Cardiorespiratory physiology

1. 1[blank_start]Pacemaker[blank_end] potential occurs between action potentials, and is the slow depolarisation of pacemaker cells of the SA node towards threshold. This is achieved by activation of [blank_start]HCN[blank_end] channels, which allow Na+ [blank_start]ENTRY[blank_end] which allows slow depolarisation. When the threshold is reached the action potential is activated.
   
   (HCN channels are active at Action potentials more negative than 50mV)

   1. APacemaker
   2. BHCN
   3. CENTRY
2. 2Non-pacemaker cells generate [blank_start]fast[blank_end] response action potentials, by rapid depolarisation. This is characteristic of atrial and ventricular [blank_start]myocytes[blank_end].
   

   1. Afast
   2. Bmyocytes
3. 3the duration of cardiac action potentials ranges from 200 to [blank_start]400[blank_end] ms.
   

   1. A400
4. 4in cardiac pacemaker cells, [blank_start]calcium[blank_end] ions are involved in the initial depolarization phase of the action potential

   1. Acalcium
5. 5(words not periodic table abbreviations)
   Fast action potentials are generated in 4 phases, 0-4 .
   In phase 0, electrochemical forces allow entry of [blank_start]sodium[blank_end] through fast sodium channels to generate upstroke.
   
   In phase 1 electrochemical forces then allow entry of [blank_start]potassium[blank_end] through channels to generate early partial repolarisation (returns it to a negative value).
   
   In phase 2 influx of [blank_start]calcium[blank_end] through calcium channels balanced by efflux of K+
   
   In phase 3 chemical forces that favour potassium efflux through channels predominate over influx of K+ I the same channels
   
   In phase 4 ionic concentration gradients restored by Na/K ATPase, 3Na+/1Ca2+ antiporter.
   

   

   1. Asodium
   2. Bpotassium
   3. Ccalcium
6. 6Slow action potentials:
   In P0 depolarisation achieved by [blank_start]calcium[blank_end] influx through Ca2+ channels
   
   In P3 calcium channels are inactivated, [blank_start]potassium[blank_end] conductance is increased.
   
   P4 Ionic concentration reset for next AP
   

   

   1. Acalcium
   2. Bpotassium
7. 7[blank_start]Absolute[blank_end] refractory period corresponds to depolarization and repolarization, whereas [blank_start]relative[blank_end] refractory period corresponds to hyperpolarization
   

   1. AAbsolute
   2. Brelative
8. 8Electrical potentials originate at the [blank_start]SA[blank_end] node and travel from one muscle cell to the next through gap junctions in the intercalated disks between cells.
   The heart cells form a functional [blank_start]syncytium[blank_end] because of this arrangement, where the electrical impulses pass freely between communicating cells, so the myocardium functions as a single contractile unit, which allows rapid spontaneous depolarisation of the myocardium.
   

   1. Asyncytium
   2. BSA
9. 9In Wolff Parkinson White syndrome, the accessory conduction pathway is called the bundle of [blank_start]Kent[blank_end]. The pathognomonic feature is the result of premature excitation of cardiac [blank_start]myocytes[blank_end], which lead to periods of rapid heart rate.

   1. AKent
   2. Bmyocytes
10. 10[blank_start]Intrinsic[blank_end] heart rate is the rate at which the heart beats when all cardiac neural and hormonal inputs are removed, and is in the range of 100-115 bpm.
    

    1. AIntrinsic

11. 11Heart rate is decreased below the intrinsic rate mainly by the activation of the [blank_start]vagus[blank_end] nerve, which innervates the SA node

    1. Avagus
12. 12A sinus rhythm is any cardiac rhythm in which depolarisation of the cardiac muscle begins at the sinus node. It is characterised by the presence of correctly oriented [blank_start]P[blank_end] waves on the electrocardiogram (ECG).

    1. AP
13. 13The normal duration of the cardiac cycle is [blank_start]0.8[blank_end] seconds, which gives resting heart rate of ~72bpm.
    Systole lasts 0.3s and is [blank_start]shorter[blank_end] than diastole.
    This time shortens as bpm increase; short diastole has a negative impact on [blank_start]ventricular[blank_end] filling and coronary blood flow.
    

    1. A0.8
    2. Bshorter
    3. Cventricular
14. 14Normative pressure data:
    [blank_start]Right[blank_end] atrium 5/0 mm Hg
    [blank_start]Right[blank_end] ventricle 25/0mm Hg
    Pulmonary artery 25/8 mm Hg
    [blank_start]Left[blank_end] atrium 8/0 mm Hg
    [blank_start]Left[blank_end] ventricle 120/0 mm Hg
    

    1. ARight
    2. BRight
    3. CLeft
    4. DLeft
15. 15[blank_start]S1[blank_end] occurs due to AV valve closure (mitral) at the end of ventricular diastole and the onset of ventricular systole.
    [blank_start]S2[blank_end] occurs due to outflow valve closure (pulmonary and aortic), at the end of ventricular systole and onset of ventricular diastole.
    [blank_start]S3[blank_end] is normal in children and some athletes but in later life indicates cardiac problems are present such as a failing left ventricle
    [blank_start]S4[blank_end] is always abnormal; usually failing or hypertrophic left ventricle.
    

    1. AS1
    2. BS2
    3. CS3
    4. DS4
16. 16 LVEDP is important. It occurs just before the onset of ventricular systole, and indicates haemodynamic health of the left [blank_start]ventricle[blank_end]. It should be less than [blank_start]12[blank_end] mm Hg, but is raised in diastolic overload, such as left ventricular failure.
    

    1. Aventricle
    2. B12
17. 17normal value for ejection fraction is about [blank_start]60[blank_end]%.

    1. A60
18. 18The [blank_start]P[blank_end] wave on an ECG is associated with a small increase in atrial and ventricular pressures after contraction of the atria.
    The [blank_start]QRS[blank_end] segment of the ECG indicates contraction of the filled ventricles.

    1. AP
    2. BQRS
19. 19The [blank_start]end systolic[blank_end] volume is the minimum volume of blood in the ventricles during the cardiac cycle.
    

    1. Aend systolic
20. 20[blank_start]Stroke volume[blank_end] is the volume of blood ejected per heartbeat. It equals EDV – ESV. Cardiac output (CO) is the volume of blood ejected by the ventricles per minute, so it is the product of SV x HR

    1. AStroke volume
21. 21Cholesterol synthesis:
    Step 1 is the synthesis of isopentenyl pyrophosphate.
    [blank_start]Mevalonate[blank_end] is formed as an intermediate in the formation of IP.
    
    Step 2 is the condensation of 6 molecules of isopentenyl pyrophosphate to form squalene, in the reaction sequence C5, C10, C15, C30.
    
    Step 3 is the [blank_start]cyclisation[blank_end] of squalene, forming a tetracyclic product which is converted to cholesterol, by a series of concerted 1,2-methyl group and hydride shifts along the chain of squalene to bring about the formation of the four rings.

    1. AMevalonate
    2. Bcyclisation
22. 22The average healthy human has approximately [blank_start]140g[blank_end] cholesterol present in the body, mainly in cell membranes. Serum level range is [blank_start]3.7[blank_end]-5.2 mmol/L.

    1. A140g
    2. B3.7
23. 23The rate of production of cholesterol in the body is highly sensitive to cellular levels of cholesterol via a negative feedback loop, mediated mainly by changes in the activity of [blank_start]HMG[blank_end] coA reductase, which forms mevalonate from acetyl CoA (this is inhibited by [blank_start]statins[blank_end]).

