1
Q
Describe what occurs in the plateau phase phase 2) of the cardiac action potential
A
- Ca2+ enters via L-type Ca2+ channels
- Activated slowly when membrane potential more positive than ~-35mV
- Do not activate rapidly
- Reduced outward current of K+ continues
- Calcium entry essentail for contraction
2
Q
Describe what occurs in the rapid depolarisation phase (phase 3) of the cardiac action potential
A
Ca2+ influx declines and K+ outward current becomes more dominant
- Decreases rate of repolarisation taking place
3
Q
Describe what occurs during the electrical diastole phase (phase 4) of the cardiac action potential
A
Resting membrane potential restored by active pumps relocating sodium, potassium and calciu
4
Q
What is the all or none principle
A
- A stimulus must be above threshold potential in order to generate an action potential
- Strength of stimulus does not affect strength of action potential but does alter the firing frequency of action potentials
5
Q
Compare the absolute and relative refractory period
A
- Absolute is period immediately following the firing of a nerve fibre. Cannot be stimulated no matter how great a stimulus is applied
- Relative follows absolute, a new action potential can be generated under the correct circumstances
- Refractory period prevents the fusion of action potentials, period of relaxation between contractions, tetanus cannot occur
6
Q
What is the effect of he sympathetic system on the sinoatria and atrioventricular nodes?
A
- Releases noradrenaline at SA node to increase heart rate
- Increases rate of drigt towards threshold potential
- Affects whole heart
- Uses beta-receptor activation
- Higher, shorter AP and stronger quicker contractions
- Stimulation of beta-receptors increases Ca2+ entry, K+ channels open sooner and contraction is more forceful
7
Q
Describe the effects of the parasympathetic system on the sinoatrial and atrioventricular nodes
A
- Releases ACh at SAN
- Decrease heart rate and rate of drift to threshold potential
- PSNS dominant in normal dog
- Acts mainly on SAN and AVN
- Strong anti-sympathetic action on the atrial cells
- Little direct action on ventricles
- At SAN, PSNS decreases rate and AVN slows conduction and lengthens refractory period
8
Q
Outline the structural components of the cardiac conduction system and its function
A
- AP spreads from SAN through atria to AVN
- Activated ventricular myocardium through specialised conduction system
- AP delayed at AVN
- Excitation spreads to atrioventricular bund and finally to Purkinje fibres
- Delays impulse between atria and ventricle (so do not contract at same time)
- Cardiac conduction system also allows more rapid conduction of AP than in contactile muscle cells
9
Q
Describe the function of the Purkinje fibres in the heart
A
- Rapid conduction tissues
- Ensure simultaneous contraction of ventricles from apec to base of heart
- AP in Purkinje fibres is similar to that in ventricles
- Retains spontaneous activity as a result of sodium leakage but usually suppressed by SAN and AVN
10
Q
Describe the function of the SAN
A
- In charge of initiation of cardiac impulse in normal heart
- Wall of right atrium
- Lack fast Na+ channels, but have spontaneously opening Na+ channels that open when AP is finished
- Closes K+ ion chanels and influx of Ca2+ speeds up final appraoch to threshold potential
- Rate of Na+ entry controls rate of depolarisation
- Chronotropic agents can be used to increase rate of sodium entry by opening more Na+ ion channels = increase heart rate
- Resting mV ~-60mV and threshold is ~-40mV
11
Q
Describe the function of the AV node
A
- Auxillary pacemaker function
- Long refractory period prevents ventricles contracting too fast
- Sympathetic action shortens AVN delay
- Increases AV conduction by shortening AV node refractory period
