Week 23 Flashcards

1
Q

How many blood groups are there?

A

4: A, AB, B and O

(Adding Rhesus +/- groups makes it 8)

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2
Q

What are responsible for the ABO types of blood?

A

Two antigens and two antibodies.

It is determined by differet alleles

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3
Q

Who discovered blood groups?

A

Discovered by Karl Landsteiner in 1901 (University of Vienna) who tried to understand why blood transfusions sometimes caused death but at other times saved a patient

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4
Q

What happens when a blood transfusion gives the wrong blood type?

A

the antibodies bind to the new RBCs with different antigens. This causes clumping of the RBCs and antibodies (agglutination) and causes severe problems.

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5
Q

What reaction is performed to determine an individuals blood type?

A

Agglutination reactions are performed to determine blood type

Type A: will agglutinate Blood type B so cannot receive blood from Type or type AB (ie presence of Anti-B antibody to bind the antigen and cause “clumping”)

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6
Q

Who are the universal donors of blood?

A

Individuals with type O blood: universal donor

do not have A or B antigens

Type O blood is a universal donor (will not agglutinate)

Make antibodies to A and B

Agglutinates donor blood from other groups

cannot receive blood from any other blood type.

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7
Q

Who are the universal receivers of blood?

A

Individuals with type AB blood: universal receivers

have A and B antigens

do not make any A or B antibodies

Won’t agglutinate donor blood
BUT
their blood can only be given to AB recipients

Others have antibodies to A, B or both

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8
Q

What is ABO incompatibility in babies?

A

Common, mild condition that can occur in pregnancy if mother and baby’s blood types are incompatible

The RBCs are broken down causing jaundice, anaemia and sometimes death. (Mothers antibodies linger postnatal and destroy RBC of baby, causing increase in bilirubin)

Babies may need phototherapy or blood transfusion. Maternal treatment required in some.

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9
Q

Where is the heart located?

A

In the mediastinum with the lungs
Level of the 2nd rib
Roughly central, but with the base pointing towards the right and the apex towards the left.

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10
Q

What covers the heart?

A

The heart sits in a “bag”: pericardium
- Lubrication (serous)
- Mechanical protections
Ie protects it and allows it to move smoothly

Pericardium has 3 main layers:
- Fibrous pericardium
- Serous pericardium (fluid filled, allowing lubrication)
- Epicardium/Visceral layer

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11
Q

What is Pericarditis?

A

problems with the pericardium, which impact the movement and function of the heart.

Can be acute:
- Rapid inflammation and chest pain
- Detect as a scratchy sound (pericardial friction rub)
- Resolves in ~1 week with non-steroidal anti-inflammatory drugs (NSAIDS)

Can be Chronic:
- Effusive- build-up of fluid in the pericardium
- Constrictive- pericardium hardens

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12
Q

How does Pericardium form?

A

The heart sinks into the ‘bag’, creating the three layers

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13
Q

What are the three main layers of the heart wall?

A
  • Epicardium
  • Myocardium
  • Endocardium

Provide the contractile properties to the heart

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14
Q

What are the four sets of valves in the heart?

A

Atrioventricular valves: Mitral (bicuspid) and Tricuspid

Semilunar valves: Pulmonary valve, Aorta valve

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15
Q

What is the purpose Chordae tendinae in the ventricles?

A

Stop valves acting like a swing door in both directions.

So AV valves: prevent backflow from artia to ventricles
and SL valves: prevent backflow from aorta/pulmonary artery into ventricles

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16
Q

Where are the semilunar valves?

A

base of arteries: prevent back flow from arteries into ventricles

Aortic and pulmonary

Release of contraction closes valves

Prevents blood running back to refill the ventricles

Tricuspid

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17
Q

Problems with the heart valves include: Incompetent valves and Valvular stenosis. What are these?

A

Incompetent valves-
Valves (leaflets) do not fully close so there is regurgitant flow i.e. the same blood is pumped around repeatedly (leaky)

Valvular stenosis-
stiffened valves caused by repeated infection, congenital disease or calcium deposits. Opening is narrowed so insufficient blood gets through.

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18
Q

What are the three layers of arteries and veins?

A

Same basic structure in both types of vessel, but the proportion may vary.

3 layers-
Tunica adventitia/externa: supportive outer. Nerves and blood vessels

Tunica media: muscular middle, affects resistance to blood flow (ie involved in control of blood pressure)

Tunica intima: endothelial, inner, layer creates a smooth surface and involved in communication

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19
Q

What is the tunica media in blood vessels?