    1. AHMG
    2. Bstatins
24. 24Cholesterol synthesis occurs mainly in the [blank_start]liver[blank_end], and cholesterol in excess of what the liver itself needs is exported in the blood in the form of [blank_start]VLDLs[blank_end].

    1. Aliver
    2. Bkidneys
    3. Cblood
    4. DVLDLs
    5. EHDL
    6. FLDL
    7. Gchylomicrons
25. 25Bile salts are made in the [blank_start]liver[blank_end], then stored and concentrated in the gallbladder and released into the small intestine via the bile ducts, and are the major breakdown products of cholesterol.
    Bile acids eliminate [blank_start]cholesterol[blank_end] from the body.
    

    1. Aliver
    2. Bcholesterol
26. 26Bile salts are produced in the liver by conjugating bile acids with [blank_start]glycine[blank_end] or [blank_start]taurine[blank_end] forming glycocholic acid, taurocholic acid respectively.

    1. Aglycine
    2. Btaurine
27. 27Cholesterol is the precursor of vitamin D.
    In the form 7-dehydrocholesterol in the skin, it is photolyzed by UV in sunlight to pre-vitamin D3 which is then isomerised to vitamin D3, or [blank_start]cholecalciferol[blank_end]. This is converted to calcitriol in the liver by 25-[blank_start]hydroxylation[blank_end], and 1-alpha hydroxylation subsequently in the kidneys. [blank_start]Calcitriol[blank_end] is the active form of vitamin D.
    

    1. Acholecalciferol
    2. Bhydroxylation
    3. CCalcitriol
28. 28The vascular endothelium regulates vascular tone by releasing factors involved in relaxation and contraction of the vessel, as well as those involved in thrombus formation and coagulation.
    This is mediated by [blank_start]nitric oxide[blank_end], previously known as endothelium derived relaxing factor. This causes platelet deactivation and vasodilation. It is a free radical, so it can cause tissue damage due to oxidative stress at high levels.
    

    1. Anitric oxide
29. 29The vascular endothelium produces contracting factors (EDCFs), produced by the COX pathway from [blank_start]arachidonic[blank_end] acid, which circulate at low levels under normal conditions

    1. Aarachidonic
30. 30 The vascular endothelium produces [blank_start]thrombomodulin[blank_end], which can generate protein C when bound to thrombin, which causes degradation of factors 5a and 7a.
    

    1. Athrombomodulin
31. 31PGI2, [blank_start]prostacyclin[blank_end], is an eicosanoid, and a product of arachidonic acid, and is produced by cyclooxygenase. It [blank_start]inhibits[blank_end] platelet activation and functions as a potent vasodilator.
    
    
    
    It is released by healthy endothelial cells, eliciting its effect by a paracrine () signal cascade that involves a GPCR (prostacyclin receptor) on platelets and endothelial cells in proximity. Receptor binding signals adenylate cyclase to produce cAMP, which prevents platelet activation and prevents increases in cytosolic Ca2+ levels which would be caused by binding of [blank_start]thromboxane[blank_end] A2 binding its receptor, which causes platelet activation.
    
    PGI2 also binds endothelial prostacyclin receptors, and in the same way raises cytosolic cAMP levels. This activates protein kinase A (PKA) which continues the signal cascade, causing phosphorylation of the myosin light chain kinase, which inhibits its activity, inducing smooth muscle relaxation and thus vasodilation.
    When used as a drug it is known as epoprostenol.
    

    1. Aprostacyclin
    2. Binhibits
    3. Cthromboxane
32. 32NO is a gaseous signalling molecule, which was previously known as endothelium-derived relaxing factor (EDRF) because it causes vasodilation.
    It is biosynthesised from NOS enzymes and from oxygen, [blank_start]NADPH[blank_end] and L-arginine.
    It can diffuse freely across membranes.
    Sildenafil/Viagra uses the NO pathway to cause surrounding smooth muscle [blank_start]relaxation[blank_end] which causes vasodilation and increasing blood flow.
    
    

    1. ANADPH
    2. Brelaxation
33. 33[blank_start]Endothelins[blank_end] are the strongest vasoconstrictors known.
    Endothelin ETB receptors are located on endothelial cells
    ETA receptors are found in the smooth muscle tissue of blood vessels
    Both Activate [blank_start]phospholipase[blank_end] C
    ETA [blank_start]rasies[blank_end] blood pressure, ATB [blank_start]lowers[blank_end] it
    

    1. AEndothelins
    2. Bphospholipase
    3. Crasies
    4. Dlowers
34. 34[blank_start]Endothelins[blank_end] are the strongest vasoconstrictors known
    

    1. AEndothelins
35. 35[blank_start]Bosantin[blank_end] is an ETA/B receptor antagonist
    Ambrisantan and sitaxsentan are [blank_start]ETA[blank_end] selective antagonists
    Nitrovasodilators such as amyl nitrite and glyceryl trinitrate (GTN) are [blank_start]NO[blank_end] donors
    Epoxyeicosatrienoic acids (EET) are metabolites of [blank_start]arachidonic[blank_end] acid.
    
    

    1. ABosantin
    2. BETA
    3. CNO
    4. Darachidonic
36. 36The [blank_start]autonomic[blank_end] nervous system is the vegetative nervous system component; we are not acutely aware of its activity, and provides nerve activity for actions that are mainly involuntary such as breathing and heart rate.
    

    1. Aautonomic
37. 37The [blank_start]autonomic[blank_end] NS controls lung ventilation. It has two components- the parasympathetic and sympathetic nervous systems.

    1. Aautonomic
38. 38Generally the PNS causes [blank_start]vasodilation[blank_end] of blood vessels, such as the pulmonary vasculature, while the SNS causes [blank_start]vasoconstriction[blank_end].

    1. Avasodilation
    2. Bvasoconstriction
39. 39[blank_start]Parasympathetic[blank_end] fibres decrease chronotropy, inotropy and dromotropy, while the SNS acts on β1 adrenoreceptors, to increase these same factors.
    

    1. AParasympathetic
40. 40The [blank_start]cardiac[blank_end] plexus regulates chronotropy, dromotropy and inotropy. The SNS increases heart rate, increases contraction force and dilates the CA's, while the PNS takes the opposite effect.
    

    1. Acardiac
41. 41[blank_start]Sympathetic[blank_end] visceral afferents provide referred pain and also feedback on blood pressure

    1. ASympathetic
42. 42[blank_start]Cardiac output[blank_end] is the output of each ventricle per minute, equivalent to approx. 6L/ minute at rest.

    1. ACardiac output
43. 43Cardiac [blank_start]index[blank_end] is the output of ventricles per minute per m2 which is approximately 3.0 to 5.0L/min/m2. These values change depending on tissue demand.
    

    1. Aindex
    2. Boutput
44. 44[blank_start]Positive[blank_end] chronotropes increase heart rate; [blank_start]negative[blank_end] chronotropes decrease heart rate.
    

    1. APositive
    2. Bnegative
45. 45The PNS vagal tone is a tonic discharge dominant at rest, with sympathetic [blank_start]inhibition[blank_end]. It has a chronotropic effect, meaning it changes the rate of contraction in the heart.
    The SNS response is a tonic discharge that [blank_start]increases[blank_end] with stress and PNS inhibition, and has a chronotropic effect.

    1. Ainhibition
    2. Bincreases
46. 46[blank_start]Inotropes[blank_end] (not the same as ionotropes) alter the force of muscular contraction in the heart.