- AV node can act as a pacemaker in absence of dominant SAN
12
Q
Describe the nature of action potentials in the atrial cells
A
- Similar AP to ventricular cells
- Plateau is shorter
- Ca2+ slow channels open and K+ ion channels are closed for a hsorter period
- Atrial cells capable of forming more APs/min (atria beat faster than ventricles)
13
Q
Describe the functional characteristic that enables and blocks propagaion of excitation through the myocardium
A
- Anulus fibrosis is a sheet of connective tissue that electricall insulates ventricles from atria
- Allows ventricular filling to complete before initiation of ventricular systole
- Can become completely ossified in some species
- AVN, Bundle of His (atrioventricular bundle) and Purkinje fibres all enable propagation of excitation through the myocardium
14
Q
Summarise automaticity in the cardiac muscle
A
- Spontaneous electrical activity needed is product of sudden inward movement of sodium (not through fast channels)
- Rate of sodium influx affects rate of depolarisation
- Ensures dominance suppression of minor pacemakers
- SAN usually dominant, then AVN then Purkinje
15
Q
Describe how contraction of the cardiomyocytes is carried out
A
- Calcium concentration increases in sarcolemma and binds to troponin C
- Causes dissociation of toponin from actin and tropomyosin moves out of actin cleft uncovering binding sites
- Myosin can now cross bridge actin
- Tension produced is dependent on number of cross links formed and calcium concentration in the cells
16
Q
Describe the distribution of PSNS in the thorax
A
- PSNS fibres leave CNS in cranial nerves III, VII, IX, X
- Supply everything but the pelvis
- III, VII, IX run to head, only X runs to body and thorax alongisde carotid arteries
17
Q
Describe the distribution of the SNS in the thorax
A
- Originate from thoracolumbar spinal cord
- Sympathetic chain carries pairs down body
- Ganglia for these are outside of spinalcord and make up sympathetic chain
- Nerves run with blood vessels rather than making new paths
18
Q
Describe the effects of the Frank/Starling mechanism on cardiac contractility
A
- More heart is stretched, stronger force of contraction
- Increasing preload by increasing venous return, and afterload and inotropy are constant then stroke volume is increased
19
Q
Define cardiac outut and outline the factors influencing this
A
Cardiac output is the volume ofblood pumped out of the heart in one minute
- Stroke volume x heart rate
20
Q
Define blood pressure and outline factors influencing this
A
- The pressure exerted by the blood against the walls of the vessels
- Affected by contractility and heart rate
- Diameter and elasticity of arterial walls
- High BP in arteries, low BP in veins
- Necessary for blood to flow
21
Q
Define stroke volume and outline factors influencing this
A
- The volume of blood that is pumped out of the heart in one contraction
- Calculated by end-diastolic volume minus end diastolic volume
- Is affected by venous return, proload, afterload and inotropy
22
Q
What is an inotrope?
A
- An agent that alters the force of muscular contraction
- A negative inotrope weakens contractions
- Positive inotrope strengthens muscular contractions
23
Q
What effect does haemorrhage have on cardiac output, stroke volume and blood pressure
A
- Arterial blood pressure falls, reducing venous retun
- reduces cardiac output
- Decreasing mean arterial pressure
- Total peripheral resistance decreases while tissue fluid volume increase and urine output decreases due to retention of salts as blood flow to kidney is reduced
- Heart rate and contractility increase due to increased sympathetic tone
- Stroke volume reduced due to reduced venous return
- Cardiac output reduced over all
24
Q
What happens to cardiac output, stroke volume and blood pressure during exercise?
