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FBS2 > Physiology and Pharmacology of Systems > Flashcards

Physiology and Pharmacology of Systems Flashcards

1
Q

What is haematopoiesis?

A

Process by which mature blood cells are generated from precursor cells

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2
Q

What are the 3 main contents of blood and main constituents of each?

A

Plasma - soluble proteins + mediators, 50-60%
Packed cellular volume - haematocrit, 40-45%
WBS + platelets

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3
Q

What is the fancy name for platelets?

A

Thrombocytes

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4
Q

Average location and amount of:

a) RBC?
b) Platelets?
c) WBC?

A

a) Confined to blood vessels, 4-6 x 10^6 / microlitre
b) Confined to blood vessels, 1.5-4 x 10^5 / microlitre
c) Use circulation in transit to + from tissue, 4-11 x 10^3 / microlitre

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5
Q

When does haematopoiesis occur?

A

2-2.5 weeks in utero

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6
Q

What cells are the blood islands surrounded by?

Why for one of them?

A

Surrounded by mesenchymal cells
Enveloped by endothelial cells
- arranged spatially so BC group into lumen of primitive blood vessels

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7
Q

What type of cell do all blood cells arise from?

Origin of circulating blood cells?

A

Pluripotent stem cells

Haematocrit stem cells

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8
Q

What type of stem cells do not have the potential for self renewal?

A

Unipotent/Progenitor

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9
Q

What do these committed cells arise to?

a) Erythrocyte progenitor?
b) Megakaryocyte?
c) Myeloblast?
d) Monoblast?
e) B-lymphoblast?
f) T-lymphoblast?

A

a) Erythrocytes
b) Platelets
c) Neutrophils, Eosinophil, Basophil
d) Monocyte, Macrophages
e) B lymphocyte
f) T lymphocyte

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10
Q

What is the shape, size (diameter) and lifespan of:

a) RBC?
b) Platelets?
c) Megakaryocytes (only size)?
d) Monocytes?
e) Small lymphocytes (only size)?
f) Large lymphocytes (only size)?
g) Neutrophils (only shape)?
h) Eosinophils (shape + lifespan)?

A

a) Biconcave discs, 7 micrometres, 120 days
b) Anuclear, discoid shape, 2-4 micrometres, 8-12 days
c) 50-70 micrometres
d) Mononuclear (horseshoe), 20, month/years for macrophages
e) 6-9 micrometres
f) 9-15 micrometres
g) Polymorphonuclear - multilobed
h) Bi-lobed nucleus, several days

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11
Q

What is the penultimate precursor of RBC and the size?

A

Normoblast

8-10 micrometres

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12
Q

In development of RBC, when nucleus abandoned, what is cell called?

A

Reticulocyte

1-2 days for RNA + organelles to be lost

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13
Q

How do platelets form clots?

A

Adhere to fibrin filaments + damaged endothelial surfaces

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14
Q

What does Fe combine with to form haem and where?

A

Protoporphyrin

Mito

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15
Q

What types of cells act as nurse cells in development of RBC?

A

Macrophages

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16
Q

What is the half life of neutrophils in blood?

A

6-7 hours

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17
Q

When can neutrophils damage healthy tissue?

A

During chronic inflammatory diseases

e.g. RA, MS, COPD

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18
Q

What is the main function of:
a) Uropods
b) Pseudopods
in neutrophils?

A

a) Acts as anchor, traction on tissue

b) Chemokine gradient

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19
Q

What are the 4 main cytotoxic secretory products in eosinophils?

A

Major basic protein
Eosinophil cationic protein
Eosinophil derived neurotoxin
Eosinophil peroxidase

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20
Q

What are small lymphocytes sub-divided into?

A

B lymphocytes + T lymphocytes

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21
Q

What markers are present on:

a) T helper cells?
b) Cytotoxic T cells?

A

a) CD4 marker

b) CD8 marker

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22
Q

What are natural killer cells?

A

Large lymphocytes

Kill virus infected/tumour cells with no involvement of specific antigens

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23
Q

What is the relative refractory period?

A

AP overshoots to more -ve potentials

Stronger stimulation needed for another AP

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24
Q

What is the normal cardiac AP duration at rest?

A

350-380 ms

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25
Q

What should the QTc be below?

A

Less than 400 ms

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26
Q

Why can’t tetanise cardiac muscle?

A

Due to long AP

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27
Q

What is the hierarchy of pacemakers from fastest to slowest?

A

SA node
AV node
Bundle of His ==> left + right bundle branches
Purkinje fibres

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28
Q

What is diastolic depolarisation?

A

X have resting stable membrane potential

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29
Q

Name 3 features of cells from SA nodes

A

X cyto
Numerous caveolae
Lots membrane

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30
Q

What are 2 theories for diastolic depolarisation?

A

Membrane clock

Calcium clock

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31
Q

What is a funny current?

A

Inward current activated when membrane potential gets more negative (hyperpolarized)

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32
Q

What is the only drug that lowers heart rate?

A

Ivabradine

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33
Q

What stimulates and inhibits funny current?

A

Stimulate - adrenaline

Inhibit - AcH

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34
Q

What is the function of the AV pause?

A

Allows ventricles to fill

Prevents transmission of fast heart rates from atria

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35
Q

What is atrial fibrillation?

A

Atria contract randomly + fast

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36
Q

What are connexons made up of?

A

2 hemi-channels

Subsequently made up 6 connexins

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37
Q

Where are connexons commonly found in the cell?

A

End of cells

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38
Q

What is anisotropic conduction?

A

Muscle cell to muscle cell contraction

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39
Q

What are the 2 electrodes of the ECG called?

A

Reference electrode

Recording electrode

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40
Q

What do each part of ECG wave represent?

A

P - Atrial Depolarisation
Q - Depolarisation of septum (towards atria)
R - Depolarisation of ventricles (towards apex)
S - Depolarisation of ventricles (towards atria)
T - Repolarization of ventricles (towards endocardium)

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41
Q

Which part of the electrical impulse doesn’t show up on an ECG?

A

When it spreads down Bundle of His and left and right bundle branches

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42
Q

Why is the Q wave negative?

A

Towards head so wave of +veness away from recording electrode

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43
Q

Why is R wave rapid?

A

Specialised rapidly conducting Purkinje fibres

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44
Q

What does the PQ interval indicate?

Pathology

A

Atrial conduction
AV node delay

AV block

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45
Q

What does the ST segment indicate?

Pathology

A

Heterogeneity of ventricular polarisation

Myocardial infarction

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46
Q

What does the QRS duration indicate?

Pathology

A

Ventricular conduction velocity
(Depolarisation of ventricles)

Bundle branch block

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47
Q

What does the QT interval indicate?

Pathology

A

Ventricular AP duration

Long QT syndrome

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48
Q

What is resting Ca level?

A

100 nM

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49
Q

Definition of:

a) Chronotropy?
b) Inotropy?
c) Lusitropy?

A

a) Heart rate
b) Strength of contraction
c) Rate of relaxation

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50
Q

What are 2 examples of +ve chronotropic agents and what is the type of stimulation?

A

Adrenaline, Noradrenaline

Sympathetic stimulation

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51
Q

What does +ve chronotropic agents cause?

A

Increase funny current
Faster rate diastolic depolarisation
Faster heart rate

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52
Q

What an example of -ve chronotropic agents and what is the type of stimulation?

A

AcH

Parasymp stimulation

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53
Q

What does -ve chronotropic agents cause?

A

Decrease funny current
Opens K-AcH channels
Slower rate of diastolic depolarisation
Slower heart rate

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54
Q

What an example of +ve inotropic + lusitropic agents and what is the type of stimulation?