    1. AInotropes
47. 47Atropine blocks muscarinic (M2) Ach receptors, [blank_start]decreasing[blank_end] heart rate.

    1. Adecreasing
48. 48Beta blockers such as atenolol block B1 adrenergic receptors, [blank_start]decreasing[blank_end] heart rate and contractility.

    1. Adecreasing
49. 49[blank_start]Afterload[blank_end] is the force opposing cardiac muscle shortening and ejection of blood during ventricular contraction.
    Affected by tension in ventricular wall and arterial impedance- the forces outside the heart that oppose ventricular ejection (arterial pressure) during ventricular contraction.
    

    1. AAfterload
50. 50Frank starling law of the heart describes the ability of the heart to change its force of contraction and therefore [blank_start]stroke volume[blank_end] in response to changes in venous return.
    The heart is able to generate a larger force of contraction at a length [blank_start]longer[blank_end] than its optimum muscle fibre length.
    

    1. Astroke volume
    2. Blonger
51. 51Protein kinase A has multiple effects in the myocyte. It phosphorylates the [blank_start]calcium[blank_end] channel in the sarcolemma and causes increased entry of Ca++ into the cell, thus increasing the force of contraction.

    1. Acalcium
52. 52Lipoproteins have an amphipathic outer shell with [blank_start]hydrophilic[blank_end] (polar) ends exposed on the surface making the particle soluble.

    1. Ahydrophilic
53. 53Lipoproteins have a neutral core containing [blank_start]triacylglycerols[blank_end] and cholesterol esters, obtained either from the diet or through de novo synthesis.
    

    1. Atriacylglycerols
54. 54[blank_start]Apolipoproteins[blank_end] are located on the external surface of lipoproteins and function as ligands for cell-surface receptors and as coenzymes for lipid metabolism enzymes.
    There are five major apolipoprotein classes- A,B,C,D,E, and each may have subclasses such as apo C-II and apo E2, E3 etc.
    

    1. AApolipoproteins
55. 55Chylomicrons are [blank_start]less[blank_end] dense than Very low density lipoproteins (VLDL)
    

    1. Aless
    2. Bmore
56. 56Vitamins A, D, E are fat [blank_start]soluble[blank_end] vitamins

    1. Asoluble
    2. Binsoluble
57. 57Chylomicrons are formed in the [blank_start]endoplasmic reticulum[blank_end] in enterocytes in the small intestine.
    

    1. Aendoplasmic reticulum
58. 58Chylomicrons in the plasma receive additional [blank_start]apolipoproteins[blank_end] by exchange with HDL particles

    1. Aapolipoproteins
59. 59Utilisation of chylomicron triglycerides by the tissues:
    Most tissues have LPL attached to the capillary walls (extracellular enzyme).
    Lipoprotein lipase is activated by [blank_start]Apo C[blank_end]-II, and degrades TG within the chylomicron
    This casues release of:
    Fatty acids: taken up by tissues for storage as TG or for energy production
    [blank_start]Glycerol[blank_end]: taken up by the liver for gluconeogenesis
    
    

    1. AApo C
    2. BGlycerol
60. 60When TGs are removed, the chylomicrons get smaller and denser
    Chylomicron remnants form as the chylomicrons lose Apo C lipoproteins back to [blank_start]HDL[blank_end]
    [blank_start]Liver[blank_end] receptors recognise Apo E on the chylomicron remnants and clear them from circulation for break down via receptor-mediated endocytosis
    

    1. AHDL
    2. BLiver
61. 61VLDL: transports endogenously synthesised [blank_start]triglycerides[blank_end]
    LDL: transports endogenously synthesised [blank_start]cholesterol[blank_end]
    HDL: transports [blank_start]cholesterol[blank_end] from the tissues to the liver- reverse cholesterol transport
    

    1. Atriglycerides
    2. Bcholesterol
    3. Ccholesterol
62. 62LDL cholesterol can be taken up by macrophages (Especially oxidised LDL)
    This is because macrophages express high levels of [blank_start]scavenger[blank_end] receptor class A (SR-A)
    SR-A has high affinity for LDL whose lipids or Apo B have been oxidised
    The macrophages become [blank_start]foam[blank_end] cells when they become engorged with Ox-LDL
    This is important for the formation of atherosclerotic plaques
    

    1. Afoam
    2. Bscavenger
63. 63HDLs are formed in blood by the addition of lipids to apolipoprotein Apo [blank_start]A1[blank_end], which is synthesised in the liver and small intestine and developed into nascent HDL
    

    1. AA1
64. 64Disorders of VLDL and chylomicrons: [blank_start]hypertriglyceridemia[blank_end]
    Disorders of LDL: [blank_start]hypercholesterolaemia[blank_end]
    

    1. Ahypertriglyceridemia
    2. Bhypercholesterolaemia
    3. Chypercholesterolaemia
    4. Dhypertriglyceridemia
65. 65 Tangier disease is a disorder of [blank_start]HDL[blank_end] cholesterol

    1. AHDL
66. 66Heterozygous familial hypercholesterolaemia is caused by a lack of production of the [blank_start]LDL[blank_end] receptor which causes high plasma cholesterol
    
    

    1. ALDL
67. 67Artery structure:
    Tunica [blank_start]intima[blank_end] is the inner, single EC layer resting on a basement membrane
    Tunic [blank_start]media[blank_end] is the middle layer, mainly smooth muscle cells, providing contractile ability
    Tunica [blank_start]adventitia[blank_end] is the outer layer, mainly connective tissue

    1. Aintima
    2. Bmedia
    3. Cadventitia
    4. Dintima
    5. Emedia
    6. Fadventitia
    7. Gintima
    8. Hmedia
    9. Iadventitia
68. 68[blank_start]Compliance[blank_end] is the ability of a hollow organ to distend and increase volume with increasing transmural pressure or the tendency of a hollow organ to resist recoil toward its original dimensions on application of a distending or compressing force

    1. ACompliance
69. 69In terms of arterial pulses,
    Peak pressure is [blank_start]systolic[blank_end] (120mm Hg in systemic and 25mm Hg in pulmonary)
    The minimum pressure is [blank_start]diastolic[blank_end] (80mm Hg systemic, 8mm Hg pulmonary)

    1. Asystolic
    2. Bdiastolic
70. 70The pulse pressure is calculated as P systolic - P diastolic: this equals approximately [blank_start]40[blank_end]mm Hg normally
    

    1. A40
71. 71The main determinant of diastolic pressure is peripheral resistance to flow, according to the [blank_start]Poiseuille[blank_end] equation
    

    1. APoiseuille
72. 72Baroreceptors are sensory receptors which respond to stretch mechanoreceptors
    They are located in the [blank_start]adventitia[blank_end] of large vessels and the [blank_start]media[blank_end] of smaller ones
    Stimulation leads to increases in both mean blood pressure and pulse pressure, caused by an increase in rate of discharge in afferent nerves
    

    1. Aadventitia
    2. Bmedia
73. 73There are 3 capillary types:
    [blank_start]Sinusoid[blank_end] capillaries
    Continuous capillaries
    Fenestrated capillaries

    1. ASinusoid
74. 74About [blank_start]8[blank_end] L moves from capillaries to the interstitial space each day, returned to circulation by [blank_start]lymphatic[blank_end] drainage (important for oedema)
    Water moves from an are of [blank_start]low[blank_end] osmotic pressure (dilute) to an area of [blank_start]high[blank_end] osmotic pressure (concentrated) by osmosis
    

    1. A8
    2. Blymphatic
    3. Clow
    4. Dhigh
75. 75[blank_start]Colloid[blank_end] osmotic pressure (oncotic pressure) is due to poorly diffusible proteins in plasma or the interstitial fluid and exerts a force on the walls of the vessels

    1. AColloid
76. 76[blank_start]Oncotic[blank_end] pressure is the opposing force to hydrostatic pressure.
    

    1. AOncotic
77. 77[blank_start]Starling’s[blank_end] law describes fluid movement across capillaries being proportional to capillary [blank_start]permeability[blank_end], trans-capillary [blank_start]hydrostatic[blank_end] pressure differences, and trans-capillary oncotic pressure differences.
    The flow of fluids across the capillary walls depends on:
    the balance between the force of blood pressure on the walls which tends to force fluids out
    And:
    the osmotic pressure across the walls with tends to force fluids in due to a greater concentration of dissolved substances in the blood (osmosis) so that the declining gradient in blood pressure from the arterial to the venous end of the capillary results in an outflow of fluids at its [blank_start]arterial[blank_end] end, with an increasing inflow towards the venous end.
    