A
- Increased stroke volume, decreased left ventricular and diastolic pressure
- End systolic volume decreases so stroke volume can be maintained
25
Define agonist
An agent that leads to a biological/physiological response when bound and has a maximum efficacy of 100%
26
Define partial agonist
An agent that leads to a biological/physiological response when boudn to a receptor but as an efficacy of less than 50%
27
Define antagonist
An agent that does not lead to a biological or physiological response when bound to a receptor. These can have the same affiinity as an agonist but will have an efficacy of 0%
28
Differentiate between receptor spcificity and selectivity
- Specificity: the number of different mechanisms of action a receptor can display (the kind of action at a site)
- Selectivity: relates to a drug's ability to target only a selective population (the site of action)
29
Differentiate between competitive and non-competitive receptor antagonism
- Competitive: blocks active site and prevents binding. Can be overcome as agonist usually has higher affinity for binding site
- Non-competitive: bind to allosteric site, not active site, but change shape of active site to prevent binding. Dose response curve shifts to right, becomes non-parallel and Emax is reduced
30
Describe facotr controlling pacemaker function and the cardiac action potential
- PSNS and SNS control
- Increased SNS tone opens more Ca2+ channels for longer meaing faster and stronger contractions and increased cardiac output
- Agonist binding to beta1receptor will cause Ca2+ channels to open earlier, more ready to contract, heart rate increases
- PSNS reduces production of cAMP, slows heart, reduces automaticity
- Decreases contraction, particularly in atria
- Increased efflux of K+ out of cells, hyperpolarisation, more difficult to reach threshold potential
31
Identify drugs and their sites of action that affect heart rate or rhythm
- Beta blockers: slow heart rate
- Muscarinic antagonists: increase heart rate (atropine to reverse heart block)
- Adenosine: binding = potassium efflux, hyperpolarises, slows heart rate
- Lignocaine: sodium channel blocker, reduces max rate of depolarisation in phase 0, slow upstroke, reduce overshoot, slows contraction of heart
- Calcium channel blockers: verapamil, block L-type, slows conduction of AP through SAN and AVN, slows rate, reduces force of contraction, shortens phase 2
- Digoxin: cardiac glycoside, inhibits Na+/K+ATPase pump, increase Na+ in cell, greater activation of Na+/Ca2+ exchange, more Ca2+ in cell, increases force of contraction and increases sympathetic tone. Slows conduction through AVN, heart rate decreased so is positive inotrope and negative chronotrope
32
Explain indication sofor use fo cardiac antidysrhythmic agents
- Presence of dysrhythia, angina or hypertension
| - Use of wrong drug can also cause a dysrhythmia
33
Outline the potential causes of a dysrhythmia
- Primary cardiac or non-cardiac disease that leads to dysrhythmia
- Damage to cardiac tissue, stretch of myocardium, high sympathetic tone
- Alterations in autonomic balance (epinephrine release due to pain or fear)
- Overloading of cells with calcium due to neoplasia or renal failure
34
State the 4 classes of antidysrhythic drugs and their mechanisms of action
Class I: sodium channel blockers
Class II: beta blockers
Class III: prolong action potential
Class IV: block voltage sensitive calcium channels
35
Describe the anatomy of the lymphatic system
- Function: assists in circulation of body fluids between cells and blood stream, return tissue fluid to circulation, protects body against foreign material, carries material/organisms to lymph nodes, transport of dietary fats
- Components: lymph, network of vessels, lymph nodes, tonsils, spleen, thymus, bone marrow
36
Explain Starling's forces and the processes leading the lymph formation
(Pc +Iii)-(Pi + IIp) where Pc = hydrostatic pressure in capillary
Iii = colloid pressure of interstitial fluid
Pi = hydrostatic pressure in the interstitial fluid
IIp = colloid pressure of the blood plasma
- Equation shows the components that affect diffusion and filtration of the fluid out of the blood vessels
37
Describe the mechanisms by which oedema may develop
- Localised or generalised
- Due to Starling's forve being out of balance
- Increased outwards filtration pressure, decreased inwards absorption pressure, leaky vessels
- Oedema causes swelling
- Increased filtration pressure may be due to increased arteral pressire (rare) or increased venous pressure or heart failure
- Increased venous pressure can be caused by obstruction of vessels locally or generalised increased in venous pressure
- Decreased absorption pressure can be caused by a fall in plasma colloid osmotic pressure due to protein loss of reduced protein synthesis
- Leaky vessel can be result of local inflammation or vasculitis
- Summary: vasogenic, lymphatic disease, hyperaemic or hydrostatic or osmotic
38
Explain the process of fluid exchange in tissues
- Hydrostatic pressure in the capillaries forces fluid out of the capillaries
- Hydrostatic pressure greater at arterial end thatn venous end
- Peripheral pressure decreases
- Difference in systolic and diastolic pressure also decreases
- By time blood reaches capillaries pressure is low and faily constant
- Generates a net outwards filtration pressure that varies along the length of the capillary
39
What is colloid osmotic pressure?