A

Adrenaline + noradrenaline

Beta receptor stimulation

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55
Q

How does PKa phosphorylation affect?

a) Pacemaker?
b) L type Ca channels?
c) ATPase subunits?
d) RYR2?
e) Myofilament?

A

a) +ve chronotropy
b) +ve chronotropy, +ve inotropy
c) +ve lusitropy
d) +ve inotropy
e) +ve inotropy, +ve lusitropy

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56
Q

What is the diastolic notch?

A

Aortic valves snapping shut

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57
Q

In a PV loop, what represents the:

a) Stroke work?
b) Stroke volume?

A

a) Integrated area bound by a PV loop

b) Difference between isovolumetric contraction and relaxation

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58
Q

What are the 2 features of a jugular venous pressure wave?

A

Biphasic

Low pressure

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59
Q 
In the JVP wave, what does the:
a) A wave
b) X descent
c) C wave
d) V wave
e) Y descent
represent?
A

a) Atrial contraction (right)
b) atrial relaXation
c) Carotid pulse - interruption of x descent
d) atrial filling during Ventricular systole - bulging of tricuspid valve
e) passive atrial emptYing - tricuspid valve open

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60
Q

What are the 2 features of a arterial pulse wave?

A

Monophasic

High pressure

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61
Q

At what hydrostatic pressure will the jugular vein collapse?

A

5 cm above heart

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62
Q

How to assess JVP in a patient?

A

Support patient 45 degrees

JVP is height of collapse of internal jugular 3 cm above manubriosternal angle

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63
Q

Why does the patient have to be at 45 degrees to assess JVP?

A

If upright, point of collapse lower

Jugular below level of clavicle so x see

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64
Q

Why is internal jugular preferable to external?

A

Closer to r atrium - external x directly drain ==> SVC
Valveless so can see pulsations - opposite external
Vasoconstriction can make external small + barely visible
External superficial + prone to kicking

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65
Q

What is tricuspid stenosis and how does the JVP wave change?

A

Narrowing of tricuspid valve opening

Atrial wave enhanced + ventricular wave diminished

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66
Q

What is tricuspid regurgitation and how does the JVP wave change?

A

Valve x close tight enough

Atrial wave diminished + ventricular wave enhanced

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67
Q

What does the S1 sound represent in a phonocardiogram?

A

Initiation of v systole + AV mitral valve closure
Low frequency
Lub

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68
Q

What does the S2 sound represent in a phonocardiogram?

A

Closure of semilunar valves
Higher frequency + shorter
Dub

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69
Q

What does the S3 sound represent in a phonocardiogram?

A

Opening of AV valves + rapid refilling

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70
Q

What does the S4 sound represent in a phonocardiogram?

A

Atrial systole, rarely heard

Except when EDP raised

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71
Q

What are the;

a) Primary heart sounds?
b) Secondary heart sounds?

A

a) S1 and S2

b) S3 and S4

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72
Q

What is the name of the rhythm when you can hear S3 and S4?

A

Gallop rhythm

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73
Q

What is a heart murmur?

A

Turbulence in blood

X always pathological, occur in young/exercise

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74
Q

What are 2 pathological causes of heart murmurs?

A

Valve stenosis

Valve regurgitation

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75
Q

What are 2 causes of diastolic murmurs?

A

Mitral stenosis - hear as ventricle fills
Aortic incompetence - early diastolic murmurs
softing + prolongation of 2nd sound

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76
Q

What are 2 causes of systolic murmurs?

A

Aortic stenosis - high pressure

Mitral incompetence - pan-systolic (lush)

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77
Q

What is atherosclerosis?

A

Buildup of cholesterol - rich plaques

Causes stenosis of arteries

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78
Q

What type of cells are blood vessels commonly made up of?

What involved in?

A

Smooth muscle cells -
Contract + relax, control diameter
Endothelial cells -
Regulate sm cells, inhibit thrombosis

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79
Q

What is 40% of human mortality caused by?

A

Disruption of vasculature structure and function

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80
Q

What 3 factors regulate vascular tone?

A

ANS
Circulating hormones
Local mechanisms

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81
Q

In regulation of vascular tone, what are 3 features of SNS?

A

Constriction - splanchnic, renal, vascular beds
Alpha -1 receptors + NANC
Activation redistributes blood flow + raises TPR

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82
Q

In regulation of vascular tone, what are 3 features of PNS?

A

Vasodilation - salivary glands, pancreas, intestinal mucosa, penis
Muscarinic receptors + NANC
Regulates blood flow organs, activation x effect TPR

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83
Q

What circulating hormones affect vascular tone?

A

Adrenaline
Angiotensin II
Vasopressin

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84
Q

Why is vascular tone regulated?

A

Maintain necessary blood flow to all organs

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85
Q

Why is CO + TPR regulated?

A

Maintain adequate pressure head (arterial BP)

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86
Q

What substance does endothelium release that relaxes surrounding sm?

A

Nitrous oxide

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87
Q

What is NO release stimulated by?

A

Bradykinin, ATP, His, H+, CO2, AcH

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88
Q

What is PGI2, what is it released by and what does it do?

A

Prostacyclin
Endothelium
Inhibits platelet aggregation + endothelin

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89
Q

What is eNOS?

A

Endothelial nitrous oxide synthase

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90
Q

What is oxidative stress?

A

Overproduction of reactive O2 species

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91
Q

What does superoxide react with and what does it form?

Why bad?

A

O2- + NO ==> peroxynitrite

Prevents NO mediated vasodilation

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92
Q

What are EETs, what released by + what do?

A

Epoxyeicosatrienoic acids
Endothelium
Activates K+ channels on vascular sm cells
Causes hyperpolarization + relaxation

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93
Q

What 2 ways do vasodilating drugs work by?

A

Blocking processes causing contraction - VG Ca2+ channel blocker
Stimulating/ mimicking pathways causing relaxation - organic nitrates

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94
Q

How is constant blood flow maintained in vascular beds over range of pressures?

A

Myogenic response

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95
Q

What effects do metabolites have on vascular function?

A

Tonic vasodilating influence on resistance vessels

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96
Q

Which is more wichtig - myogenic/metabolic regulation?

A

Metabolic increases as resistance vessel diameter decreases

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97
Q

When and where does metabolic hyperaemia occur?

What substances produced?

A

Cardiac + skeletal muscle
Increased metabolism during exercise
K+, H+, CO2, lactic acid, adenosine

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98
Q

When does reactive hyperaemia occur?

A

After static (isometric) exercise

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99
Q

What are 2 structural adaptations of coronary circulation?

A

Formation coronary collaterals after ischaemia

High capillary density - 1 capillary/myocyte

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100
Q

Why is blood flow in cardiac wall occluded during systole?

A

Rise in wall tension compresses intramyocardial arterioles

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101
Q

What is the Circle of Willis made up of?

A

Anterior + Posterior cerebral
Internal carotid
Anterior + Posterior communicating arteries

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102
Q

What are 2 functional adaptations of cerebral circulation?

A

Strong metabolic hyperaemia - excess blood supply to organ

Weak regulation by ANS

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103
Q

What is diameter of typical capillary?

A

8 microns

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104
Q

What are the 2 main layers in capillary?

A

Basal lamina - fibrous protein, supports endothelium

Monolayer of endothelial cells - x sm cells (same venules)

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105
Q

What extra layer can capillaries in CNS have?

A

Pericytes

Contractile cells

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106
Q

What layer does veins have?

A

Thin tunica media

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107
Q

What is diameter of typical vein?