    1. AStarling’s
    2. Bpermeability
    3. Chydrostatic
    4. Darterial
78. 78Oedema is an increase in [blank_start]interstitial[blank_end] fluid volume due to alteration in one or more of the starling forces
    The interstitial fluid (fluid between cells), is derived from capillaries with a similar solute content to plasma except for protein content.
    Capillary pressure forces fluid from the capillaries into the interstitium where the arterial end pressure is higher than the venous end
    Oedema is believed to be the outward filtration predominating the arterial end of the capillary, and as hydrostatic pressures fall, fluid reverts to the capillary from the interstitium driven by the oncotic pressure gradient.
    

    1. Ainterstitial
79. 79Flat Alveolar Cells ([blank_start]Type I[blank_end] granular pneumocytes) form the alveolar wall in a single cell layer.
    Each alveolus is surrounded by a single cell capillary network. Large and thin cells with a central nucleus, 95% of the epithelial lining of the respiratory zone. Fuse with the pulmonary endothelium. Responsible for gas exchange-fusion with PE allows diffusion. Terminally differentiated so can't replicate.

    1. AType I
80. 80Type [blank_start]II[blank_end] alveolar cells secrete pulmonary surfactant from [blank_start]microvilli[blank_end]. PS is a phospholipid protein complex which facilitates lung expansion.

    1. AII
    2. Bmicrovilli
81. 81[blank_start]Goblet[blank_end] cells and submucosal glands secrete mucus in the upper respiratory tract.

    1. AGoblet
82. 82[blank_start]Hysteresis[blank_end] means that lung volume at any given pressure during inhalation is less than the lung volume at any given pressure during exhalation; this is because filling empty lungs with air requires more pressure to maintain a given volume because you have to overcome the surface tension of the wet alveolar walls which are "stuck" to each other. There's an energetic cost to breaking that liquid-liquid surface tension.
    
    

    1. AHysteresis
83. 83The Law of [blank_start]Laplace[blank_end] essentially states that the tension within the wall of a sphere filled to a particular pressure depends on the thickness of the sphere. Consequently, even at a constant pressure, the tension within a filled sphere can be decreased simply by increasing the thickness of the sphere's wall
    

    1. ALaplace
84. 84At the end of expiration, compressed surfactant phospholipid molecules decrease the surface tension to near-zero levels, which increases [blank_start]compliance[blank_end] to allow the lung to inflate more easily.
    

    1. Acompliance
85. 85[blank_start]DPPC[blank_end] is the strongest surfactant molecule in the pulmonary surfactant (higher compaction capacity because the apolar tail is less bent). Made and secreted by Type II pneumocytes. It comprises 40% of surfactant, with another 40% being phospholipids such as phosphatidylcholine.
    

    1. ADPPC
86. 86Surfactant is stored in [blank_start]lamellar[blank_end] bodies. These then develop tubular [blank_start]myelin[blank_end] ( highly ordered surfactant structure that is lung specific and produced in the alveolar airspace). Surfactant can then be recycled or degraded by type II alveolar cells and macrophages.
    

    1. Alamellar
    2. Bmyelin
87. 87Alpha 1-antitrypsin is a protease inhibitor which acts on [blank_start]elastase[blank_end] and trypsin.
    

    1. Aelastase
88. 88Alveolar [blank_start]dead[blank_end] [blank_start]space[blank_end] is sum of the volumes of those alveoli which have little or no blood flowing through their adjacent pulmonary capillaries, i.e., alveoli that are ventilated but not perfused, and where, as a result, no gas exchange can occur.
    Negligible in healthy individuals, but can increase dramatically in some lung diseases due to ventilation-perfusion mismatch.

    1. Adead
    2. Bspace
89. 89Fick's law of diffusion:
    The greater the [blank_start]surface[blank_end] [blank_start]area[blank_end] and the shorter the distance (thickness of the membrane) the greater the rate of [blank_start]diffusion[blank_end].
    Rate of diffusion is directly proportional to SA, inversely proportional to distance.
    

    1. Asurface
    2. Barea
    3. Cdiffusion
90. 90Reduced [blank_start]alveolar[blank_end] surface [blank_start]area[blank_end] is seen in some pathologies such as emphysema, collapsed lung, lung resection. This leads to a decrease in the rate of gaseous exchange.

    1. Aalveolar
    2. Barea
91. 91Increased thickness of the space between air and blood may be seen in pulmonary [blank_start]oedema[blank_end] due to pulmonary inflammation, reducing the rate of gaseous exchange. This causes accumulation of interstitial fluid between alveoli and pulmonary capillaries. In pulmonary fibrosis, irritants cause lung tissue to become fibrotic and thick, increasing the thickness of the membrane.

    1. Aoedema
92. 92V/Q ratio: The ratio of the amount of air reaching the alveoli (V) to the amount of blood reaching the alveoli (Q). 1L of blood/air has approximately [blank_start]200[blank_end]mL of O2.
    

    1. A200
93. 93The V/Q ratio is also variable in different regions of the lung. It is affected by [blank_start]gravity[blank_end]- at the apex, VQ>1, while at the base VQ<1. in the middle the ratio is close to 1. this is because ventilation is greater by approximately [blank_start]50[blank_end]% at the base than at the apex because the lower lungs are better adapted for gaseous exchange.
    

    1. Agravity
    2. B50
94. 94The V/Q ratio is also variable in different regions of the lung, due to the position of the [blank_start]heart[blank_end] in relation to the lungs- as you move from the apex to the base of the lungs, ventilation and perfusion [blank_start]increase[blank_end], but perfusion increases at a greater rate, which results in a lower V/Q ratio. This allows increased perfusion and higher rate of gas exchange during exercise in the [blank_start]apical[blank_end] and middle zone of the lungs.

    1. Aheart
    2. Bincrease
    3. Capical
95. 95The ideal VQ ratio is [blank_start]1[blank_end], but it is closer to [blank_start]0.8[blank_end] in humans due to the differences in the ratio In different regions of the lungs.
    

    1. A0.8
    2. B1
96. 96[blank_start]Pleural[blank_end] pressure is higher at the base of the lungs, which leads to higher compliance of the alveoli and increased ventilation. [blank_start]Hydrostatic[blank_end] pressure is decreased at the apex of the lungs, which results in a decrease in flow and perfusion in this region.
    