Pressure exerted by plasma proteins and promotes fluid reabsorption into the circulatory system
40
Define pulse pressure
The difference between systolic and diastolic pressure in the heart. The pressure in the arteries during one contraction and can be calculated by systolic pressure - diastolic pressure
41
Define arterial compliance
The elasticity of arteries
42
State the Starling law of the heart and explain the intracellular mechanisms underlying the Frank-Starling effect (length tension curve)
- Increased preload leads to increase stroke volume
- Increase preload leads to increased exposure of myosin to actin at sarcomeres
- Means there is increased cross-bridge formation and an incresed force of contraction
- Too much stretch and exposure of myosin to actin will be minimised
- Reduced cross bridge formation and decreased force of contraction
43
Give a working definition o contractility.
The strenght of a contraction and is influence by the sympathetic nervous system
44
Explain why a coordinated control of both heart and peripheral circulation is necessary to achieve optimal cardiac output
- CO is volume of blood pumped in 1 minute
- Usually close to total blood volume
- Affected by rate and stroke volume
- Preload, afterload and contractility affect stroke volume
- Preload depends on venous return of blood (low preload, low stroke volume)
- Poor peripheral circulation, stroke volume negatively affected
- Increased heart rate reduces time for ventricular filling, reduces cardiac output
- Decreased heart rate reduces venous pressure so preload decreases decreasing CO
45
Define the relationship between mean arterial pressure, cardiac output and total peripheral resistance
Mean arterial pressure = cardiac output x peripheral resistance
46
Describe the effects of changes in preload on cardiac output
- Increased preload increases contractility of heart
- Increases cardiac output
- Decrease in preload will decrease stroke volume and thus cardiac output
47
Describe the effects of cahnges in afterload on cardiac output
- increased afterload is result of increased stroke volume
- Is resistance against which ventricle pumps
- Influenced by blood in circulation as is affected by vasomotor and primarily arteriolar tone
- Greater afterload decreases stroke volume and hence decrease cardiac output
48
Describe the mechanisms that regulate cardiac output and blood pressure
- CO influenced by heart rate and stroke volume
- Heart rate controlled by SNS and PSNS
- High blood pressure: PSNS stimulated, heart rate (and thus CO) reduced
- Low BP: SNS system stimulated, heart rate and vascular tone increase, increases cardiac output
- Baroreceptors in carotid artery
49
Describe how arterial tone affects cardiac function
- Afterload affected by pressure of blood in circulation
- Affected by vasomotor tone but mainly arteriolar tone
- Arteriolar tone determined by diameter of arterioles
- High BP leads to reduced stroke volume and therefore increased afterload
50
Describe how venous return contributes to cardiac function
- Increased venous return = increased preload
- Increased preload = increased stroke volume
- Increaed stroke volume = increased cardiac output
- Venous return is under sympathetic and muscular control
- Contraction of skeletal muscles forces blood through venous system
- Increased sympathetic tone leads to vasoconstriction, increasing central venous pressure and thus increasing preload.
51
Define preload
Preload is the volume of blood in the heart at the end of diastole
52
Define afterload
Afterload is the blood left in the heart after systole
53
Describe a systematic approach to the reading of an ECG
- Rate
- Rhythm (regular/irregular/regularly irregular etc)
- P for every QRS?
- Are Ps and QRSs consistently related
- Are all Ps alike
- Are all QRSs alike
- Are QRSs narrow and upright in leads 2, 3, AVF
- Are QRSs wide and bizarre?
54
What are the endividual elements of the normal P-QRS-T complex?
```
P = atrial contraction
QRS = ventricular contraction
T = ventricular diastole
```
55
Define ectopic activity in an ECG and determine its origin
- Ectopic activity can be caused by premature contractionof atria or ventricles
- In premature contraction of atria, single P wave will appear different from the other while QRST looks normal
- In premature ventricular contraction, very few or no Ps will be visible as abnormal wide and bizarre QRSs cover Ps on ECG
56
Describe how the mean electrical axis can be calculated from an ECG
- Find isoelectric lead (most flat)
- Use circle diagram to find perpendicular lead
- On ECG, is the perpendicular lead more positive or negative?