A

5mm

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108
Q

What happens to venules near sites of infection?

A

Permeable to leukocytes
Enter tissues via diapedesis - passage of cells via capillaries
Immune response

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109
Q

What is the respiratory pump related to venous system?

A

Inspriration reduces pressure within thorax
Decreases pressure within vena cava
Increase pressure gradient from venules ==> vena cava

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110
Q

What 3 factors can CVP vary due to?

A

Blood volume
Venous constriction
Posture

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111
Q

What is haemostasis?

A

Arrest of blood loss from damaged vessels

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112
Q

What is thrombosis?

A

Formation of occlusive thrombi, leading to MI, ischaemic stroke

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113
Q

What is primary haemostasis?

A

Aggregation of platelets + vasoconstriction

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114
Q

What receptors are present on platelets and what do they bind to?

A

GP1b - vWF
GPVI - collagen binding
Integrin alpha2beta1 - collagen 1

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115
Q

What are platelets exposed to in the ECM which they aren’t usually?

A

Collagen

Von Willebrand Factor

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116
Q

What is role of thrombin?

A

Catalyzes conversion fibrinogen ==> fibrin

Activates procoagulant factors V, VI, XI, XIII

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117
Q

What is COX and what does it activate?

A

Cyclooxygenase enzyme

Activate prostanoid thromboxane (TXA2)

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118
Q

What does 5 hydroxytryptamine do?

A

Vasoconstriction blood vessels

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119
Q

What does ADP do to platelets?

A

Activate adjacent platelets
Functional confirmation of receptor GP IIb/IIIa
Adjacent platelets come together by fibrinogen crosslinking

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120
Q

What is secondary haemostasis?

A

Clotting pathway

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121
Q

What causes initiation of clotting pathway?

A

Tissue Factor (TF)

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122
Q

What causes amplification of clotting pathway?

A

Thrombin

Activates factors FV, FVIII, FIX, FX

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123
Q

What are
a) Arterial
b) Venous
thrombi associated with?

A

a) Atherosclerosis

b) Stasis of blood/vascular injury following surgery/trauma

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124
Q

What are the main components of:

a) Arterial thrombi?
b) Venous thrombi?

A

a) Platelets

b) Fibrin, RBC

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125
Q

What is the prophylaxis for:

a) Arterial thrombi?
b) Venous thrombi?

A

a) Anti-platelet drugs

b) Anti-coagulants

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126
Q

What makes up Virchow’s triad?

A

Endothelial/vascular damage
Low blood flow (stasis)
Hypercoagulabilty

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127
Q

What is the action of aspirin?

A

Irreversible inhibition of COX-1

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128
Q

What does TXA2 do?

A

Platelet agonist

Vasoconstrictor

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129
Q

What are 4 side effects of aspirin?

A

Blood disorders
GI haemorrhage
GI irritation
Increased bleeding time

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130
Q

What are 2 irreversible P2Y12 antagonists?

A

Clopidogrel

Prasugrel

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131
Q

Why is Clopidogrel reduced pharmacological effect on 20-30% of pop?

A

Genetic polymorphisms CYP450 + CYP2C19

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132
Q

What are 2 P2Y12 antagonists developed by design?

A

Ticagrelor - oral

Cangrelor - i.v

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133
Q

Why do the P2Y12 antagonists developed by design have a rapid onset action?

A

Non-thienopyridine derivatives

X require metabolism

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134
Q

What are 2 types of GP IIb -IIIa antagonists and examples?

How taken?

A

F-ab fragments - aboximab, tirofiban

Small molecule inhibitors - Eptifibatide

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135
Q

What are 3 sub-optimal problems with current antiplatelet drug therapy?

A

Limited clinical efficacy
Variable in patient response + toxicity
Risk major haemorrhage

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136
Q

What does HIT stand for?

A

Heparin induced thrombocytopaemia

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137
Q

What is heparin made up of?

A

Glycodaminoglycans

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138
Q

Pros and cons of unfractionated heparin?

A 
Pro:
Cheap, shrt 1/2 life, reversible with protamine
Con:
Continuous infusion
HIT
Haemorrhage
Unpredictable pharmacokinetics
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139
Q

Pros and cons of low molecular weight heparin (LMWH)?

A 
Pro - 
Low chance HIT
High bioavailability
Con - 
Expensive
Haemorrhage
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140
Q

What factor on platelets bind to heparin to cause HIT?

A

Platelet Factor 4 (PF4)

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141
Q

What does the binding of PV4 to heparin complex cause?

A

Heparin-induced thrombocytopenia type 2

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142
Q

What does coumarin (Warfarin) inhibit?

A

Inhibit Vit K dependant epoxide-reductase

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143
Q

What does epoxide-reductase do?

A

Modifies FVII, FIX, FX, FII during synthesis in liver

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144
Q

What can affect Warfarin activity?

A

Diet

Genetic variation

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145
Q

What is the antidote for major bleeding event caused by warfarin?

A

Vit K

Replace clotting factors by plasma transfusion

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146
Q

What factor Xa inhibitors directly inhibit and examples?

A

Orally available
Rivaroxaban, Apixaban, Edoxaban
X frequent blood monitoring

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147
Q

What are examples of factor Xa inhibitors via injection?

What effect?

A

Fondaparinux, idraparine
Pentasaccharides
Act indirectly via antithrombin

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148
Q

What does antithrombin do?

A

Produced liver

Inactivates FX + FII

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149
Q

What type of thrombin does thrombin inhibitor work on?

A

Clot bound + free thrombin

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150
Q

Examples of:

a) I.V thrombin inhibitor?
b) Orally active thrombin inhibitor?

A

a) Hirudin, Lepirudin, Desirudin

b) Dabigatran

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151
Q

What things do traditional anticoagulants require?

A

Monthly blood tests
Dietary consultations
Possibility uncontrolled bleeding

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152
Q

What are DOAC?

A

Directly oral anticoagulant

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153
Q

What DOAC has an antidote?

A

Dabigatran

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154
Q

What does fibrinolytics do?

A

Activate plasminogen

Remove arterial thrombi

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155
Q

What is the risk of fibrinolytics and how treat?

A

Haemorrhage

Tranexamic acid

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156
Q

2 example of fibrinolytics + properties

A 
Streptokinase: 
non enzyme protein from streptococci
Plasminogens ==> plasmin
Allergenic
Alteplase: 
non-allergenic
Clot selective - only activate plasminogens bound to fibrin in thrombus
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157
Q

What is the common rhesus group peeps have and why?

A

Rh+ (85%)

Gene for D antigen dominant

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158
Q

How is antibody to D antigen formed?

A

Exposure to D antigen and sensitisation

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159
Q

When does antigen to D antigen formed?

A

Transfusion

Rh- mother birth to Rh+ baby + blood mixes

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160
Q

What are 5 complications with blood transfusions?

A 
Blood type incompatible
Transmission of infection
Fe overload
Fever
Impaired clotting
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161
Q

What percentage of stroke volume is stored in aorta and large arteries after systole?

A

75%

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162
Q

What percentage of stroke volume is pushed forward into smaller arteries during systole?

A

25%

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163
Q

4 short term factors that affect BP?

A

Sleep
Posture
Exercise
Stress

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164
Q

Where are baroreceptors located?

A

Carotid sinus in upper arch

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165
Q

What is orthostasis?

A

Decrease in BP soon after standing

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166
Q

What is afterload?

A

Force against which left ventricle pumps to eject blood into aorta

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167
Q

What is preload?

A

Degree of cardiac stretch

Amount of blood in ventricles before they contract

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168
Q

What is the IX cranial nerve?