A

Smooth muscle:
Helps move blood along the arteries
Vasoconstriction of smooth muscle decreases lumen size
Vasodilation of smooth muscle increases lumen size

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20
Q

How does lumen size affect blood flow?

A

Species with low mobility:​ will not be able to shift their distributions

Affects single vessel, not whole system.

Small lumen size = inc blood pressure.

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21
Q

Features of large arteries?

A

More muscular walls push blood along to organs. Distribution role. Renal, carotid, mesenteric. Don’t affect BP. Elastic to absorb high volume and pressure from heart. Capacitance

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22
Q

Features of small arteries?

A

Distribution and resistance. Highly innervated. Regulate arterial Pressures. Receptors for circulating hormones and locally produced signals ie K+ and NO

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23
Q

Features of Arterioles?

A

smaller; when constricted, blood flow to organs can be bypassed. Resistance vessels. Same as small arteries

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24
Q

Features of capillaries?

A

small and thin to allow for exchange of materials. Exchange vessels. No smooth muscle. High exchange

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25
What are the different types of capillaries features?
Capillaries: small. High resistance, BP low Continuous Capillaries: - Most common - Continuous. Gaps only between endothelial cells (tight junctions) - CNS, lungs, muscle tissue, skin Fenestrated Capillaries: - Pores of 70-100nm in the capillary wall - Choroid plexus, kidneys, endocrine glands, villi and ciliary processes of the eye Sinusoid Capillaries: - Wider gaps in the vessel walls (Lets blood cells through) - Bone marrow, endocrine glands, placenta
26
What are the three different types of capillaries?
Continuous Capillaries Fenestrated Capillaries Sinusoid Capillaries
27
Features of veins (venous system)?
Under less pressure Less smooth muscle (less resistance) Stretchy (high capacitance vessels) Larger veins have valves to prevent blood flowing backwards. 
28
Features of venules (venous system)?
8-100µm in diameter, more porous than arterioles. Capillaries drain into venules Continued loss of BP, almost 0 by the time it gets to the vena cava. Resistance is key.
29
What blood vessels make up the venous system?
Veins and Venules
30
Where is the blood in the body at rest when upright?
Vein = 65% Arteries = 13% Arterioles = 2% Capillaries = 5% Central blood volume = 15%
31
Where is the blood in the body at rest when supine?
Vein = 54% Arteries = 10% Arterioles = 1% Capillaries = 5% Central volume = 30% * 12% in heart * 18% in lung In the supine position there is: - Less blood in peripheral veins - More blood in central volume
32
When blood exists the heart, what three distribution systems can it be split into?
Pulmonary Circulation (RHS) Systemic Circulation (LHS) Coronary Circulation (from aorta)
33
Briefly, What is the RHS pulmonary circulation after blood exits the heart?
Positioned towards back of the heart. Crescent shaped Blood in through Venae cavae Back out through pulmonary artery
34
Briefly What is the LHS systemic circulation after blood exits the heart?
At front and apex More circular (thicker walls) In through pulmonary veins Out through Aorta to aortic arch
35
Briefly what is coronary circulation system after blood exits the heart?
L and R Coronary arteries from the base of the aorta. Shut during contraction Coronary arteries branch to supply the heart Arteries supply the capillaries for gas and nutrient transfer before draining into the veins
36
What is a complete cardiac cycle?
One complete heart beat
37
Systole is what?
Contraction. (Generally taken to mean ventricular contraction and ejection
38
What is diastole?
Relaxation. Or the rest of the cycle: ventricular relaxation and filling
39
Basic steps of the cardiac cycle?
- Atrial contraction (Atria at systole) - Isovolumetric contraction (Ventricles at systole) - Ventricular ejection (Ventricles at systole) - Isovolumetric relaxation - Ventricular filling
40
Summarise the cardiac cycle's timins?
At a heart rate of 75bpm, each whole cardiac cycle lasts 0.8 second. The whole heart is in diastole for 0.4 seconds, atrial systole lasts 0.1 seconds and ventricular systole lasts 0.3 seconds
41
Why may blood pumped out of the heart decrease the faster the heart is going?