    1. AHydrostatic
    2. BPleural
97. 97Hypoxia ABG: Arterial pO2 is less than [blank_start]60[blank_end]mmHg
    Arterial hypoxemia: Arterial pO2 is lower than [blank_start]80[blank_end]mm Hg
    Hypercapnia: Increase in arterial pCO2 above the normal range, >[blank_start]40[blank_end]mmHg
    Hypocapnia: Abnormally low arterial pCO2, <[blank_start]35[blank_end]mm Hg
    

    1. A60
    2. B80
    3. C40
    4. D35
98. 98Pleural pressure is [blank_start]less[blank_end] than pulmonary pressure, because the lungs are stretched under tension, pulling inwards and the chest wall is also under tension, pulling outwards.
    The pressure differentials required for inspiration and expiration are established by mechanical force via the muscles of respiration.
    

    1. Aless
99. 99Events of inspiration:
    
    Inspiratory muscles contract
    Diameter of the thoracic cage [blank_start]increases[blank_end]
    Intrapleural pressure becomes more [blank_start]negative[blank_end] (PPL)
    Transmural pressure [blank_start]increases[blank_end], alveoli swell or open (PTM)
    Intraalveolar pressure falls relative to [blank_start]atmospheric[blank_end] pressure
    Air flows [blank_start]down[blank_end] the pressure gradient from atmosphere to alveoli
    Tidal volume of about [blank_start]500[blank_end]ml is added to the resting volume (FRC=functional residual capacity) (VT)
    End of inspiration- no airflow, Intraalveolar pressure= atmospheric pressure
    

    1. Aincreases
    2. Bnegative
    3. Cincreases
    4. Datmospheric
    5. Edown
    6. F500
100. 100During breathing, the [blank_start]scalenes[blank_end] raise the first two ribs, and the [blank_start]sternocleidomastoid[blank_end] raises the sternum. These are known as the accessory Inspiratory muscles.
     

     1. Ascalenes
     2. Bsternocleidomastoid
101. 101Spirometry Key volumes:
     TV: [blank_start]tidal[blank_end] volume
     IRV: inspiratory [blank_start]reserve[blank_end] volume
     IC: [blank_start]inspiratory[blank_end] capacity
     ERV: expiratory [blank_start]reserve[blank_end] volume
     RV: [blank_start]residual[blank_end] volume
     FRC: functional residual volume
     VC: [blank_start]vital[blank_end] capacity
     TLC: total lung capacity
     FEV1: Forced [blank_start]expiratory[blank_end] volume in one second (% of forced vital capacity)

     1. Atidal
     2. Breserve
     3. Cinspiratory
     4. Dreserve
     5. Eresidual
     6. Fvital
     7. Gexpiratory
102. 102Compliance= measure of the change in lung volume which occurs due to a change in [blank_start]transmural[blank_end] pressure.
     A compliant lung stretches further than a non-compliant lung.
     Disease alters compliance, causing a decrease leading to more work.

     1. Atransmural
103. 103[blank_start]Hysteresis[blank_end]: phenomenon in which the value of a physical property lags behind changes in the effect causing it. So, filling empty lungs with air requires more pressure to maintain a given volume because you have to overcome the surface tension of the wet alveolar walls which are "stuck" to each other

     1. AHysteresis
104. 104[blank_start]Elastic[blank_end] forces account for roughly 70% of the total work of breathing, with the remainder being NEFs.
     

     1. AElastic
105. 105The optimal value of respiratory rate is [blank_start]15[blank_end]/min in order to minimise work, because higher rate produces higher flow and increases non elastic work.

     1. A15
106. 106[blank_start]Law[blank_end] of [blank_start]Laplace[blank_end]: pressure in alveoli is directly proportional to the surface tension and inversely proportional to the radius of the alveoli. So, pressure in a smaller alveolus would be higher than in a larger alveolus, if surface tension is the same in both.

     1. ALaw
     2. BLaplace
107. 107surfactant components SPA and SPD enhance [blank_start]immune[blank_end] [blank_start]system[blank_end] activity in the lung
     

     1. Aimmune
     2. Bsystem
108. 108Determinants of airway resistance:
     Radius
     Cross sectional area of the [blank_start]bronchial[blank_end] tree
     Lung [blank_start]volume[blank_end]
     [blank_start]Pattern[blank_end] of airflow
     Lower airway [blank_start]diameter[blank_end]
     [blank_start]Bronchial[blank_end] smooth muscle tone
     Thickness of the [blank_start]mucous[blank_end] lining and submucosa
     

     1. Abronchial
     2. Bvolume
     3. CPattern
     4. Ddiameter
     5. EBronchial
     6. Fmucous
109. 109According to the Hagen-poiseuille law, [blank_start]radius[blank_end] has a strong influence on airway resistance (relates flow rate to airway radius and to the distance air is transported).
     resistance can therefore be defined as the ratio between driving pressure and the associated flow rate.
     If the airway radius is reduced by [blank_start]50[blank_end]%, resistance increases 16-fold.
     

     1. Aradius
     2. B50
110. 110[blank_start]Obstructive[blank_end] airway diseases:
     Interfere with movement of air through the airways
     Increases flow-resistive work
     No effect on elastic work
     Decreases FEV1 but not FVC (ratio decreases)
     
     [blank_start]Restrictive[blank_end] airway diseases:
     Interfere with the ability to expand the lungs
     Increases elastic work
     No effect on flow-resistive work
     Decreases FEV1 and FVC (ratio remains normal)
     
     

     1. AObstructive
     2. BRestrictive
111. 111Each haemoglobin molecule is made up of [blank_start]four[blank_end] heme groups surrounding a globin group, forming a tetrahedral structure.
     There are [blank_start]four[blank_end] iron atoms in each molecule of haemoglobin, which accordingly can bind four atoms of oxygen. Globin consists of two linked pairs of polypeptide chains (2 [blank_start]alpha[blank_end] and 2 [blank_start]beta[blank_end] chains).

     1. Afour
     2. Bfour
     3. Calpha
     4. Dbeta
112. 112The % saturation is the O2 [blank_start]content[blank_end]/ O2 [blank_start]capacity[blank_end].
     Oxygen content in arterial blood is approximately 20 ml% in health.
     

     1. Acapacity
     2. Bcontent
113. 113The [blank_start]sigmoid[blank_end] (S) shape of the curve for oxygen saturation means that at the plateau where % saturation is near 100%, the pO2 can fall, but the % saturation won't change much. This is a protection mechanism against [blank_start]hypoxia[blank_end] because in air with low O2 levels, O2 levels are maintained in Hb.
     The [blank_start]steep[blank_end] part allows for O2 unloading in the tissues- low pO2 allows dissociation of the O2 from the haem molecule into the tissues, from an area of high O2% (blood) to low (tissue).
     
     
     

     

     1. Ahypoxia
     2. Bsigmoid
     3. Csteep
114. 114The [blank_start]Bohr[blank_end] effect refers to the shift in the oxygen dissociation curve caused by changes in the concentration of carbon dioxide or the pH of the environment.
     Haemoglobin's oxygen binding affinity is inversely related both to [blank_start]acidity[blank_end] and to the concentration of carbon dioxide.
     Since carbon dioxide reacts with water to form carbonic acid, an increase in CO2 results in a decrease in blood pH, resulting in haemoglobin proteins releasing their load of oxygen.
     