- If more negative, then will be the more negative answer on the graph, if more positive then will be more positive answer on the graph
- 12 points on graph
- Lead I = 0 -> +/- 180
- Lead AVL = -30
- Lead III = -60
- Lead AVF = -90
- Lead II = -120
- Lead AVR = -150
- Normal in dog is 40 - 100
57
Going anticlockwise starting at lead I, what are the leads and their degress to calculate MEA?
- Lead I = 0
- AVL (one to the left of Lead I) = -30
- Lead III (third lead anticlockwise) = -60
- AVF (has 90 degrees in F) = -90
- Lead II (second from the right of Lead I going clockwise from 180) = -120
- AVR (to right of lead I at 180) = -150
58
What is the rate calculation when paper speed on an ECG is 2.5cm/sec
1500/#boxes
59
What is the rate calculation when paper speed on an ECG is 5cm/sec
3000/#boxes
60
Describe the common reasons why complexes may be wide and bizarre
- Left ventricular enlargement leads to increased time taken for the impulse to move through the heart, therefore leading to wide QRS complex
- Ventricular tachycardiac is when there is a run of 3 or more VPCs on an ECG (ventricular premature contractions)
61
List some common artefacts affecting ECGs
Electrical interference from other electrical equipment, muscle tremors, coughing, normal respiration, panting, purring
62
Describe the placement of the leads for a surface ECG
- Lead 1: RF and LF
- Lead 2: RF and LH
- Lead 3: LF adn LH
63
Explain the circulatory response to reduced cardiac output
- Reduced pressure detected by baroreceptors in vascular system
- Increase sympathetic tone
- Increase heart rate and contractility
- Will increase cardiac output (as long as venous return also increases, not the case in blood loss)
64
Explain the circulatory response to increased cardiac output
- Increased blood pressure detected by baroreceptors in vascular system
- PSNS stimulated
- Decreases heart rate and contracility
- Reduces cardiac output and blood pressure returns to normal level
65
Recognise clinical indicators of hypotension
- Poor CRT
- Tacky and pale mucous membranes
- Increased heart rate (shock, attempt to increase blood pressure)
- Decreased temeperature (decreased flow to extremities)
- Poor pulse pressure
- Dyspnoea
- Anuria
- Tachypnoea
- Central depression
- Weakness
- Thirst
- Minimum blood pressure needed to supply brain is 60mmHg, hypotension can lead to hypoxia
- In acute hypotension skin tenting, altered PCV and signs of dehydration will not be occuring
66
Explain the principles of angiogenesis
- Sprouting of new capillaries from pre-existing vessels
- Occurs in response to hypoxia
- Controlled by hypoxia inducible factor
- Endothelial cell tip secretes proteolytic enxymes and allows migration through ECF
67
Define and describe the process of vasculogenesis
- Formation of blood vessels from endothelial progenitor cells
- Cardinal veins form laterally and arterial angioblasts form dorsal aorta
- Vasculogenesis controlled by vascular endothelial growth factor
- Formation of blood vessels from angioblasts involves complex ineractions between cells, growth factors and ECM
68
Give the origin of and describe cardiovascular development
- Derived from splanchnic mesoderm
| - Forms angiogenetic clusters that undergo canalisation to form blood vessels and heart tubes
69
Describe how obliteration and fusion of major arteries in the early embryo produces the adult pattern
- Initially, dorsal aortae form in response to VEGF (vascular endothelial growth factor)
- 6 pairs and truncus arteriosus in the middle
- Form within pharyngeal arches alongside cranial nerves
- 1st pair: form maxillary artery
- 2nd pair: strapedial artery by moving cranially
- 3rd pair: common, internal and external carotid arteries
- Right 4th: right subclavian and right dorsal orta
- Left 4th: aortic arch (ascending aorta leading to descending aorta)
- Right 6th: straight pulmonary artery
- Left 6th: left pulmmonary artery and ductus arteriosus
- Right 7th: distal end of right subclavina
- Left 7th: left subclavian artery
- Right dorsal aorta regresses in part an forms part of lsubclavian artery
- Left forms descending thoracic aorta
- Aortic sac forms ascending aorta and brachiocephalic trunk
70
List the abnormalities that can occur as a result of a failure of the obliterationand fusion of major arteries in the early embryo to produce the adult patter
