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Year 1 > Medical Science > Flashcards

Medical Science Flashcards

1
Q

What is the movement of fluid known as?

A

Convection

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2
Q

What is the movement of dissolved molecules known as?

A

Advection

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3
Q

What is the way blood flows after blood vessels split known as?

A

Portal systems

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4
Q

What is the initial layer of blood vessels?

A

Endothelial cells (endothelium) and a basement membrane called the Basal Lamina

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5
Q

What is the medial layer of a blood vessel?

A

SMC, fibrous proteins (collagen and elastin). Elastin allows stretching (organized in sheets on inside and outside), collagen provides mechanical strength

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6
Q

What is the adventitial layer of blood vessels?

A

Nervous cells to stimulate VSMC

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7
Q

What is the Law of Laplace

A

Tension = Pressure x Radius

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8
Q

What is the purpose of larger elastic artery’s?

A

Maintain constant BP by recoiling due to large elastic tissue. Smoothing pulse

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9
Q

Adaptation of smaller muscular arteries?

A

More VSMC to spasm to reduce blood loss if cut and control diameter

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10
Q

Arteriole function in blood flow?

A

Control flow of blood with thick SMC walls to control diameter

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11
Q

Diffusion equation for distance?

A

Time = (x^2) /2D
D = diffusion coefficient

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12
Q

Capillary function and adaptation

A

Only intimal layer (endothelial cells) for exchange

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13
Q

Purpose and adaptation of veins?

A

Capacitance vessel with thin stretchy walls to expand to store blood

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14
Q

What equation links airflow, resistance and pressure difference

A

Flow = delta P / R

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15
Q

What membrane surround the lungs and what is found inside this membrane?

A

Pleural membrane with inter pleural space contain inter pleural fluid (liquid)

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16
Q

How does pressure change in inspiration?

A

Diaphragm contracts and so do intercostal muscles. This tries to expand the intra pleural fluid (Volume can’t change) therefore pressure decreases (becomes more negative compared to atm) pulls on lungs increasing volume

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17
Q

How does expiration differ to inspiration process?

A

Inspiration in reverse and usually only passive process due to only relaxation of muscles

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18
Q

What is resting tidal volume?

A

Change in volume when normally breathing

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19
Q

What is expiratory/inspiratory reserve volume?

A

The extra volume capable of being breathed in/out

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20
Q

What is vital capacity?

A

The maximum amount of volume that can be breathed in and out

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21
Q

What is the resistance in airways to airflow and why is it this value?

A

Low resistance due to airways being short, wide and air having low viscosity

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22
Q

What is compliance equation?

A

Compliance = delta V / delta P

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23
Q

What is compliance?

A

The measure of how easily a container changes volume based on pressure

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24
Q

What determines complaince in lungs?

A

The surface tension of the liquid lining the surface of the lungs (75m^2)

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25
Q

What is purpose of type 2 cells in lungs?

A

Secrete detergent (surfactant) to lower liquid tension of the liquid lining the lungs

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26
Q

What issue can arise in early birthed baby’s related to surfactant?

A

Baby’s don’t secrete detergent so can be born with respiratory-distress

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27
Q

What is the minute ventilation equation?

A

Tidal volume (500ml/breath) x Resp rate (10 br/m) = minute ventilation (5L/min)

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28
Q

What is deadspace in airways?

A

Volume of airways not involved in gas exchange (150ml in human)

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29
Q

What do coronary artery’s do?

A

Bring blood to the muscles of the heart

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30
Q

What blood vessels lead to left atria?

A

Pulmonary veins (2 from each lung)

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31
Q

What blood vessels bring blood back to right atria?

A

Vena cava (superior and inferior)

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32
Q

What blood vessels leaves right ventricle?

A

The pulmonary artery, it then splits into 2

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33
Q

What blood vessel leaves left ventricle?

A

Aorta

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34
Q

What are the AV valves called ?

A

A-V valves: left is a bicuspid (mitral)
Right is a tricuspid

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35
Q

What valves are located in the aorta and pulmonary artery and what’s their purpose?

A

Aortic valve
Pulmonary valve
To prevent back flow after ventricular relaxation

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36
Q

How are AV valves stopped from being pushed the wrong way when ventricles contract?

A

Cardiac Muscle extensions called chordae tendinae

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37
Q

What is the fibrotendinous ring?