A

Glossopharyngeal

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169
Q

What are baroreceptors?

A

Fine nerve endings with mechanoreceptors

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170
Q

If BP decreases, what receptors are affected on parasympathetic drive?

A

M2

Beta-1

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171
Q

If BP decreases, what is effect of parasympathetic drive?

A

HR increase
Force increase
CO increase

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172
Q

If BP decreases, what receptors are affected on sympathetic drive?

A

Beta 1

Alpha 1

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173
Q

If BP decreases, what is effect of sympathetic drive?

A

Venoconstriction
CVP increase
Arterial constriction - TPR increase

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174
Q

What is the blood level of adrenaline?

A

0.2-1nM

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175
Q

What receptors does noradrenaline effect?

A

Beta - 1

Alpha - 1

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176
Q

What receptors does adrenaline effect?

A

Beta - 1
Alpha - 1
Beta -2

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177
Q

What is the effect of these receptors when activated?

a) Beta 1
b) Alpha 1
c) Beta 2

A

a) Increase HR, Cardiac contractility
b) Vasoconstriction in most vascular beds
c) Vasodilation in skeletal muscle

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178
Q

What is used for long term regulation of arterial BP?

A

Maintenance of constant ECF volume

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179
Q

What is pressure natriuresis?

A

Increased renal perfusion due to higher BP

180
Q

What 4 things directly affect cardiac output?

A

Preload
Afterload
Contractility
HR

181
Q

What is Starling’s Law of heart?

A

Energy released during contraction depends in initial fibre length

182
Q

What is skinned cardiac muscle?

A

Removes cell membrane

183
Q

What are 3 consequences of Starling’s law?

A

SV of l and r ventricles are perfectly matched
Any given rate + functional state of heart, CVP will determine CO
Helps maintain CO even in face of increased afterload/decreased contractility

184
Q

What happens to the Starling curve in heart failure?

A

Becomes depressed

185
Q

What are 3 compensatory mechanisms for heart failure?

A

Reduce in pressure natriuresis - retention of Na + H2O
Activation of SNS + RAAS
Greater venous blood volume + vasoconstriction increase CVP

186
Q

What is the abbreviation for:

a) Atmospheric pressure?
b) Alveolar pressure?
c) Mouth/nose pressure?

A

a) Pb
b) PA
c) Pm

187
Q

What is Boyle’s law?

A

Pressure of fixed number of molecules (at constant temp) related to volume of a container in which they’re placed
PV = constant

188
Q

What value is -ve intrapleural pressure?

A

-5cm H2O at resting end expiration

Relative to Pb

189
Q

What type of muscles are used at rest during inspiration and what are they?

A 
Obligate Inspiratory Muscle
Diaphragm
External Intercostal muscles
Scalenes
Parasternal intercostal
190
Q

What muscles are used for inspiration if need increase resp intake?

A

Accessory intercostal muscle

Sternocleidomastoid

191
Q

What is FRC?

A

Functional Residual Capacity

Volume of lung at end of normal expiration

192
Q

What is the meaning of these abbreviations?

a) Pw
b) Pl
c) Prs
d) Ppl

A

a) Trans chest wall
b) Transpulmonary pressure
c) Trans total system
d) Intrapleural pressure

193
Q

How to calculate:

a) Pw
b) Pl
c) Prs

A

a) Ppl - Pb
b) PA - Ppl
c) PA - Pb

194
Q

What 4 factors change with inspiratory pressure?

A

Intrapleural pressure
Alveolar pressure
Transpulmonary pressure
Inspiratory muscles

195
Q

What is a pneumothorax?

A

Collapsed lung due to air in pleural cavity

Lungs inwardly directed elastic recoil

196
Q

What are the typical values for:

a) Vt?
b) VC?
c) IRV?
d) ERV?
e) IC?
f) TLC?
g) FRC?
h) RV?

A

a) 500ml
b) 5500ml
c) 3300ml
d) 1700ml
e) 3800ml
f) 7300ml
g) 3500ml
h) 1800ml

197
Q

What measurement cannot be taken by spirometry - what is technique?

A

TLR
FRC
RV
Bodyplevismography

198
Q

What is dead space and it’s abbreviation?

A

Airway volume with no gas exchange

Vd

199
Q

Calculation for physiological dead space?

A

Anatomical Vd - Alveolar Vd

200
Q

What is
a) Anatomical
b) Physiological
dead space?

A

a) All except alveoli + respiratory bronchioles - 15oml approx
b) Areas where GE dysfunctional

201
Q

Calculation for alveolar ventilation?

A

Total ventilation p/min - dead space ventilation

202
Q

Calculation for total ventilation?

A

Vt x frequency

203
Q

What are the 2 main sources of resistance the lung needs to overcome?

A

Elastic resistance of lung

Airway resistance of lung

204
Q

What is elastic resistance of lung?

A

Resistance to stretch of lung tissue + air-liquid interface lining alveoli

205
Q

What is airway resistance of lungs?

A

Resistance due to friction between layers of flowing air + airway walls

206
Q

Calculation for lung compliance?

A

Change in lung volume/ Change in transmural pressure gradient

207
Q

Calculation for airway resistance (RAW)?

A

(Alveolar pressure - mouth pressure)/ Airflow at mouth

208
Q

What 3 factors can disrupt laminar flow and lead to turbulence?

A

Increased velocity
Sharp edges
Branch points

209
Q

What causes lung sounds?

A

High velocity airflow due to narrowed airways

210
Q

What lung sounds are heard in asthma and how are they generated?

A

Wheezing

Oscillations in walls of airways near point of closure

211
Q

Why is silent chest ominous is asthma?

A

X generate enough airflow to breath

212
Q

What factors can affect bronchodilation on airway smooth muscle?

A

CO2
Inhibitory NANC nerves (NO, VIP)
Beta-adrenergic agonists via beta-2 receptors - adrenalin + salbutamol

213
Q

What factors can affect bronchoconstriction on airway smooth muscle?

A

Pulmonary stretch receptors (inhibit) + Airway irritant receptors (activate) on brain stem
Excitatory NANC nerves (SP, neurokinins)
His, prostaglandins, leukotrienes - Mast cells + eosinophils

214
Q

What equipment can be used measure Ppl?

A

Oesophageal balloon

215
Q

In a static pressure volume loop, when is compliance:

a) Max?
b) Min?

A

a) Around normal tidal volume

b) At high and low lung volume

216
Q

Calculation for compliance?

A

Change in lung volume/Change in transmural pressure

217
Q

What is the shape of a static pressure volume loop?

A

Hysteresis shape

Lines x touch

218
Q

Where is the most compliant part of a static pressure volume loop?

A

Middle bit where line steepest

219
Q

What special about volume of lung in expiration in a static pressure volume loop?

A

Greater at any given transmural pressure than inspiration

220
Q

What factors can:

a) Increase lung compliance?
b) Decrease lung compliance?

A

a) Emphysema - destroy elastic fibres

b) Stiff lungs, lung fibrosis (TB, asbestosis)

221
Q

In what condition does the honeycomb appearance of the lungs occur?

A

UIP fibrosis

Usual Interstitial Pneumonia

222
Q

What conditions are associated with COPD?

A

Bronchiolitis

Emphysema

223
Q

What is bronchiolitis?

A

Thick, narrow bronchioles mit excess mucus

224
Q

Where does centrilobular emphysema occur?

A

Affects upper lobes of lungs

225
Q

What is LaPlace equation?

A

P = 2T/R

226
Q

What is surfactant produced by?

A

Type II alveolar cells

227
Q

What is surfactant made up of?