Diastole doesn't occur for long enough for the heart to fully fill with blood, therefore less is released into arteries after this.
42
What are the sounds of the heart: Korotkoff?
4 sounds, only 2 are loud enough to be heard (auscultation) First heart sound ('LUBB')– turbulence caused by closure of the AV valves (happens when the ventricles contract)​ Second heart sound ('DUPP') – turbulence caused by semilunar valves closing (when the ventricles stop contracting)​ 3rd and 4th sounds from ventricular filling and atrial systole. 4th Sound audible when ventricles are stiff​ (helps with diagnosis of conditions)
43
Step one of the cardiac cycle: Atrial Systole (Cardiac Dyastole)?
Atria contract, squeezing blood into the ventricles, through the valves.​ AV valves open. Pulmonic and Aortic closed​ Slight increase in atrial pressures​ End Diastolic Volume = Ventricular Vol + Atrial Contribution (10% at rest) 105ml +25ml = 130ml​
44
Step two of the cardiac cycle: Isovolumetric Contraction?
All valves closed. ​ Beginning of systole. ​ Increase in intraventricular pressure from contraction. ​ Heart shape change but no blood is ejected. ​ Pushes AV valves closed. First sound ​
45
Third step of the cardiac cycle: Rapid (ventricle) ejection?
AV valves closed , others open.​ When intraventricular P is higher than the aortic and Pulmonary P, the valves open and blood is ejected. ​ Atria continue to fill.​
46
Explain the difference in left and right ventricle ejection in the cardiac cycle?
L: LVP exceeds aortic P of 80mm/Hg for SL valves to open and ejection. P increase to 120mm/Hg​ R: RVP exceeds pulmonary P of 20mm/Hg for SL valves to open and ejection. P increases to 25-30mm/Hg
47
Step four of the cardiac cycle: Reduced (ventricular) ejection?
Aortic and pulmonary valves stay open and AV valves stay closed. No movement of blood​ Ventricular muscle relaxation. Ventricular P decreases slightly but blood still leaves the heart (kinetic energy). Atrial P increasing as atria continue to fill​
48
Step 5 of the cardiac cycle: Isovolumetric relaxation?
Valves close ( Heart sound 2). Aortic first, then pulmonic valve. Ventricle volume remains the same as valves are closed (dicrotic wave). Atrial pressure and volume increase from venous return​ End Systolic Volume = volume remaining in the ventricles after ejection​ Ie ESV = (EDV)130ml – 70ml = 60ml​
49
What is step 6 of the cardiac cycle: Rapid (ventricular) filling?
AV valves open. Aortic and pulmonary valves close.​ Ventricular filling. Relaxation phase (still.) ​ Amount of filling decreases when HR increases. ​ Atrial P falls​ Third sound (not usually audible without specialist equipment)​
50
What is the seventh step of the cardiac cycle: Reduced (ventricular) filling?
Difficult to distinguish these phases. ​ When filling is nearly finished , ventricles at full stretch so P rises. P in large vessels drops as blood flows into circulation​
51
In order to figure out cardiac output, we need to know stroke volume How to calculate stroke volume?
SV = End-diastolic vol (EDV) – (ESV) End-systolic vol​ EDV: Amount of blood collecting in ventricle (~130ml)​ Related to filling time and rate of venous return​ ESV: amount remaining after contraction (~60ml)​ Preload, Contractility, Afterload ​
52
How to calculate cardiac output?
Stroke volume (mL/beat) x Heart rate (beats/min) = Cardiac Output (mL/min)
53
Cardiac output is affected by the control of heart rate. how do neurons affect this?
Neural control: physical or emotional stress​ Sympathetic nervous system stimulates heart rate (SA node). Up to 100-200%​ Parasympathetic nervous system steadies HR
54
Cardiac output is affected by the control of heart rate. how do ions affect this?
ion levels: ​ Calcium: too little: weak. Too much: long contractions ​ Potassium: involved in muscle contraction and nerve conduction.​
55
What is Frank-Starling's law state?
Frank Starlings law: bigger SV ejected if there is a larger degree of filling at the end of diastole. ​
56
Explain Frank-Starling's law in terms of stroke volume?
When the rate at which blood flows into the heart from the veins changes, the heart automatically adjusts its output to match the inflow​ If an increase in end-diastolic volume occurs, the force of ventricular contraction rises, producing an increase in stroke volume and cardiac output​ Stretching of muscle fibres increases contraction force and ejection​
57
Regulation of stroke volume: preload (how stretchy is the heart at max fill)?