- Persistent right aortic arch - constricts oesophagus
- Aberrant right subclavian (similar to perisistent right aortic arch)
- Transposition of arties (aorta arises from RV and takes oxygenated blood to lungs)
- Patent ductus arteriosus (normally forms ligamentum arteriosum. Can increase risk for endocarditis, heart failure and development of Eisenmenger's complex)
71
Define arteriogenesis
The remodelling of newly formed or pre-existing vascular channels into larger and well-muscularised arterioles and collateral vessels
72
Describe the development of the venous system in the embryo
- Develops from capillary network
- Split into 4 systems
- Cardinal, umbilica, omphalomesenteric and pulmonary veins
- Cardinal has complex modifications, superior cardinal veins from head and inferior cardinal vein from body
- Drains into sinus venosum and into atrium via sinus horns
- Umbilical system bring sin oxygen and nutrient rich blood from placenta
- Initially unpaired umbilical vein within cord, then divides into paired, then just right UV
- Later, vein regresses entirely to combine with omphalomesenteric vessels within liver
- Omphalomesenteric system forms drainage system from duodenum, liver and umbilicus, foms ductus venosus (to bypass liver)
- Pulmonary veins separate the venous system
- Development pooly understood
- 4 vessels empty into the left atrium
73
Explain why the foetal circulation differs from the adult
- Lungs are collapsed, not necessary, high resistance to air and blood flow
- Foetal liver not fully required, important in late metabolic stages
- Developing organs and tissues are fragile and therefore most blood kept away and pressure low
- Organs in feotus very soft
- Uses a series of shunts in order to perfuse only areas necessary
74
Explain the consequences of parturition on the circulatory system and list all the major circualtory changes that occur
- Immediate need for independent aeration of lungs
- Pulmonary vascuar resistance decreases secondary tolung expansion
- Increase pulmonary blood flow
- Increases LA pressure to higher than that of inferior vena cava
- Pulmonary walls become thinner (lungs stretch when breathing)
- Independent gas exchange necessary
- 2 modifications from foetal system: blood circulates to lungs, direct flow from RA to LA prevented
- Alveoli open, decrease pressure in pulmonary tissue and right heart
- Increases pressure in left heart as blood return from lungs to LA
- Shunts close to maintain cardiac output
- Prevent dilution of oxygenated blood
75
Describe the mechanisms that regulate changes in circulation at birth
- Changes in pressures of teh lungs and heart
- Cause closure of some shunts
- Changes the pathway of circulation
76
Describe the shunt system and flow of blood in the foetus
- Oxygenated blood from the placenta enters foetus through umbilical vein
- Bypasses liver via ductus venosus
- Combines with deoxygenated in inferior vena cava
- Joins deoxygenated from superior vena cava
- Empties into RA
- Blood shunted through foramen oval to LA
- Bypasses pulmonary arteries, direct to aorta from pulmonary artery via ductus arteriosus
- Deoxygenated blood returns to placenta via umbilical arteries originating from internal iliacs near bladder
77
Describe the closure of the forament ovale
- Nncreased blood flow to lungs
- Increases pressure in left atrium
- Closure of foramen ovale
- Continues contact between septae (primum and secundum) leads to fibrosis of septum
- Anatomical closure relatively slow
- No shunting persists in normal animal
78
Describe the closure of the ductus venosus
- DV weakly responsive to PGE2 and PGI1 (vasodilators)
- Ability to influence lost with improved pulmonary clearance and loss of umbilical blood supply
- Full closure occurs within hours to days of birth
- Loss of blood from umbilical vein leads to constriction of sphincter in DV
- Divert blood flow to liver
- DV becomes ligamentum venosum
79
Describe the anatomical remnants of the foetal cardiovacular system after parturition
- Umbilical arteries become round ligaments of bladder, while umbilical vein becomes round ligament of the liver
- DV becomes ligamentum venosum
- DA becomes ligamentum arteriosum
- Blood enters capillary bed and so blood pressure in IVC drops