A

Phospholipids e.g phosphatidylcholine

Surfactant proteins

228
Q

How do surfactants work?

A

Reduce surface tension in proportion to surface concentration

229
Q

What are the 3 effects of surfactants?

A

Increase compliance
Reduces tendency for alveoli to collapse
Reduces tendency to suck fluid into alveoli

230
Q

What is neonatal respiratory distress syndrome?

A

Occurs premature babies due inadequate surfactant production

Increased work breathing due reduced compliance + alveolar collapse

231
Q

What is alveolar dependency?

A

Joining of alveoli to each other to help resist collapse

232
Q

What are the airways like in asthma?

A

Narrowed bronchoconstriction

Mucosal oedema

233
Q

What are the airways like in chronic bronchitis?

A

Wall damage
Hypertrophied glands
Mucus production

234
Q

What are the airways like in emphysema?

A

Poorly supported

235
Q

What are the alveoli like in:

a) Asthma?
b) Chronic bronchitis?
c) Emphysema?

A

a) Normal
b) Normal
c) Destroyed

236
Q

What are the airways like in:

a) Lung fibrosis?
b) Respiratory muscle weakness?

A

a) Normal

b) Normal

237
Q

What are the alveoli like in:

a) Lung fibrosis?
b) Respiratory muscle weakness?

A

a) Stiff

b) Normal

238
Q

What is the difference between obstructive lung disease and restrictive lung disease?

A

Obstructive - Airflow impeded

Restrictive - Poor lung expansion

239
Q

Calculation for forced expiratory ratio?

A

FEV1/FVC

240
Q

In a peak flow meter, if patient has reduced expiratory flow, what can this suggest?

A

Resistance in lungs has increased

241
Q

What happens to FEV1, FVC and FEV1/FVC ratio in:

a) Obstructive disease?
b) Restrictive disease?

A

a) FEV greatly decrease, FVC decrease/normal, FEV1/FVC decrease
b) FEV + FVC decrease, FEV1/FVC normal

242
Q

Features of maximum flow-volume loops of obstructive disease?

A

Concave appearance of forced expiratory curve

Forced inspiratory flow less affected than forced expiratory flow

243
Q

What is the name of the chest shape in emphysema?

A

Barrel chest

244
Q

What is dead space in lungs?

A

Airway volume with x gas exchange

245
Q

What is the name and abbreviation for the total pressure of air?

A

Barometric pressure

PB

246
Q

Equation for Henry’s law and meaning of letters?

A 
C = kP
C = conc of dissolved gas at equilibrium
k = Henry's law constant
P = pp of gas
247
Q

What is the constant water vapour pressure in the lungs?

A

6.3 kPa

248
Q

What rate does CO2 diffuse at compared to oxygen and why?

A

85% of rate of O2

Higher molecular weight

249
Q

What is the value of the solubility coefficient of:
a) CO2
b) O2
in plasma?

A

a) 0.7ml/L/mmHg

b) 0.03 ml/L/mmHg

250
Q

What is DLCO?

A

CO diffusing capacity

251
Q

What 3 things is DLCO reduced by?

A

Reduction in alveolar-capillary membrane area
Increased thickness of alveolar-capillary membrane
Anaemia

252
Q

What 2 things is DLCO increased by?

A

Increased pulmonary blood volume (exercise)

Polycythaemia - mehr RBC, mehr ability pick up O2

253
Q

How much oxygen does the mitochondria need?

A

PO2 > 1mmHg (0.13kPa)

254
Q

What happens to tissue if capillary PO2 falls too low?

A

Hypoxic

255
Q

What 3 factors cause O2-Hb curve to shift left?

A

Increase pH, low pCO2
Low temp
Low 2,3 DPG

256
Q

What 3 factors cause O2-Hb curve to shift right?

A

Decrease pH, high pCO2
High temp
High 2,3 DPG

257
Q

What are the neural controls of ventilation?

A

Role of brain stem

Lung receptors + other inputs

258
Q

What are the chemical controls of ventilation?

A

Responses to changes in pCO2, pO2, pH
Central chemoreceptors
Peripheral chemoreceptors

259
Q

What is apnoea?

A

Temporary cessation in breathing, esp in sleep

260
Q

What is eupnoea?

A

Normal pattern of breathing

261
Q

What is apneusis?

A

Deep, gasping inspiration with pause at full inspiration followed by a brief, insufficient release.

262
Q

What are the 4 main respiratory nuclei in the medulla?

Full descrip

A

Dorsal resp group (DRG) within nucleus tractus solitarius (NTS)
Ventral resp group (VRG) containing nucleus ambiguus (NA) + nucleus retroambiguus (NRA)
Pre-Botzinger (PBC) + Botzinger complex located near nucleus retrofacialis (RTN)

263
Q

What neural input does the DRG receive?

A

Chemoreceptors
Lung mechanoreceptors
Higher brain centres

264
Q

Where are the stretch receptors located?

A

Smooth muscle of bronchial walls

265
Q

What do the stretch receptors do?

A

Make inspiration shrter/shallower

Delays next inspiratory cycle

266
Q

What reflexes are the stretch receptors involved in?

A

Hering-Breuer inflation reflex - inflation inhibits inspiration
Deflation reflex - deflation augments inspiration

267
Q

Where are the juxtapulmonary receptors located?

A

Alveolar/bronchial walls, close to capillaries

268
Q

What do the juxtapulmonary receptors do?

A

Apnoea/rapid shallow breathing
Fall HR + BP
Laryngeal constriction
Relaxation skeletal muscle

269
Q

Where are the irritant receptors located?

A

Throughout airways between epithelial cells

270
Q

What do the irritant receptors do?

A

Receptors in trachea lead to cough
Reflex bronchial + laryngeal constriction
Deep augmented breaths every 5-20 min at rest - reverse slow collapse of lung in quiet breathing

271
Q

Where are the proprioceptive receptors located?

A

Respiratory muscles

272
Q

What do the proprioceptive receptors do?

A

Wichtig coping mit increased load + achieving optimal tidal volume + frequency

273
Q

What are 3 other types of receptors in the control of ventilation?

A

Pain receptors
In Trigeminal region + larynx
Arterial baroreceptors

274
Q

Why is there a plateau of ventilation in the ventilatory response to CO2?

A

Always breathing, never 0

275
Q

Why is the combination of hypoxia and hypercapnia synergistic?

A

Combined effect greater than sum of individual effects

276
Q

Do the peripheral chemoreceptors respond to O2?

A

No

277
Q

What are the 2 types of cells found in the carotid bodies?

A

Type 1/Glomus cells

Type 2/Sheath cells

278
Q

What are the 3 functions of the carotid bodies

A

Increase in pCO2/H+ increases discharge
Decrease in pCO2 increases discharge
V fast response

279
Q

What are 3 examples of breathing disorders?

A

Loss of CO2 drive
Cheyne-Stokes respiration
Central sleep apnoea

280
Q

What occurs in obstructive central sleep apnoea?

A

Muscles relax + airways collapse
Snore, x airflow
O2 sats fall so wake up

281
Q

What is the curse of Odine?

A

Brain x respond to changes in CO2 + O2

282
Q

What is ventilation-perfusion relationship?

A

Va/Q

Alveolar ventilation per min + Blood flow per min

283
Q

What percentage of venous blood passes through lungs?

A

98%

284
Q

What veins are involved in normal R==>L shunt?

A

Bronchial veins

Thebesian veins

285
Q

What are Thebesian veins?

A

Small veins draining wall of l ventricle

286
Q

What are 3 causes of abnormal R==>L shunt?