A

Non conductive material can that includes the tricuspid and bicuspid (mitral) valves

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38
Q

What are the stages of cardiac cycle?

A
  1. Mid diastole
  2. Atrial contraction
  3. Isovolumetric ventricular contraction
  4. Ventricular ejection
  5. Isovolumetric ventricular relaxation
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39
Q

How is the cardiac cycle split time wise and what are they?

A

Takes approx 1 sec.
Systole contraction of ventricles (1/3 of cycle)
Diastole relaxation (2/3 of cycle)

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40
Q

What is Mid diastole?

A

Aortic valve closed (PAorta > Pv), mitral valve open (Pa > Pv), blood flows from atria to ventricle, ventricular pressure increase slightly due to blood flow.

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41
Q

What happens in atrial contraction?

A

Blood forced out of atria into ventricles, slamming mitral valve shut (1st heart sound)

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42
Q

What happens in Isovolumetric ventricular contraction?

A

No valves open (mitral or aortic) but ventricles contract leading to rapid Pressure increase opening aortic valve
No volume change

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43
Q

What happens in ventricular ejection?

A

Pressure rises slightly but then begins to decrease, volume also decreases as blood leaves into aorta. The P drop leads to closing of aortic valve

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44
Q

What happens in Isovolumetric ventricular relaxation?

A

No valves are open but blood flows into atrium from pulmonary vein. When Pa > Pv mitral valve opens and ventricle volume increases

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45
Q

How to calculate stroke volume?

A

SV = EDV - ESV
EDV is end diastolic volume
ESV is end systolic volume
SV is therefore amount pumped per beat

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46
Q

What is the respiratory quotient?

A

CO2 out / O2 in — at the cells

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47
Q

Importance of partial pressure in respiration?

A

Pp drives diffusion and is responsable for conc of gas dissolved in liquid
C = pp x Solubility

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48
Q

What is the makeup of oxygen in the air?

A

0.21 mole fraction
760 mmhg

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49
Q

How much oxygen per liter of arterial blood and how is it stored?

A

200 ml of O2
3ml dissolved in blood with pO2 of 100mmhg
Remaining 197ml associated with Haemoglobin in RBC (erythrocytes) each Hb can bind with 4 O2

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50
Q

What alters the saturation of Hb with oxygen and what way does the curve shift?

A

Factors include [H+], Temp and pCO2 as these increase oxygen dissociation curve shifts right and O2 is harder to bind.

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51
Q

What is pO2 in alveolar gas and respiring tissue and why is it important?

A

105mmhg roughly in gas so high Hb saturation so lots of O2 associated to Hb
40 mmhg at respiring tissues leading to O2 dissociating.

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52
Q

How much CO2 in venous blood (1L) and how is it stored?

A

520ml per L
1. Dissolved (~10%)
2. CO2 combines with amino groups in all proteins (30%)
3. As hydrogen carbonate ions (bicarbonate) (60%)

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53
Q

How are bicarbonate ions produced in blood?

A

CO2 reacts with water to produce carbonic acid (in equilibrium)
Carbonic acid dissociates into HCO3- and H+ ions

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54
Q

What is the Donan equilibrium?

A

When electrical gradient of diffusion is equal to concentration diffusion gradient so no net movement

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55
Q

What is the ratio of the Na/K pump and it’s resting potential?

A

3 Na for 2 K ions
Resting potential 80mv

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56
Q

What are the potentials if all of specific ion channels are open?

A

Na+ 51mv
Ca2+ 133mv
K+ -94mv

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57
Q

What is the threshold value ?

A

Voltage required for an action potential to be generated

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58
Q

What type of feedback occurs when Na+ channels open?

A

Positive

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59
Q

What helps maintain the plateau of an action potential?

A

Ca2+ channels opening.
K+ channels closing

60
Q

What type (fast/slow) of voltage gates channels are the channels involved in action potential?

A

Ca and K are slow voltage gated channels
Na is fast voltage gated channels

The speed tells us how quickly they respond to changes in membrane potential

61
Q

What is the refractory period and its importance?

A

Where the cells are unable to be stimulated, important as it prevents the A.P traveling backwards due to ions moving along membrane via diffusion

62
Q

What is the change in ions required (what ion) for muscle contraction and how is it achieved?