- FO closes to form the complete septum between RA and LA
80
What is meant by "amount of substance" and what units should be used to describe an amount
Amount of substance can refer to the amount of things in a substance or can refer to the mass of a substance
81
Give the conversions for commonly used lab units
- Milli = 1/1000
- Micro = 1/1000000
- Nano = 10^-9
- Pico = 10^-12
- Kilo = x1000
82
Describe how to perform dilution calculations
- Find the dilution factor
| - The total number of unit volume in which the material is dissolved
83
Describe the anatomy of the vascular tree
- Split into 2 parts
- Systemic and pulmonary
- Blood sent around body in parallel
- Each tissue receives fresh blood from the heart and not from other tissues
- Delivery system of arteries and arterioles
- High pressure
- Exchange system made up of capillaries
- Intermediate pressure
- Return system make of venules and veins
- Low pressure, contain most blood and are reservoir for blood
- Deoxygenated blood enters heart via cranial and caudal vena cava into right atrium, into right ventricle, to lungs
- Oxygenated blood from the lungs to the left atrium, left ventricle, to body
84
Identify major routes of blood flow
- Divided based on physiological purpose and metabolic needs
- GI -> kidneys -> skeletal muscle -> braiin -> skin/heart -> bones
- Deoxygenated blood flows through right heart to lungs
- Oxygenated from lungs to body via left side of heart
85
Describe the anatomical remnants of the foetal cardiovacular system after parturition
- Umbilical arteries become round ligaments of bladder, while umbilical vein becomes round ligament of the liver
- DV becomes ligamentum venosum
- DA becomes ligamentum arteriosum
- Blood enters capillary bed and so blood pressure in IVC drops
- FO closes to form the complete septum between RA and LA
86
What is meant by "amount of substance" and what units should be used to describe an amount
Amount of substance can refer to the amount of things in a substance or can refer to the mass of a substance
87
Give the conversions for commonly used lab units
- Milli = 1/1000
- Micro = 1/1000000
- Nano = 10^-9
- Pico = 10^-12
- Kilo = x1000
88
Describe how to perform dilution calculations
- Find the dilution factor
| - The total number of unit volume in which the material is dissolved
89
Describe the anatomy of the vascular tree
- Split into 2 parts
- Systemic and pulmonary
- Blood sent around body in parallel
- Each tissue receives fresh blood from the heart and not from other tissues
- Delivery system of arteries and arterioles
- High pressure
- Exchange system made up of capillaries
- Intermediate pressure
- Return system make of venules and veins
- Low pressure, contain most blood and are reservoir for blood
- Deoxygenated blood enters heart via cranial and caudal vena cava into right atrium, into right ventricle, to lungs
- Oxygenated blood from the lungs to the left atrium, left ventricle, to body
90
Describe the structure and function of capillaries
- No collagen or elastin
- Relatively low blood pressure in capillaries
- Fragile and permeable
- High pressure can tear or force a lot of fluid oout (oedema)
- Small blood flow over a large surface area = good ability to exchange substances
- Delivery of nutrients and removal of wastes
- Slow flow allows time for molecules to diffuse across the capillary wall
91
Describe the struction and function of veins
- High collagen, low elastin
- Do not need to recoil
- Fill with blood and stay strong
- Venous return depends on pressure differences between venules and RA
- Smooth muscle contraction in tunica media, inspiration/lower diaphragm compression, existence of venous valves, skeletal muscles and gravitation (head)
92
Describe the importance of anastomoses
- Anastomoses are bridges between 2 vessels
- Survival of an organ relies on blood flow
- If blood flow stopped or dramatically reduced organ becomes necrotic and dies
- Anastomoses provide collateral supply of blood to organs
93
Describe the portal systems of blood flow
- A few organs connected in series
- Obtain blood second hand from the venous outflow of another organ
- Main advantage: enables transportation of a solute from one place to another without dilution in general circulation
- Hepatic portal vein is present in all vertebrates