     1. ABohr
     2. Bacidity
115. 115[blank_start]HbF[blank_end] binds O2 better than HbA because 2,3 BPG binds poorly to HbF gamma chains, which improves transfer of O2 across the placenta
     
     

     1. AHbF
116. 116Fe2+ in Hb can be oxidised to Fe3+ (ferric iron) by certain drugs/ chemicals such as nitrates and nitrites and some local anaesthetics
     This forms [blank_start]methaemoglobin[blank_end], which doesn’t bind O2, causing methemoglobinemia

     1. Amethaemoglobin
117. 117Haemoglobin binds carbon monoxide [blank_start]240[blank_end]x more avidly than o2, forming carboxyhemoglobin, which can't bind O2 leading to carbon monoxide toxicity
     

     1. A240
118. 118[blank_start]Cyanosis[blank_end] occurs when arterial blood is 85% saturated (pO2= 50mmHg), or when capillary blood is 70% saturated

     1. ACyanosis
119. 119There are three ways carbon dioxide is carried in the bloodstream from the peripheral tissues back to the lungs:
     (1) as a dissolved gas (10%)
     (2) as [blank_start]bicarbonate[blank_end]
     (3) bound to [blank_start]hemoglobin[blank_end] (and other proteins) as carbaminohemoglobin
     

     1. Abicarbonate
     2. Bhemoglobin
120. 120
     
     The [blank_start]haldane[blank_end] effect: Oxygenation of blood in the lungs displaces carbon dioxide from haemoglobin which increases the removal of carbon dioxide. Consequently, oxygenated blood has a reduced affinity for carbon dioxide.
     

     1. Ahaldane
121. 121The medullary respiratory centre consists of two neuron clusters called the [blank_start]dorsal[blank_end] respiratory group and the [blank_start]ventral[blank_end] respiratory group

     1. Adorsal
     2. Bventral
122. 122Neurons in the [blank_start]pons[blank_end] can modify respiratory rhythm; the pneumotaxic centre sends signals to the DRG, which helps silence the inspiratory neurons
     The [blank_start]apneustic[blank_end] centre conversely prevents inspiratory neurons from being switched off
     

     1. Apons
     2. Bapneustic
123. 123[blank_start]Central[blank_end] Chemoreceptors are Located in the medulla.
     [blank_start]peripheral[blank_end] chemoreception are located at the carotid body.
     Both regulate arterial PCO2 within normal limits in response to primary changes in CO2 and regulate blood and body pH (in the ECF) in response to acid-base disturbances; this is achieved because CO2 can permeate the BBB into the CSF which leads to eventual hyperventilation to blow off CO2.
     
     
     

     1. ACentral
     2. Bperipheral
124. 124Peripheral chemoreceptors are generally located in the [blank_start]carotid[blank_end] [blank_start]sinus[blank_end] region and [blank_start]aortic[blank_end] arch. They respond to changes in (arterial) PO2, PCO2 and pH.
     They trigger respiratory drive changes aimed at maintaining normal partial pressure levels.
     
     

     1. Acarotid
     2. Bsinus
     3. Caortic
125. 125Pulmonary stretch receptors are [blank_start]mechanoreceptors[blank_end] found in the lungs.
     When the lung expands, the receptors initiate the [blank_start]Hering[blank_end]-[blank_start]Breuer[blank_end] reflex, which reduces the respiratory rate.
     Increased firing from the stretch receptors also increases production of pulmonary surfactant.
     

     1. Amechanoreceptors
     2. BHering
     3. CBreuer
126. 126PO2 at atmospheric is [blank_start]160[blank_end]mm Hg, N2 600 mm Hg, CO2 negligible
     Alveolar Po2 is [blank_start]100[blank_end]mm Hg, due to dilution with H2O vapour and dead space (150mL)
     

     1. A160
     2. B100
127. 127[blank_start]Hypoxic[blank_end] [blank_start]Drive[blank_end]:
     As the arterial level of carbon dioxide changes, this results in a change seen with the pH of the cerebrospinal fluid.
     This triggers a reaction in the central chemoreceptors located near the medulla.
     These sensory receptors are responsible for regulating respiratory function so excess CO2 in blood can be “blown off”, to raise pH to normal levels, and monitoring the levels of arterial carbon dioxide.
     [blank_start]Haldane[blank_end] [blank_start]effect[blank_end]:
     Haemoglobin binds most of the H+ formed in RBCs when no O2 is bound (hbO2), so unloading of O2 means Hb can collect H+ generated by CO2.
     If this did not occur, venous blood would be much more acidic than arterial blood (there is little O2 in the blood, so the Hb can collect acidic ions)
     Deoxygenation of blood increases its ability to carry COs and H+, maintaining a normal pH.
     

     1. AHypoxic
     2. BDrive
     3. CHaldane
     4. Deffect
128. 128
     
     Arterial Blood Gas Analysis Normal Values:
     pH: [blank_start]7.35[blank_end]-[blank_start]7.45[blank_end]
     PO2: [blank_start]75[blank_end]-100mm Hg
     PCO2: [blank_start]40[blank_end]mmHg
     HCO3: ~24 mEq/L
     O2 sat %: [blank_start]94[blank_end]-[blank_start]100[blank_end]%
     
     
     
     

     1. A94
     2. B100
     3. C7.35
     4. D7.45
     5. E75
     6. F40
129. 129As altitude increases, PB and PO2 [blank_start]decrease[blank_end]. Air composition remains the same (21% O2), but the O2 decrease means PAO2 (partial pressure of the alveoli) and PaO2 (partial pressure of arterial blood) decrease. The rate of ventilation increases by [blank_start]65[blank_end]% at high altitude because of this; PACO2 and PaCO2 decrease and eventual [blank_start]hypercapnia[blank_end] occurs.
     
     

     1. A65
     2. Bdecrease
     3. Chypercapnia
130. 130At high altitude brain function decreases because [blank_start]Anoxic[blank_end] [blank_start]depolarization[blank_end] occurs, which is induced by the loss of neuronal selective membrane permeability and the ion gradients across the membrane that are needed to support neuronal activity.

     1. AAnoxic
     2. Bdepolarization
131. 131In acute hypoxia, peripheral chemoreceptors [blank_start]increase[blank_end] ventilation and activate sympathetics which [blank_start]increase[blank_end] heart rate (and CO), as well as blood pressure.

     1. Aincrease
     2. Bincrease
132. 132Dexamethasone (glucocorticoid-unknown mechanism), nifedipine (Ca channel blocker- reduces pulmonary arterial pressure) are used to treat [blank_start]altitude[blank_end] sickness.
     Prophylactic [blank_start]acetazolamide[blank_end]- inhibits renal carbonic anhydrase (CA), leading to increased bicarbonate excretion, which prevents hypercapnia by maintaining normal acid-base balance.

     1. Aacetazolamide
     2. Baltitude
133. 133At altitude given sufficient time, cardiac output and heart rate return to normal but not [blank_start]pulmonary[blank_end] [blank_start]arterial[blank_end] pressure. There is increased tissue vascularity, EPO, HCT, Hb, blood volume and diffusing capacity. Renal compensation also occurs to counteract the [blank_start]hypercapnia[blank_end]- more HCO3- is released.
     