A

[Ca2+] inside must increase to contract, Ca from 2nd inward current not enough so it’s released from sarcoplasmic reticulum

63
Q

What changes make the sarcoplasmic reticulum permeable to Ca?

A

1.AP alters reticulum membrane allowing Ca diffusion
2. 2nd inward current makes reticulum permeable

64
Q

What is the 2nd inward current?

A

Movement of Ca ions into cell via calcium channels

65
Q

How is an AP initiated?

A

Some cells have unstable potential (pacemaker), and depolarize spontaneously

66
Q

How do pacemaker cells depolarise and how does this differ from other heart depolarisation?

A
  1. K channels spontaneously close
  2. Na channels open when cell is polarized “funny current”
    Only slow channels so don’t plateau and depolarize slower
67
Q

How does an impulse travel across the heart?

A

Through heart cells until the nonconductive fibro tendinous ring
The AV node then receives the impulse and after delay generated impulse that travels to apex of ventricles and up

68
Q

What are the parts on the ECG reading?

A

P wave is atrial polarization
QRS complex is ventricular depolarization
T wave is ventricular repolarisation
Atrial repolarisation is too small

69
Q

Where do muscular impulses for breathing come from?

A

Medullary inspiration neurons which stimulate skeletal muscle

70
Q

What factors in blood determine breathing rate?

A

pO2, pCO2 and [H+] in artery plasma in a negative feedback loop

71
Q

Where are the peripheral chemoreceptor and what do they detect?

A

In the carotid sinus and aortic arch, detect CO2 changes very sensitively and O2 changes less sensitively

72
Q

What change is made to breathing if pCO2 is high or pO2 is low?

A

Increased firing from the medullary inspiratory neurons

73
Q

How is ventilation controlled locally in the lungs?

A

Ventilation is matched to perfusion (blood flow)

74
Q

What do baroreceptors measure?

A

They detect pressure changes in the body, measure stretch are artery’s which due to elastic nature is equal to pressure

75
Q

Where are barorecpetors located?

A

Aortic arch and carotid sinus

76
Q

Where in the brain is responible for receiving baroreceptor signals and what branch of NS responsible for changing?

A

Medullary cardiovascular center revives signals
Parasympathetic and sympathetic NS respond and control BP

77
Q

What is bernoullis principle?

A

Delta P = Q x R
P1 - P2 = Cardiac output x Total peripheral resistance
Cardiac output = SV x HR

78
Q

What changes occur to alter BP?

A

To Inc pressure Inc HR,SV or decrease resistance

79
Q

What nervous system responsible for effecting BP and how does it do it?

A

SNS:
1. Increases HR
2.Constricts Blood vessels
PNS:
Limits heart rate (firing limits HR)

80
Q

How does constricting blood vessels lead to increased BP?

A

If constriction occurs Resistance Inc so delta P increases
Peripheral vein constriction stroke volume and CO so Inc BP

81
Q

What are the changes to BP produced by barorecptors categorized as?

A

Short-term (baroreflex) and after altering BP for 1-3 days accepts anomalous BP as correct and maintains

82
Q

What are long term solutions to BP changes?

A

Kidneys altering blood volume and diuretics causing urine Inc as BP Inc

83
Q

How does ECG work (3 steps)?

A
  1. Measures PD between 2 points on the body
  2. Uses PD data to measure charge in the heart
  3. Measures extra cellular potential
84
Q

In a 3 lead ECG where are the leads located and what do they form?

A

Both arms and the left leg
Einthovens triangle

85
Q

What ways are the lead vectors in einthoves triangle

A

Lead 1 Ra -> La
Lead 2 La -> LL
Lead 3 Ra -> LL

86
Q

What is cardiac out put equation and rough values

A

CO = HR x SV
5 L/min = 70bpm x 70ml/beat

87
Q

What are the effect of SNS and PNS on HR?

A

PNS firing Inc HR decrease
SNS firing Inc HR Inc

88
Q

How the PNS alter heart rate?

A

Releases Acetyl choline (neurotransmitter) which opens K channels slowing the slope to threshold value, decrease heart rate

89
Q

How does SNS and adrenal gland cause HR increase?

A

Release NorAd which opens Ca and Na channels making threshold hold value easier to reach
Adrenal gland releases ADR and NorAd follows same mechanism

90
Q

What is contractility?

A

How vigorously the heart contact and the key factor determining SV and therefore CO

91
Q

How is contractility changed by nervous system?