- Passes from GIT to liver
- Newly absorbed compounds filtered
- Renal portal vein present in all non-mammalian vertebrates and goes from hindlimbs to the kidney for the reabsorption of salt, water etc
94
Describe the different types of capillaries
- 3 types
- Continuous: lining of endothelial cells except for clefts between cells. Found in majority of body
- Fenestrated: fenestrations where cell membrane compressed to permit great fluid transmission
- Discontinuous sinusoid: wider intercellular gaps permit increased exchange within surrounding tissues. Are found in liver, bone marrow, lymphoid tissue and some endocrine glands
95
Describe the structure and function of arterioles
- Cells contractile - can reduce radius of arterioles
- Increase blood pressure
- Composed of smooth muscle cells
- Can reduce high BP by relaxing smooth muscle
- Decrease in arteriolar radius will lead to increase in blood pressure
- Arterioles regulate blood pressure and provide resistance to blood flow
96
Describe how hydrophobic signalling factors can act directly at the nucleus
- Receptor is intracellular within cytoplasm nucleus
- Lipid soluble hormones able to pass through memrbane and act on receptor
- Forms hormone receptor complex
- Once bound, complexes can bind to sites on DNA causing DNA replication and production of proteins
- Protein synthesised leading to a biologial response
97
Describe the struction and function of veins
- High collagen, low elastin
- Do not need to recoil
- Fill with blood and stay strong
- Venous return depends on pressure differences between venules and RA
- Smooth muscle contraction in tunica media, inspiration/lower diaphragm compression, existence of venous valves, skeletal muscles and gravitation (head)
98
Identify the 3 main classes of cell surface receptors
- G-protein linked
- Ion channel/ligand gates
- Enzyme linked
99
Describe the cellular signalling mecahnism of endothelium derived hyperpolarising factor
- EDHF mysterious
- Most likley only important in arterioles
- If all of nitric oxide and prostacyclin activity is blocked
- Some vasodilation persists when ACh and brady kinin are administered
- Due to EDHF but an be revered by K-channel antagonists
100
Describe G-protein linked receptors
Pheromones, hormone, NTs, cAMP
| - Receptor linked with G protein which carries out effect such as opening ion channels or activating an enzyme
101
Describe enzyme linked receptors
- Transmembrane element
- Activates intracellular enzyme
- Enzymes acitvated within cell
- Causes chain reaction
102
Describe how hydrophobic signalling factors can act directly at the nucleus
- Receptor is intracellular within cytoplasm nucleus
- Lipid soluble hormones able to pass through memrbane and act on receptor
- Forms hormone receptor complex
- Once bound, complexes can bind to sites on DNA causing DNA replication and production of proteins
- Protein synthesised leading to a biologial response
103
Lis examples of endothelial derived factors that influence vasomotor tone
- Nitric oxide
- INtracellular Ca
- Angtiotensin II
- Prostaglandins
- Endothelin
104
Describe the cellular signalling mechanism of PGI2 and its effect on the vascular system
- Prostaglandin
- Acts on G-protein coupled receptor
- Released in response to ACh
- Stimulated an increase in [Ca]
- This stimulated endothelium to release prostacyclin
- Activated adenylate cyclase to increase cAMP in vacular smooth muscle cells
- Decreases [Ca] in CSMC
- Relaxation of VSMC and vasodilation
105
Describe the cellular signalling mecahnism of endothelium derived hyperpolarising factor
- EDHF mysterious
- Most likley only important in arterioles
- If all of nitric oxide and prostacyclin activity is blocked
- Some vasodilation persists when ACh and brady kinin are administered
- Due to EDHF but an be revered by K-channel antagonists
106
Describe the cellular signalling mechanism of endothelins
- Family of peptides from 3 different genes (ET-1, ET-2, ET-3)
- Act as potent vasoconstrictors
- Isoforms of endothelins differentially expressed in different organs
- ET-1 is only endothelin present in endothelial cells
- Action is short term, local and specific
- Antagonists of their receptors promote dilation
- Bind to calcium channels and open them
- Allow constriction of VSMCs