A

Collapsed lung
Consolidation
Congenital heart disease

287
Q

What is atelectasis?

A

Collapse of lung tissue with loss of volume

288
Q

What is Fallot’s tetralogy?

A 
4 congenital abnormalities
Ventricular septal defect
Misplaced aorta
Pulmonary vein stenosis
Thickened r ventricular wall
289
Q

If r border heart x visible on chest x-ray, what can you say about the pneumonia?

A

Lobar pneumonia of r middle lobe

290
Q

What is an air bronchogram?

A

Aerated bronchi surrounded by solid consolidated lung

291
Q

What causes L==> R shunts?

A

Atrial septal defects

Ventricular septal defects

292
Q

What percentage of live births have VSDs?

A

0.2%

293
Q

What septal defect can turn into a R==>L shunt + why?

A

VSDs
Increase in pressure in pulmonary circulation lead to pulmonary vascular remodelling + increased resistance e.g r ventricle hypertrophy

294
Q

Effect of increased ventilation/FIO2 in R==>L shunt?

A

Low PaO2, normal/low CO2

295
Q

Why does breathing 100% O2 have a modest effect on arterial PO2 in R==>L shunt?

A

Doesn’t reach shunted blood

296
Q

How do these effects alter VA/Q?

a) Dead space effect
b) Shunt effect?

A

a) High VA/Q

b) Low VA/Q

297
Q

What is the response of
a) Pure R==>L shunt
b) Ventilation perfusion mismatch
to O2 enriched inspired air?

A

a) Little improvement to arterial pO2

b) Marked improvement, PO2 in under ventilated areas improved

298
Q

What area of the lung is the VA/Q higher?

A

Top of lungs

299
Q

Where is the relative change of the alveoli greater?

A

Bottom of lung

300
Q

What do the pulmonary blood vessels do in response to hypoxia + why?

A

Vasoconstrict

Divert blood flow from poorly ventilated areas ==> well ventilated areas

301
Q

When is hypoxic pulmonary vasoconstriction not useful?

A

In global hypoxia

e.g. Hypoxic lung disease, resp failure, altitude

302
Q

What 5 mechanisms lead to arterial hypoxia?

A 
Low inspired pO2
Hypoventilation
Diffusion impairment
R==>L shunt
Ventilation-perfusion mismatch
303
Q

What mechanism increases PaCO2?

A

Hypoventilation

304
Q

What mechanisms increase A-a pO2 gradient?

A

Diffusion impairment
R==>L shunt
Ventilation-perfusion mechanism

305
Q

Why does blood continue to flow while we stand up?

A

At any given level above/below heart, arterial pressure greater than venous pressure

306
Q

What happens to the venous valves in the lower limbs when we stand?

A

Shut transiently

Shrt time, outflow blood from heart greater than inflow

307
Q

What 3 mechanisms limit effect of orthostasis?

A

Lowered stroke volume + C,O, blood flow to brain, MABP in upper prt body
Arterial constriction reduces blood flow on standing
Skeletal muscle pumping

308
Q

What leads to varicose veins?

A

Valve failure in tributary superficial veins exposes them to chronic high pressures

309
Q

By what percentage does cerebral blood flow reduce by when standing?

A

20%

310
Q

What does gravity do to CSF?

A

Downward displacement within subarachnoid space

Creates -ve intracranial pressure, prevents veins within cranium collapsing

311
Q

Why is negative pressure within cerebral veins dangerous in neurosurgery?

A

Risk of air embolism if opened

312
Q

What 3 things occur during prolonged standing?

A

Progressive venous pooling
Progressive fall in pulse pressure
Progressive rise in heart rate + TPR

313
Q

What is vasovagal syncope?

A

Fainting that occurs to response in to sudden drop in heart rate/blood pressure
Vagally mediated bradycardia - v slow heart rate

314
Q

Why is it bad to keep a person upright when they’re fainting?

A

BP remains low and brain damage possible

315
Q

How to calculate O2 consumption?

A

O2 consumption =

C.O (arterial - mixed venous blood O2 content)

316
Q

How are these factors affected by exercise?

a) Arterial O2 content
b) Venous O2 content
c) Cardiac output

A

a) Unaffected
b) Falls progressively as exercise intensity increases
c) Increases progressively with increasing exercise intensity

317
Q

What is the main factor determining VO2 max?

A

Max cardiac output produced

318
Q

What happens to blood flow in active muscle?

A

Vasodilation + capillary recruitment due local metabolites

319
Q

What happens to blood flow in inactive muscle + splanchnic circulation?

A

Sympathetic vasoconstriction

320
Q

What happens to blood flow in skin during exercise?

A

Vasoconstriction then vasodilation due temp rise

At max exercise, vasoconstriction dominates

321
Q

What 3 factors can increase stroke volume?

A

Enhanced filling of heart
Increased CVP, increases skeletal muscle pump
Enhanced emptying

322
Q

How is BP affected in dynamic exercise?

A

Little change diastolic
Systolic increased
Mean BP moderate increased

323
Q

How is BP affected in isometric exercise?

A

Systolic + diastolic increase

Any given O2 consumption, BP greater than dynamic + fails to plateau

324
Q

Why may TPR rise during isometric exercise?

A

Compression of blood vessels in contracting muscles

325
Q

What is the difference between:

a) Revealed haemorrhage
b) Concealed haemorrhage

A

a) Obvious bleeding, quantity hard to measure

b) E,g, ruptured organs, can be due to trauma

326
Q

What is the result of:

a) Chronic, slow persistent bleeding?
b) Acute large blood loss?

A

a) Fe deficiency anaemia

b) Reduced circulatory volume + circulatory shock

327
Q

What is the most common cause of circulatory shock and the others?

A 
Haemorrhage
Sepsis
Cardiogenic
Anaphylaxis
Other hypovolemic e.g. burns, severe vomiting/diarrhea
328
Q

What is pulse pressure?

A

Difference between systolic and diastolic pressure

329
Q

What is the average blood volume in:

a) Men?
b) Women?

A

a) 77 ml/kg

b) 67 ml/kg

330
Q

What is the reverse stress contraction in immediate compensation for blood loss?

A

Veins shrink around reduced blood volume
Helps maintain venous pressure, therefore venous return
Maintains CO

331
Q

What are cardio-pulmonary stretch receptors and what do they do?

A

Mechanoreceptors in heart + large pulmonary vessels

Respond to changes in blood volume

332
Q

Why is arterial BP normal in moderate haemorrhage?

A

Low C.O offset by high TPR

333
Q

What is a reticulocyte and its normal number in body?

A

Immature RBC

<2% of RBC

334
Q

What is non-progressive shock?

A

Shock gets better without treatment

e.g. donating blood

335
Q

What is haemodilution?

A

Increased blood volume but lower conc of RBC

336
Q

How quickly should blood transfusion be given in shock?

A

1 hour (golden hour)

337
Q

What are 4 cardiovascular effects of aging?

A

Atherosclerosis
Rise in systolic BP + fall in diastolic BP
Reduced baroreflex sensitivity
Impaired cardiac performance during exercise

338
Q

What happens to the forward pressure wave and reflected pressure wave in:

a) Youth + normotension?
b) Age + hypertension?

A

a) Prt of pulse wave reflected almost immediately

b) Forward + reflected pressure waves summate

339
Q

Why is heart less able to increase cardiac output when stressed?
What reasons?

A

Max attainable HR falls (220- age in years)
Fall in cardiac contractility reduces stroke volume
Decreased response to beta-1 receptor activation + loss of myocytes

340
Q

What are drugs in term of exogenous + endogenous?