A

SNS and adrenal gland release NorAd and adrenaline(only adrenal) which increase contractility

92
Q

What is the frank-starling mechanism and how does it relate EDV and SV?

A

Ensure the correct volume of blood is pumped by heart due to EDV stretching heart muscles determining contraction strength.

93
Q

What is the hydrostatic pressure equation?

A

P = h p g
h is height
p is fluid density
g is acceleration due to gravity

94
Q

What is the entrance length?

A

When the flow isn’t fully developed

95
Q

What is the no slip condition?

A

The idea that fluid in contact with the vessels don’t move due to interactions

96
Q

How does a velocity profile change in a vessel?

A

Starts quite blunt then smoothens to a parabola shape when fully developed

97
Q

What is the boundary layer?

A

Region of fluid near solid boundary, where viscosity and no slip are significant and develops as fluid moves until reaching eqb

98
Q

What is laminar flow and turbulent flow ?

A

Laminar flow: When flow rate is linear to the pressure drop
Turbulent flow: When flow is proportional to root Pressure drop (plateaus with very little change due to pressure)

99
Q

What is the equation for resistance in poise flow?

A

R = (128 x Viscosity x Length) /
Pi x diameter^4

100
Q

How does a collection of vessels alter resistance cumulatively?

A

In series sum all the resistances
In parallel 1/R = 1/R1 + 1/R2 …

101
Q

What is the entrance length of blood vessels and why type of flow is occurring here?

A

60cm (most of the aorta). Most blood is in laminar flow

102
Q

What effects does blood being a suspension have on flow?

A

Velocity profiles are blunter than expected
Viscosity isn’t constant

103
Q

What does blood being pulsatile flow mean for types of flow inside it?

A

It’s made of both steady and oscillatory flow

104
Q

How is resistance of blood flow altered?

A

SMC work to change diameter of vessels (Vasodilation and vasoconstriction)

105
Q

Why would only SOME arterioles alter diameter and why would lots?

A

Lots would to alter BP by changing resistance
Only some would do it to divert flow

106
Q

What is the return rate of water by the lymphatic duct and the thoracic duct and where do they return the water to?

A

Lymphatic duct 20ml/h
Thoracic duct 100ml/h
Return lymph into subclavian vein

107
Q

What proportion blood is in capacitance vessels and what properties make vein capacitance vessels?

A

2/3
Veins have low compliance and are low pressure system so can accommodate volume changes and have little pressure change

108
Q

How is the amount of blood in capacitance vessels altered

A

SMC action and pressure changes

109
Q

What are the methods of pumping in veins and how are they caused?

A

Extrinsic pumping and valves to drive blood to heart
Extrinsic: Gut peristalsis, muscle action(exercise) and breathing (P changes in thorax)

110
Q

What is the starling Balance?

A

Jv = Lp.S [(Pc-Pi)-g(oncotic pressure)]
Jv is volume to water flux
Lp= hydraulic conductivity
S = surface area
g=Reflection co-efficient

111
Q

What is oncotic pressure?

A

Osmotic pressrue (plasma) - Osmotic pressure (interstitial space)

112
Q

What causes Osmotic pressure in interstitial space?

A

Plasma proteins in interstitial space

113
Q

What are 3 properties of lymphatic capillaries?

A

Endothelial cells overlapping forms these
They are surrounded by SMC
Have valves created by overlapping cells

114
Q

What types of pumping occur in lymphatic capillaries?

A

Intrinsic due to SMC rhythmic contraction
Extrinsic due to muscle action, arterial pulse and gut peristalsis

115
Q

For what Pc value is Jv positive (starling eq)

A

Pc> 12.5 mmhg

116
Q

Why does standing cause Pv to change?

A

Pc increases due to hydrostatic pressure, P = QxR means R is increased via Vasoconstriction. Lowers Pc again but doesn’t completely stop change

117
Q

Why does excercise change Jv?

A

Arterioles dilate to increase blood flow, increasing Pc and Jv (if goes wrong causes oedema (swelling))

118
Q

How does a change in capillary wall alter Jv?

A

Capillary hydraulic co-efficient increases or reflection coefficient decrease

119
Q

How does low lymph flow change Jv?

A

Lymph flow responsible for -Pi so lowering flow lowers that, this can lead to oedema

120
Q

How does “active hyperaemia” lead to a change in arterial tone?