     1. Apulmonary
     2. Barterial
     3. Chypercapnia
134. 134Chronic mountain sickness is characterised by increased HCT and HPV ([blank_start]Hypoxic[blank_end] [blank_start]pulmonary[blank_end] [blank_start]vasoconstriction[blank_end]). The HPV in combination with high HCT increase leads to severe [blank_start]pulmonary[blank_end] HTN.
     Right heart failure (hypertrophy) occurs due to generalised pulmonary vasoconstriction, resulting in increased vascular resistance
     This leads to a decrease in peripheral [blank_start]arterial[blank_end] pressure
     This condition can evolve in to [blank_start]cor[blank_end] [blank_start]pulmonale[blank_end] and congestive heart failure
     

     1. AHypoxic
     2. Bpulmonary
     3. Cvasoconstriction
     4. Dpulmonary
     5. Earterial
     6. Fcor
     7. Gpulmonale
135. 135Venous return is [blank_start]Increased[blank_end] during exercise by increased:
     Muscle blood flow
     Muscle pump function
     Respiratory pump function
     Venoconstriction
     

     1. AIncreased
136. 136Cardiac output is [blank_start]increased[blank_end] during exercise due to increased venous return, [blank_start]sympathetic[blank_end] nerve activity and circulating catecholamines.
     Max cardiac output is approximately [blank_start]25[blank_end]-[blank_start]30[blank_end]L/min, or just >40L/min for elite athletes
     There is a redistribution of blood flow to exercising muscles with vasoconstriction in the gut, kidney, inactive muscles and skin initially
     Later when body temperature increases, skin vessels dilate to try and get rid of some of the excess heat
     

     1. Aincreased
     2. Bsympathetic
     3. C25
     4. D30
137. 137When [blank_start]ATP[blank_end] is used up in working muscles, the muscles themselves produce metabolic byproducts (for example, [blank_start]adenosine[blank_end], hydrogen ions and carbon dioxide).
     As these byproducts leave the muscle cells, they cause small, thin-walled blood vessels (capillaries) within the muscle to expand or dilate, which is called vasodilation.
     The dilated capillaries allow increased blood flow, which delivers more oxygenated blood to the working muscle
     

     1. AATP
     2. Badenosine
138. 138O2 demand during exercise can be met by increasing:
     -Blood flow
     -The rate of O2 extraction from the blood
     -Amount of O2 present in the blood
     
     The rate of O2 extraction from the blood can be increased by Decreasing the diffusion distance between blood and cells
     Increasing the [blank_start]diffusion[blank_end] gradient
     Increasing exchange area of the [blank_start]capillary[blank_end] bed
     Increased bohr and haldane effect
     Increased levels of 2,3[blank_start]BPG[blank_end]
     
     

     1. ABPG
     2. Bdiffusion
     3. Ccapillary
139. 139During exercise, [blank_start]diffusing[blank_end] [blank_start]capacity[blank_end] is increased 3x because of increased CO and pulmonary arterial pressure, which opens capillaries, improving the VQ ratio
     

     1. Adiffusing
     2. Bcapacity
140. 140[blank_start]VO2[blank_end] [blank_start]max[blank_end] is the measurement of the maximum amount of oxygen a person can utilize during intense exercise.
     Calculated by Measuring the VO2 plateau which occurs as exercise intensity is raised.
     [blank_start]40[blank_end]ml/min/kg is average, athletes can be >[blank_start]80[blank_end]ml/min/kg
     
     

     1. AVO2
     2. Bmax
     3. C40
     4. D80
141. 141[blank_start]Anaerobic[blank_end] [blank_start]threshold[blank_end] is reached during exercise when the metabolic demand for O2 exceeds O2 delivery so that muscles begin to use glycolysis in addition to aerobic metabolism.
     As a result, lactic acidosis occurs.
     
     

     1. AAnaerobic
     2. Bthreshold
142. 142VO2 at rest, Diffusing capacity, Maximum heart rate, CO at rest, Hb concentration in blood are factors which are [blank_start]unaffected[blank_end] by training
     

     1. Aunaffected
     2. Baffected
143. 143Veins are small vessels with an internal diameter of ~0.5mm. They have High [blank_start]compliance[blank_end], and are innervated by [blank_start]sympathetic[blank_end] constrictor nerves which influence venous return and cardiac output.
     
     

     1. Acompliance
     2. Bsympathetic
144. 144Lymph vessels are lined by [blank_start]endothelial[blank_end] cells and have a thin layer of smooth muscles and adventitia that bind the lymph vessels to the surrounding tissue.
     

     1. Aendothelial
145. 145Lymphatics are vessels which return the interstitial fluid to the venous system at a rate of [blank_start]8[blank_end]L a day.
     They drain proteins and particulate matter, including pathogens, as well as absorbing fat in the form of [blank_start]chylomicrons[blank_end].
     

     1. A8
     2. Bchylomicrons
146. 146Small lymphatic vessels are found in all organs except the CNS and [blank_start]cornea[blank_end]
     

     1. Acornea
147. 147The composition of lymph: PEC
     P: [blank_start]protein[blank_end]
     E: [blank_start]electrolytes[blank_end]
     C: [blank_start]cells[blank_end]

     1. Aprotein
     2. Belectrolytes
     3. Ccells
148. 148In terms of cerebral circulation, the regulation of blood flow to any organ over a period of time commensurate with metabolic activity in the setting of a wide range of perfusion pressure is termed [blank_start]Autoregulation[blank_end]

     1. AAutoregulation
149. 149Autoregulation is controlled by several factors:
     "SLEEP"
     
     [blank_start]SNS[blank_end] vasoconstrictor tone
     [blank_start]Local[blank_end] mediators
     [blank_start]Endothelial[blank_end] cell factors
     [blank_start]Endocrine[blank_end] factors
     [blank_start]Paracrine[blank_end] factors
     

     1. ASNS
     2. BLocal
     3. CEndothelial
     4. DEndocrine
     5. EParacrine
150. 150Normal Cerebral Blood Flow: [blank_start]750[blank_end] cc/min
     The brain is highly metabolically active: [blank_start]3.3[blank_end]mL O2 per 100g required; grey matter more active than white
     

     1. A750
     2. B3.3
151. 151CBF autoregulation: believed to occur via a [blank_start]myogenic[blank_end] mechanism whereby an increase in MAP increases the transmural vessel tension causing [blank_start]depolarization[blank_end] of vascular smooth muscle and constriction of the precapillary resistance vessels.
     The reverse happens when the MAP and transmural tension decreases.
     Mean cerebral arterial P is ~ [blank_start]77[blank_end] mmHg
     
     

     1. Amyogenic
     2. Bdepolarization
     3. C77
152. 152The brain oxygen consumption accounts for [blank_start]20[blank_end]% of basal oxygen consumption at rest

     1. A20
153. 153[blank_start]Cushing[blank_end] reflex: Rising ICP leads to [blank_start]bradycardia[blank_end] and hypertension
     

     1. Abradycardia
     2. BCushing
154. 154Total resting flow of the coronary arteries is [blank_start]250[blank_end] cc/ min
     

     1. A250
155. 155Determinants of myocardial oxygen demand: CHAPT:
     [blank_start]Contractility[blank_end]
     [blank_start]Heart[blank_end] rate
     [blank_start]Afterload[blank_end]
     [blank_start]Preload[blank_end]
     [blank_start]Tension[blank_end]
     

     1. AContractility
     2. BHeart
     3. CAfterload
     4. DPreload
     5. ETension
156. 156Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes.
     The nucleus tractus solitarii of the brainstem is activated directly or indirectly by the triggering stimulus, resulting in simultaneous enhancement of [blank_start]parasympathetic[blank_end] nervous system (vagal) tone and withdrawal of sympathetic nervous system tone.
     This results in a spectrum of haemodynamic responses, either [blank_start]cardioinhibitory[blank_end] due to enhanced parasympathetic tone, or [blank_start]vasodepressor[blank_end] responses where blood vessels dilate due to withdrawal of sympathetic NS tone.