A

Drugs are exogenous molecules that mimic/block action of endogenous molecules/systems

341
Q

What are 3 types of pharmacological receptors?

A

Physiological receptors
Other proteins e.g. enzymes, ion channels,
Nucleic acids

342
Q

What are physiological receptors?

A

Endogenous proteins that are receptors for endogenous chem signalling compounds e.g. hormones/NT

343
Q

What is an:

a) antagonist?
b) agonist?

A

a) Bound drug prevents receptor from being activated

b) Bound drug activates receptor to provoke response

344
Q

What type of drug interactions are:

a) Reversible?
b) Irreversible?

A

a) Ionic interactions + hydrophobic interactions

b) Covalent bonding

345
Q

What is pharmacodynamics?

A

What drug does to an organism

Sum of all actions of drugs

346
Q

What is pharmacokinetics?

A

What organism does to drug

Absorption, distribution, metabolism + excretion of drug

347
Q

What is the main:

a) metabolic organ?
b) excretory organ?

A

a) Liver

b) Kidney

348
Q

What 5 factors influence the amount of drg absorbed and the speed of absorption?

A 
Chem properties of drug
Molecular size
Lipid solubility.ionization
Chem + metabolic vulnerability
Route of administration
349
Q

What are the 3 names given to conventional drugs?

A

Proprietary names
Common name
Chemical name

350
Q

What therapeutic uses can drugs be grouped to?

A

Analgesic - pain killer
Anti-inflammatory
Antipyretic (lowers temp in fever)
Anti-platelet

351
Q

How many phases are there in clinical trials?

A

5

Phase 0 then Phase I, II, III, IV

352
Q

What is Emax?

A

Max effect/response a drug can produce

353
Q

What is EC50?

A

Conc of drug that produces 50% of max response

354
Q

What shape is given in the plotted graph of proportion of receptors occupied (p) vs drug conc [D]?

A

Rectangular hyperbola

355
Q

What shape is given in the plotted graph of proportion of receptors occupied (p) vs log drug conc (Log[D])?

A

Symmetrical sigmoid

356
Q

What is the affinity of a drug to its receptor quantified as and what is the symbol?

A

Molar conc of drug required to occupy 50% of receptors at equilibrium
KD

357
Q

What is the value of KD of a drug with a high affinity for its receptors?

A

Low KD

In micro-/nanomolar range

358
Q

What is efficacy and what types of drugs have it?

A

Ability of drug to activate receptor

Agonists

359
Q

What molecules in body are agonists?

A

NTs, hormones

360
Q

What is the difference between:

a) Partial agonist?
b) Full agonist?

A

a) Low efficacy, less effective

b) High efficacy, v effective producing biological response

361
Q

What is the difference in response between:

a) Partial agonist?
b) Full agonist?

A

a) Fail produce full response despite occupy all receptors

b) Max response, activate fraction of available receptors

362
Q

What is the difference between:

a) Competitive antagonist?
b) Non-competitive antagonist?

A

a) Compete for same site, x activate - affinity but 0 efficacy
b) Act at diff site on receptor

363
Q

What are reversible competitive inhibitors used for?

A

Inhibit effects of NT/hormones

364
Q

What effect does an reversible competitive antagonist have on Log[agonist] vs response graph?

A

Parallel shift to right

365
Q

What is the dose-ratio?

A

Ratio of conc of agonist producing same response on presence + absence of antagonist

366
Q

What is pA2?

A

Quantified affinity of antagonist

-ve logarithm of molar conc of antagonist that necessitates that you double agonist conc to produce same response

367
Q

What effect does an irreversible competitive antagonist have on Log[agonist] vs response graph?

A

Right shift but x parallel

Block x surmountable

368
Q

Calculation for probability of adverse event to drug?

A

Total exposure x likelihood

369
Q

What is acceptable benefit:risk ratio dependant on?

A

Efficacy
Toxicity
Disease

370
Q

What is Reye’s syndrome?

A

Swelling in liver + brain.

Oft affects children + teenagers recovering from viral infection e.g. flu/chickenpox

371
Q

What is Torsades de Pointes?

A

Polymorphic ventricular tachycardia mit long QT interval

Rapid, irregular QRS complexes, appear to be twisting around ECG baseline

372
Q

What are the 3 structures in microcirculation?

A

Terminal arterioles
Capillaries
Lymphatic capillaries

373
Q

What are the 3 types of capillaries?

A

Continuous
Fenestrated
Sinusoidal (discontinuous)

374
Q

Where are these capillaries found?

a) Continuous
b) Fenestrated
c) Sinusoidal

A

a) Most tissues
b) Kidneys, joints, intestinal mucosa
c) Liver, bone marrow, spleen

375
Q

How is the endothelium arranged in these capillaries?

a) Continuous
b) Fenestrated
c) Sinusoidal

A

a) Monolayer covering entire surface of capillary
b) Contains pores, 10x more permeable to smol hydrophilic molecules
c) Spaces between endothelial cells, large molecules readily diffuse

376
Q

What is the glycocalyx?

A

Glycoprotein layer covering luminal surface of endothelium

377
Q

How do small lipophobic molecules cross capillary wall?

A

Fenestral route

Paracellular route

378
Q

How do large lipophobic molecules cross capillary wall?

A

Vesicular transport
Trans-endothelial channel
Wide intercellular gap (acute inflammation)

379
Q

How do lipophilic molecules cross capillary wall?

A

Transcellular route

380
Q

What is Fick’s 1st law?

A

Diffusion =

diffusion constant x area x (change in conc/diffusion distance)

381
Q

How many litres of plasma pass through capillaries each day?

A

4000L

382
Q

How many litres of fluid flow across capillary walls in both directions?

A

80,000L

383
Q

How is filtered fluid returned to the bloodstream?

A

Lymphatic system

384
Q

What is an oedema?

A

Net filtration increases locally/systemically or lymphatic system blocked, fluid accumulates in tissue

385
Q

What 2 pressure gradients does fluid filtration rely on?

A

Hydrostatic pressure

Osmotic pressure gradient

386
Q

What is the hydrostatic pressure in an open capillary?

A

Arterial end - 140 mmHg

Venous end - 15 mmHg

387
Q

What is the hydrostatic pressure in tissue spaces?

A

0 (atmospheric)

388
Q

What is effect of these pressures on water flow?

a) Hydrostatic pressure
b) Osmotic pressure

A

a) Draws water out of capillaries

b) Draws water into capillaries

389
Q

What is the Starling equation?

A

Jv proportional to (Pcap - Pint) - sigma(pi-cap - pi-int)

390
Q

What are the capillaries doing in tissues where the arterioles are open?

A

Mainly filtering

391
Q

What are the capillaries doing in tissues where the arterioles are contracted?

A

Capillary hydrostatic pressure falls

Absorption more important

392
Q

What are the 4 factors that promote oedema?

A

Increased capillary hydrostatic pressure
Increased capillary/venular permeability
Decreased plasma oncotic pressure
Lymphatic obstruction reduces lymphatic flow

393
Q

What are 3 functions of the lymphatic system?

A

Preserves fluid balance
Transfers fat absorbed in SI to circulatory system
Transports foreign materials to lymph nodes for immunosurveillance

394
Q

What is the function of the intercellular clefts on the lymphatic capillaries?

A

1 way entry of fluid driven by tissue compression

395
Q

What is a lymphangion?

A

Functional unit of lymph vessel that lies between 2 semilunar valves

396
Q

By how much does the lymphangion need to be compressed to prevent pumping?
When would be useful?

A

40-50 mmHg

Stop envenomation - exposure to poison/toxin from bite/sting

397
Q

How can lymphocytes be activated?