A

Products of metabolism inc, causing vasodilation.
Resp prods and ATP breakdown cause vasodilation because as no. of particle inc so does osmotic pressure, then vasodilation

121
Q

How does pressure autoregulation affect arteriole tone?

A

P arteriole inc, flow inc, arterioles constrict to maintain bloodflow

122
Q

What is myogenic control of arteriole tone?

A

When the muscles cells are stretched by P inc then contraction occurs

123
Q

Why does reactive hyperaemia cause vasoconstriction?

A

Blood supply is blocked and therefore resp prods build up causing dilation

124
Q

How does local temp control lead to arteriole tone changing?

A

If limb temp inc, vasodilation
If limb temp dec, vasoconstriction

125
Q

How does injury/illness lead to changes in artieole tone?

A

Dilation caused by inflammation, cells release histamine which causes dilation
Constriction caused by blood clotting releasing 5HT -> helps prevent blood loss

126
Q

How does endothelial action lead to constriction?

A

Endothelin released by endothelial cells lead to constriction

127
Q

How do endothelial cells cause vasodilation?

A

Cells release ‘Endothelial-Dependent-Relaxing-Factor’ (EDRF) = NO free radicals

128
Q

What causes endothelial cells to release EDRF?

A

Chemicals that lead to release of EDRF are histamine, ACh (ac chol), Bradykinin and frictional force of flowing blood

129
Q

How does SNS (sym) affect arteriole tone?

A

Nerves go to most arteriole and stimulate release of NorAd causing constriction by binding to alpha receptors (contains basal rate so can increase/decrease)

130
Q

How does PNS (para) affect arteriole tone?

A

Innervates a few arterioles. Ach released causing EDRF and vasodilation

131
Q

How do hormones (adr and norad) lead to arteriole tone changes?

A

Adrenal gland releases Adr and NorAd, both bind to alpha receptors and cause constriction. ADR also binds to beta receptor to dilate (heart,liver and skeletal muscle) for fight or flight

132
Q

What are the diameters of a RBC and capillary and what does this mean?

A

RBC is 8 um and Capillary is 5-8 um so RBC must be deformed

133
Q

What is the intercellular junction in a capillary?

A

Gap Between endothelial cells that make up capillary wall (15-20nm)

134
Q

What is an open surface vesicle?

A

A vesicle attached to membrane which is 20nm at neck and 60nm at bulbous part

135
Q

What is the glycocalyx?

A

Glycoproteins and proteoglycans in capillary’s

136
Q

What is the basal lamina of a capillary made of and its purpose?

A

Collagen type 4 and provides mechanical strength.

137
Q

How do small lipid insoluble molecules travel across capillaries?

A

Through ICJ via diffusion

138
Q

What are the 3 methods that could move large insoluble lipids across capillaries?

A
  1. Ferry boat vesicles- molecule enters OSV and is transported and deposited
  2. Vesicles fuse to form tube across cell
  3. ICJ widens when cells pull apart due to inflammation, cell death or division
139
Q

Why and How does transport of molecules in the blood brain barrier differ?

A

Tight junctions are continuous and fewer vesicles and ICJ blocked by astrocytes
The cells contain carrier molecules to transport

140
Q

How does exchange differ in fenestrated capillaries vs regular and where are they found?

A

Increased transport of small lipid insoluble molecules so have 2 very close membranes with pores (shorter diffusion dist)
Found in kidney and glands

141
Q

How do discontinuous capillaries differ from others and why?

A

Gaps in the epithelial cells and no basal lamina
To allow for transport of cells (spleen, bone marrow and liver)

142
Q

How can flow lead to altering transport of solutes?

A

By increasing flow, flow limited solutes which can fully transport across membrane are provided more often so more diffuses.(O2)
However no effect on diffusion limited solute (eg albumin)

143
Q

What are Krogh cylinders?

A

The region around a capillary that can be supplied by the capillary

144
Q

How does capillary recruitment change Krogh cylinders?

A

By increasing amount of capillary’s recruited krogh cylinder shrinks decreasing diffusion distance and increasing SA for diffusion

145
Q

What is vaso motion ?

A

The rhythmic closing and opening of blood supply for capillaries

146
Q

What is the threshold value in heart cell depolarisation?

A

Roughly -65 mv

Year 1 (5 decks)

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