     1. Aparasympathetic
     2. Bcardioinhibitory
     3. Cvasodepressor
157. 157The pulse pressure is the [blank_start]systolic[blank_end] pressure minus the [blank_start]diastolic[blank_end] pressure, and the mean pressure is the diastolic pressure plus 1/2 of the pulse pressure (for arteries only).
     Absolute pressure in veins is an order of magnitude lower than in major arteries. In health, Central Venous Pressure (CVP) is normally low. It is a [blank_start]complex[blank_end] waveform, with a,c,v waves and x and y descents. These values reflect venous return and heart function.
     

     1. Asystolic
     2. Bdiastolic
     3. Ccomplex
158. 158Flow can be derived from ohm's law, as BP/CO x TPR, where TPR is [blank_start]total[blank_end] [blank_start]peripheral[blank_end] [blank_start]resistance[blank_end].

     1. Atotal
     2. Bperipheral
     3. Cresistance
159. 159Turbulence occurs when [blank_start]laminar[blank_end] flow is replaced by [blank_start]turbulent[blank_end] flow.
     

     1. Alaminar
     2. Bturbulent
160. 160If the LVEDP is high or MR Is chronic, the LA [blank_start]enlarges[blank_end]. It is a [blank_start]low[blank_end] pressure chamber.
     

     1. Alow
     2. Benlarges
161. 161[blank_start]Haematocrit[blank_end] is the main determinant of viscosity. Viscosity is also determined by
     blood vessel [blank_start]diameter[blank_end], velocity of blood flow and high plasma protein concentrations
     

     1. AHaematocrit
     2. Bdiameter
162. 162[blank_start]Compliance[blank_end] refers to the ability of a vessel to respond to an increase in pressure by to distending or swell and increase the volume of blood it can hold, or with decreased pressure, a decrease in volume

     1. ACompliance
163. 163Abnormal compliance causes [blank_start]oedema[blank_end]
     

     1. Aoedema
164. 164Cardiac output at Rest: Volume is [blank_start]5[blank_end] L/min per ventricle
     

     1. A5
165. 165[blank_start]Left[blank_end] ventricular dysfunction:
     Systolic: impaired contractility and ejection
     ~⅔ of HF patients have systolic dysfunction
     Diastolic:
     Impaired filling and relaxation
     
     Primary problem: low cardiac output, particularly in exertion
     A lot of the problems with HF occur due to the homeostatic response to the syndrome in order to compensate
     

     1. ALeft
166. 166[blank_start]Coronary[blank_end] [blank_start]artery[blank_end] disease accounts for 70% of HF in developed societies.
     Causes [blank_start]Left[blank_end] [blank_start]Ventricle[blank_end] Remodelling which occurs as compensatory hypertrophy, which is then followed by:
     Significant hypertrophy
     Dilatation
     Progressive dysfunction
     
     

     1. ACoronary
     2. Bartery
     3. CLeft
     4. DVentricle
167. 167[blank_start]HTN[blank_end] is the Second most common cause of HF behind CAD.
     Pathology is characterised by LV hypertrophy and [blank_start]fibrosis[blank_end]; Cardiac amyloidosis may affect the way electrical signals move through the heart leading to abnormal [blank_start]contraction[blank_end]
     
     

     1. AHTN
     2. Bfibrosis
     3. Ccontraction
168. 168[blank_start]Dilated[blank_end] [blank_start]cardiomyopathy[blank_end] is characterised by LV dilatation with decreased ejection fraction. It is the final common morphology after a variety of insults such as MI
     
     
     

     1. ADilated
     2. Bcardiomyopathy
169. 169[blank_start]Valvular[blank_end] cardiomyopathy occurs when volume overload causes chamber dilation, leading to left ventricular remodelling.
     [blank_start]Hypertrophic[blank_end] cardiomyopathy is a relatively common condition but rarely causes HF. it is characterised by hypertrophy of LV with or without RV, with systolic anterior motion of the mitral valve.
     
     
     
     

     1. AValvular
     2. BHypertrophic
170. 170Standard values for blood volume:
     Normal 70kg man:
     70mls per kg
     [blank_start]4900[blank_end] mls in total
     

     1. A4900
171. 171Classification of shock:
     [blank_start]Cardiogenic[blank_end]: failure of the heart as a pump
     [blank_start]Distributive[blank_end]: changes in vascular tone
     [blank_start]Hypovolemic[blank_end]: reduction in circulating fluid volume- either whole blood, plasma, extracellular or intracellular
     

     1. ADistributive
     2. BCardiogenic
     3. CHypovolemic
172. 172Tension pneumothorax, Constrictive pericarditis and Cardiac tamponade cause [blank_start]obstructive[blank_end] [blank_start]cardiogenic[blank_end] shock
     
     
     
     

     1. Aobstructive
     2. Bcardiogenic
173. 173In shock, if sBP < 70 mm Hg, [blank_start]norepinephrine[blank_end] is administered. If sBP 70–100 mm Hg, [blank_start]dopamine[blank_end] is administered.
     
     

     1. Anorepinephrine
     2. Bdopamine
174. 174[blank_start]Distributive[blank_end] shock is characterised by redistribution of fluid from the intravascular to the extravascular compartment, leading to underperfusion of the organs. Occurs even though the output of the heart is at or above a normal level.
     According to the cause, there are 4 types of [blank_start]distributive[blank_end] shock:
     
     Neurogenic shock: Decreased sympathetic stimulation leading to decreased vasal tone.
     Anaphylactic shock
     [blank_start]Septic[blank_end] shock
     Shock due to adrenal crisis
     
     

     1. ADistributive
     2. Bdistributive
     3. CSeptic
175. 175[blank_start]Hypovolemic[blank_end] shock: Fluid loss may affect either extra or intracellular compartments and may be associated with many different issues, such as whole blood loss, plasma loss or fluid loss.

     1. AHypovolemic
176. 176In shock, [blank_start]compensation[blank_end] is due to Redistribution of cardiac output
     The initial response protects the [blank_start]cerebral[blank_end] and myocardial circulation at the expense of reduced perfusion to major organs

     1. Acerebral
     2. Bcompensation
177. 177[blank_start]Compensation[blank_end] in hypovolemia is Neural and hormonal.
     Activation of the [blank_start]sympathetic[blank_end] NS diverts blood away from noncritical organs and tissues to preserve blood supply to vital organs such as the heart and brain, prolonging heart and brain function.
     Vasoactive hormones such as Angiotensin II, [blank_start]ADH[blank_end], catecholamines (NA/ adrenaline) and metabolically active hormones such as [blank_start]cortisol[blank_end] are released to maintain cardiovascular control, provide of adequate metabolic fuel and restore of volume
     
     
     
     
     

     1. ACompensation
     2. Bsympathetic
     3. CADH
     4. Dcortisol
178. 178Capillary fluid shift or internal [blank_start]transfusion[blank_end] occurs to mobilise tissue fluid by a decrease in [blank_start]hydrostatic[blank_end] pressure, leading to increased plasma [blank_start]osmolarity[blank_end]. Up to 500mL of fluid can be released this way, absorbed into the capillaries. However, this really dilutes plasma proteins impairing their function.
     

     1. Atransfusion
     2. Bhydrostatic
     3. Cosmolarity
179. 179[blank_start]Decompensated[blank_end] shock is an irreversible phase occurs after the body has endured tissue injury so severe that survival is unlikely, due to multiorgan failure.
     Metabolic [blank_start]acidosis[blank_end] blunts the CV response and the arterioles dilate, causing microcirculatory pooling and disseminated intravascular coagulation

     1. ADecompensated
     2. Bacidosis

Beschreibung

Quiz am Cardiorespiratory physiology , erstellt von Phil Howard am 10/05/2020.

Autor

Phil Howard

Sprache

English

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