A

In lymph glands by antigen entering via afferent lymphatics

398
Q

How much O2 do tissues remove from blood?

A

5 ml dl-1

399
Q

What is peripheral cyanosis?

A

Reduced blood flow to region resulting in hypoxic tissue

Blueish tinge in extremities

400
Q

What are 4 causes of reduced blood flow?

A

Cardiovascular shock
Low temp
Reduced cardiac output
Poor arterial supply

401
Q

What is central cyanosis?

A

Arterial hypoxaemia, reduction in O2 content

Buccal mucosa + lips best sites to spot

402
Q

What are 2 causes of central cyanosis?

A

COPD

R==>L shunt

403
Q

What is the solubility of CO2 in blood?

A

0.52 ml dl-1 kPa-1

404
Q

What are 3 ways CO2 is carried in blood?

A

Dissolved CO2
Bicarbonate
Carboamine compound

405
Q

What is the Haldane effect?

A

At any given PCO2, quantity of CO2 carried is greater in partially deoxygenated blood (venous) than in oxygenated blood (arterial)

406
Q

What is the Haldane effect due to?

A

Hb forms carbamino compounds more readily when deoxygenated so can carry more CO2.
Hb binds to H+ better when deoxygenated, favours formation of HCO3-, increasing CO2 carriage

407
Q

What are 3 features of the shape of the CO2 dissociation curve?

A

X sigmoid
X plateau
Approx linear over physiological range

408
Q

Name 3 features of the CO2 dissociation curve

A

More total CO2 carrying capacity than for O2
Haldane effect
At rest, tissue produces 4ml of CO2 for 100 ml blood passing through

409
Q

How much HCO3- is in arterial blood?

A

24mM

410
Q

What is the relationship between alveolar CO2 and alveolar ventilation?

A

Inversely proportional

411
Q

What are 2 ways to measure O2 consumption?

A

Fick’s principle

Respiratory mechanisms

412
Q

What is hyperventilation?

A

Over ventilation in proportion to metabolism

Measured with respect to arterial pCO2

413
Q

What is hypoventilation?

A

Under ventilation in proportion to metabolism

Results in higher arterial pCO2 levels

414
Q

What are 2 causes of hyperventilation?

A

Anxiety, pain, excessive mechanical ventilation

Diseases contributing to mechanical acidosis

415
Q

What are 2 consequences of hyperventilation?

A

Low paCO2 - leads cerebral construction ==> cerebral hypoxia

Alkalosis -

416
Q

What are the causes of hypoventilation?

A

Head injury impairing respiration
Anaesthetics
Drugs
Chronic lung disease

417
Q

What are the consequences of increased pCO2 due to hypoventilation?

A

Increasing arterial pCO2 - peripheral vasodilation

V high pCO2 - depresses CNS function

418
Q

What is the pCO2 and pO2 in:

a) Inhaled air?
b) Exhaled air?
c) Inspired air in airways?

A

a) pO2 = 21, pCO2 = 0
b) pO2 = 16, pCO2 = 3.5
c) pO2 = 20, pCO2 = 0

419
Q

What is the pCO2 and pO2 in:

a) Mixed venous blood?
b) Alveolus?

A

a) pO2 = 5.3, pCO2 = 6.1

b) pO2 = 13.3, pCO2 = 5.3

420
Q

What is the pCO2 and pO2 in:

a) Mixed venous blood?
b) Alveolus?

A

a) pO2 = 5.3, pCO2 = 6.1

b) pO2 = 13.3, pCO2 = 5.3

421
Q

What is the pCO2 and pO2 in:

a) Arterial blood?
b) Capillary/tissues?

A

a) pO2 = 12.5, pCO2 = 5.3

b) pO2 = 5.3 /less, pCO2 = 6.1/more

422
Q

What substances follow:

a) Zero order kinetics?
b) First order kinetics?

A

a) Most drugs, don’t accumulate

b) Alcohol, phenytoin, overdose, accumulate

423
Q

What type of kinetics do most drugs follow?

A

First order

424
Q

What substances follow 0 order kinetics?

A

Alcohol, phenytoin, in overdose

425
Q

What are 2 features of 1 compartment?

A

Instantaneous distribution

Monophasic decline in in plasma conc

426
Q

What is 1 feature of 2 compartment?

A

Biphasic decline

427
Q

What is half life and its symbol?

A

Time taken for plasma conc of drug to fall by half

T(1/2)

428
Q

In what conditions can you see a monoexponential decline?

A

Drug cleared according to 1st order kinetics

Only distributed by 1st compartment

429
Q

What is absorption?

A

Process by which drug moves from site of administration to site of action

430
Q

What factors can absorption depend on?

A

Solubility + pH dependant

431
Q

Calculation for volume of distribution?

A 
Vd = Total amount drug dosed / plasma conc at t0
Vd = Dose A /A0
432
Q

What happens in:
a) Phase I
b) Phase II
in drug metabolism?

A

a) Body makes mehr H2O soluble so easier to excrete

b) Body conjugates H2O soluble molecule onto drug so easier to excrete

433
Q

What is clearance and it’s calculation?

A

Volume of plasma cleared of drug per unit of time

Cl = k x Vd

434
Q

What is clearance limited by?

A

Organ blood flow

435
Q

How to calculate clearance using extraction ratio?

A 
Clearance = Q x Eh
Q = organ blood flow
Eh = hepatic ratio (diff 2nd letter represents which system)
436
Q

What is human liver blood flow?

A

1.4 L/min

437
Q

How to calculate maximum oral bioavailability?

A

F = 1 - Eh

438
Q

What condition occurs when there is extra-hepatic clearance?

A

Total blood clearance > Q

439
Q

What is human renal blood flow?

A

1.1L/min

440
Q

What is bioavailability (F)?

A

Fraction of unchanged drug reaching systemic circulation

441
Q

What 2 factors limit bioavailability in oral dosing?

A

Absorption from gut

Gut/hepatic metabolism/excretion

442
Q

How to calculate bioavailability (F)?

A

F = AUC oral / AUC iv

443
Q

Intrapleural pressure is:

a) always positive​
b) positive during inspiration​
c) negative during inspiration​
d) always negative​
e) cannot be estimated

A

d) always negative

444
Q

Relative to PB, during expiration PA is approximately:

a) 2 cmH2O​
b) 1 cmH2O​
c) 0 cmH2O​
d) -1 cmH2O​
e) -2 cmH2O

A

b) 1cmH2O

445
Q

What is the name of the protein that mediates contraction in smooth muscle?

A

Calmodullin

446
Q

Which combination of valves cause which heart sounds?

a) S1 - Aortic and Mitral, S2 - Pulmonary and Tricuspid​
b) S1 - Aortic and Pulmonary, S2 - Mitral and Tricuspid​
c) S1 - Mitral and Pulmonary, S2 - Aortic and Tricuspid​
d) S1 - Mitral and Tricuspid, S2 - Aortic and Pulmonary​

A

d) S1 - Mitral + Tricuspid, S2 - Aortic + Pulmonary

447
Q

Describe smooth muscle contraction

A

Ca2+ enters cell (through sarcolemma/from SR)​
Binds to calmodulin in cell, activates myosin kinase
Phosphorylates myosin heads to start contraction
Ends when Ca2+ pumped out of cell by ATP-dependent pump on membrane.​
Some stays in cell bound to calmodulin to maintain muscle tone - less energy required to maintain contraction.​
Also get ‘latch bridges’ between some myosin + actin filaments - stay contracted w/ no energy use - wichtig in some tracts + vessels

FBS2 (3 decks)

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