The more the heart fills with blood, the more the muscle is stretched. Exercise increases venous return via: - Rapid breathing forcing reoxygenated blood into heart quicker ​ - Skeletal muscle pump forcing venous return​
58
Regulation of stroke volume: Afterload (the pressure against which the heart need to pump, to expel blood)?
The higher the arterial pressure, the lower the stroke volume​ Arteries are elastic to keep BP stable and absorb volume. If arteries are blocked it increases the amount of force (P) needed to move blood.​
59
Regulation of stroke volume: Contractility (the ability of the muscle to produce a force)?
The more forcefully the muscle contracts, the more blood is expelled 1.Ions like Ca and K affect muscle activity. ​ 2. Adrenalin and the sympathetic nervous system increase contractility​ 3. Increased stretch leads to increased contractility
60
What is the skeletal muscle pump?
Lack of muscle in veins limits the force of venous return. Contraction of the skeletal muscle in the tissue surrounding the veins compress them. Compression closes upstream valves and opens downstream valves. Compressed veins = increases pressure Venous return increases during exercise
61
What is blood pressure?
Directly describes the pressure of blood on the wall of the Blood Vessels. ​ It does not describe changes in cardiac pressure during the cardiac cycle​
62
How do you calculate blood pressure?
Cardiac Output X Total Peripheral Resistance ​
63
What is classified as normal blood pressure?
- “normal” BP is 120/80​ - High is >130/ >85​ BUT​ - Females have lower BP than men​ - BP increases (/decreases) with age​ - Children have low BP until adolescence (neonates could be 60/20)​
64
What is peripheral resistance in terms of the cardiac cycle?
the degree of friction encountered by blood ie the resistance to flow​
65
What causes peripheral resistance in terms of the cardiac cycle?
Constriction or narrowing- initiated by action of the Sympathetic Nervous System or atherosclerosis, or stiffening​ Increased blood volume (eg increased retention from high NaCl)​ Viscosity (cold, increased red blood cells)​
66
True or false: anything increasing CO or PR, decreases BP​
False! anything increasing CO or PR, increases BP​
67
What increases pulse pressure?
massively increases as arteries become less stretchy​
68
How do you calculate pulse pressure?
PP = systolic BP – Diastolic BP​ ie = 120-80​ = 40mm Hg​
69
What is the mean atrial pressure? How do you calculate it?
more useful to work out as this is the pressure at which blood is actually delivered to the tissues​ MAP = Diastolic Pressure + (Pulse Pressure/3)​
70
How can we control blood pressure when changes in pressure occurs?
Baroreceptors in the Arterial carotids and aortic arch​ detect pressure change. Each is sensitive to a different pressure. ​ Small changes therefore increase firing frequency A decrease in pressure is also detected (via decreased frequency)​ due to triggering of the SNS or the PNS, pressure changes are 'fixed'. ​
71
How can we control blood pressure: chemoreceptors?
1. Peripheral chemoreceptors : carotid bodies in carotid artery. No receptors in veins​ 2. Central chemoreceptors: medulla​ Detect changes in PO2, PCO2, pH​ Low PO2 is associated with changes in pulmonary pressure, so changes in lung stretch receptor activity will also respond to low O2 levels.​
72
How can blood pressure be modified by vasoconstriction?
Contraction of smooth muscle in the vessel walls, also precapillary sphincters in arterioles​ Activation of Sympathetic Nervous activity​ Causes narrowing of the diameter of the blood vessel​ Increases the resistance of blood vessels to blood flow​ Increases Blood Pressure​
73
How can blood pressure be modified by vasodilation?
Relaxation of smooth muscle in the vessel walls, also precapillary sphincters in arterioles​ Causes widening of the diameter of the blood vessel​ Caused by withdrawal of sympathetic nerve activity and locally released chemicals e.g. nitrous oxide and lactic acid​ Decreases the resistance of blood vessels to blood flow​ Decreases Blood Pressure​
74
Why would you need to raise blood pressure?
Counteract the pressure change from getting up too quickly (orthostatic hypotension)​ Haemorrhage: can cause problems medically​ Stress or exercise.
75
How can you decrease blood pressure?
Low salt diet ( regulation of blood volume)​ Decrease stress and effects of sympathetic nervous system​ Therapeutically with ACE inhibitors- interacting with the Renin Angiotensin Aldosterone System (RAAS) that regulates blood volume and BV constriction.​
76