on the bronchi by the surrounding lung parenchyma.
Also depends on the size and posture of the person.
Functional - disease
Physiological - both - parts of lung with ventilation but no perfusion, volume of the lung that does not eliminate CO2
Why is volume physiological deadspace important
greater total ventilation an individual must generate to ensure an adequate amount of air enters the alveoli to participate in gas exchange
Cardiac conducting system
SA, AV, LBB, RBB
SA node - junction of the SVC and RA
AV node - R post interatrial septum.
3 bundles of atrial fibres connect SA to AV
AV node is continuous with the bundle of His, which gives off LBB and RBB
LBB divides into an anterior and a posterior fascicle.
Branches and fascicles run subendocardially down septum and come
Purkinje fibers spread to all parts of the ventricular myocardium.
Cardiac cycle phases vs ECG
P wave : Atrial depolarisation
PR interval : AV conduction
QRS : Ventricular depolarisation
ST segment: plateau portion of ventricular depolarisation
QT : ventricular action potential
T wave: Ventricular repolarisation
Membrane changes in infarcted myocytes
Rapid repolarisation due to accelerated opening of K+ channels (seconds to few minutes)
Decreased resting membrane potential due to loss of intracellular K+
Slow depolarisation of the affected cells compared to surrounding normal cells
LV changes and cardiac cycle
Atrial systole: Contraction of atria, blood flows into R and L ventricles via open AV valves
Isovolumetric ventricular contraction:
AV valves close, pulmonary and aortic remain closed. Ventricles are contracting without a change in volume
–> sharp rise in pressure.
Ventricular ejection: Aortic valve opens when pressure in LV exceeds the aortic pressure, 80mmHg. The stroke volume is ejected, LV peaks at 120mmHg
Isovolumetric relaxation: End of systole and beginning of diastole. Aortic valve closes once LV pressure below 80mmHg. AV valve remains closed. Rapid pressure drop, no change in volume.
Ventricular filling: AV valves open once vent pressures fall below atrial pressures. Blood flows into ventricles from atria.
When does the aortic valve open and shut
opens once LV pressure exceeds aortic pressure at 80mmHg marking the end of isovolumetric contraction.
Closes once LV pressure drops below 80mmHg during isovolumetric relaxation.
Factors affecting insulin secretion
Increased by: glucose, AAs, GIP, glucagon, theophyline, sulfonylureas
Decreased by: somatostatin, hypokalaemia, beta blockers, thiazides, alpha agonists (adr and norad)
Principle actions of insulin
Seconds: increased glucose and AA uptake cells, inc K uptake cells
Minutes: inc protein synth, dec protein degradation, activation glycolytic enzymes
Hours: inc mRNA for lipogenic enzymes
Effects of insulin on carbohydrate regulation and metabolism in tissues
*Adipose: inc glucose entry, inc fatty acid synthesis, inc K uptake
*Muscle: inc glucose entry, inc AA uptake, inc protein synthesis
*Liver: decreased ketogenesis, inc protein synthesis, dec gluconeogenesis
What are baroreceptors and where
Stretch receptors
Aortic arch and carotid sinus
Atria
MOA of baroreceptors
Stretch leads to neuronal discharge
inhibits sympathetic and increases vagal
Leads to vasodilation, dec BP, bradycardia
Normal CSF pressure
10-25 cm
Mechanism of fever
toxins act on monocytes, macrophages and kupffer cells –> cytokine release
Endogenous pyrogen e.g. IL6 and TNFalpha independently cause fever
CNS pyrogens act on hypothalamus causing PG release
Causes in reduced preload
Dec venous return - dec blood volume, venous pooling, gravity, vasodilation
Dec ventricular filling - inc thoracic/ pericardial pressure, dec ventricular compliance, dec filling time tachycardia, loss atrial kick AF
Potassium reabsorption in collecting ducts
H-K ATPase reabsorb K in exchange for H
How does aldosterone increase K secretion in urine
Aldosterone secretion triggered by high K
Acts on DCT and cortical collecting duct
Stimulates NaKATPase BLM
Causes K and Na channels to form apical membrane principal cells
Transport CO2 in blood
90% bicarb
5% carbamino compounds
5% dissolved
Chloride shift
- Ionic dissociation carbonic acid to bicarb and H in red cell
- Bicarb diffuses out, H+ stays in as impermeable to cations
- Cl- diffuses in to maintain neutrality
Draw and lael pressure volume curve LV
Y axis pressure 10 - 120
X ais volume 50 - 130
Arterial supply to cardiac conducting system
SA node- RCA 60%, circumflex 40%
AV node and bundle- RCA, AV nodal artery
Right and Left Bundles and Purkinje fibres- LAD
Consequences impaired renal function
Proteinuria and hypoalbuminaemia - inc perm glomerular capillaries
Uraemia - impaired exc products protein breakdown
Acidosis and hyperkalaemia
Abnormal Na handling with inc retention
Cause impaired ability kidney to conc urine in renal failure
disruption counter current mechanism
loss of nephron function
Synthesis of ACh at NMJ
- synthesized in pre synaptic terminal and stored in synaptic vesicles
- acetyl co A + choline catalysed by choline acetyltransferase