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VetMed Year 1 > CRS 4 > Flashcards

CRS 4 Flashcards

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
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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

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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

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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
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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
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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
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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
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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
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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
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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
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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
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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)
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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
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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
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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
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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
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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
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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
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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

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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
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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
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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
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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
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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
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25
Q

Define agonist

A

An agent that leads to a biological/physiological response when bound and has a maximum efficacy of 100%

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26
Q

Define partial agonist

A

An agent that leads to a biological/physiological response when boudn to a receptor but as an efficacy of less than 50%

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27
Q

Define antagonist

A

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%

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28
Q

Differentiate between receptor spcificity and selectivity

A
  • 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)
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29
Q

Differentiate between competitive and non-competitive receptor antagonism

A
  • 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
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30
Q

Describe facotr controlling pacemaker function and the cardiac action potential

A
  • 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
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31
Q

Identify drugs and their sites of action that affect heart rate or rhythm

A
  • 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
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32
Q

Explain indication sofor use fo cardiac antidysrhythmic agents

A
  • Presence of dysrhythia, angina or hypertension

- Use of wrong drug can also cause a dysrhythmia

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33
Q

Outline the potential causes of a dysrhythmia

A
  • 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
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34
Q

State the 4 classes of antidysrhythic drugs and their mechanisms of action

A

Class I: sodium channel blockers
Class II: beta blockers
Class III: prolong action potential
Class IV: block voltage sensitive calcium channels

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35
Q

Describe the anatomy of the lymphatic system

A
  • 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
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36
Q

Explain Starling’s forces and the processes leading the lymph formation

A

(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

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37
Q

Describe the mechanisms by which oedema may develop

A
  • 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
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38
Q

Explain the process of fluid exchange in tissues

A
  • 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
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39
Q

What is colloid osmotic pressure?

A

Pressure exerted by plasma proteins and promotes fluid reabsorption into the circulatory system

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40
Q

Define pulse pressure

A

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

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41
Q

Define arterial compliance

A

The elasticity of arteries

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42
Q

State the Starling law of the heart and explain the intracellular mechanisms underlying the Frank-Starling effect (length tension curve)

A
  • 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
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43
Q

Give a working definition o contractility.

A

The strenght of a contraction and is influence by the sympathetic nervous system

44
Q

Explain why a coordinated control of both heart and peripheral circulation is necessary to achieve optimal cardiac output

A
  • 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
Q

Define the relationship between mean arterial pressure, cardiac output and total peripheral resistance

A

Mean arterial pressure = cardiac output x peripheral resistance

46
Q

Describe the effects of changes in preload on cardiac output

A
  • Increased preload increases contractility of heart
  • Increases cardiac output
  • Decrease in preload will decrease stroke volume and thus cardiac output
47
Q

Describe the effects of cahnges in afterload on cardiac output

A
  • 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
Q

Describe the mechanisms that regulate cardiac output and blood pressure

A
  • 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
Q

Describe how arterial tone affects cardiac function

A
  • 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
Q

Describe how venous return contributes to cardiac function

A
  • 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
Q

Define preload

A

Preload is the volume of blood in the heart at the end of diastole

52
Q

Define afterload

A

Afterload is the blood left in the heart after systole

53
Q

Describe a systematic approach to the reading of an ECG

A
  • 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
Q

What are the endividual elements of the normal P-QRS-T complex?

A 
P = atrial contraction
QRS = ventricular contraction
T = ventricular diastole
55
Q

Define ectopic activity in an ECG and determine its origin

A
  • 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
Q

Describe how the mean electrical axis can be calculated from an ECG

A
  • 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
Q

Going anticlockwise starting at lead I, what are the leads and their degress to calculate MEA?

A
  • 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
Q

What is the rate calculation when paper speed on an ECG is 2.5cm/sec

A

1500/#boxes

59
Q

What is the rate calculation when paper speed on an ECG is 5cm/sec

A

3000/#boxes

60
Q

Describe the common reasons why complexes may be wide and bizarre

A
  • 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
Q

List some common artefacts affecting ECGs

A

Electrical interference from other electrical equipment, muscle tremors, coughing, normal respiration, panting, purring

62
Q

Describe the placement of the leads for a surface ECG

A
  • Lead 1: RF and LF
  • Lead 2: RF and LH
  • Lead 3: LF adn LH
63
Q

Explain the circulatory response to reduced cardiac output

A
  • 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
Q

Explain the circulatory response to increased cardiac output

A
  • 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
Q

Recognise clinical indicators of hypotension

A
  • 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
Q

Explain the principles of angiogenesis

A
  • 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
Q

Define and describe the process of vasculogenesis

A
  • 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
Q

Give the origin of and describe cardiovascular development

A
  • Derived from splanchnic mesoderm

- Forms angiogenetic clusters that undergo canalisation to form blood vessels and heart tubes

69
Q

Describe how obliteration and fusion of major arteries in the early embryo produces the adult pattern

A
  • 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
Q

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

A
  • 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
Q

Define arteriogenesis

A

The remodelling of newly formed or pre-existing vascular channels into larger and well-muscularised arterioles and collateral vessels

72
Q

Describe the development of the venous system in the embryo

A
  • 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
Q

Explain why the foetal circulation differs from the adult

A
  • 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
Q

Explain the consequences of parturition on the circulatory system and list all the major circualtory changes that occur

A
  • 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
Q

Describe the mechanisms that regulate changes in circulation at birth

A
  • Changes in pressures of teh lungs and heart
  • Cause closure of some shunts
  • Changes the pathway of circulation
76
Q

Describe the shunt system and flow of blood in the foetus

A
  • 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
Q

Describe the closure of the forament ovale

A
  • 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
Q

Describe the closure of the ductus venosus

A
  • 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
Q

Describe the anatomical remnants of the foetal cardiovacular system after parturition

A
  • 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
Q

What is meant by “amount of substance” and what units should be used to describe an amount

A

Amount of substance can refer to the amount of things in a substance or can refer to the mass of a substance

81
Q

Give the conversions for commonly used lab units

A
  • Milli = 1/1000
  • Micro = 1/1000000
  • Nano = 10^-9
  • Pico = 10^-12
  • Kilo = x1000
82
Q

Describe how to perform dilution calculations

A
  • Find the dilution factor

- The total number of unit volume in which the material is dissolved

83
Q

Describe the anatomy of the vascular tree

A
  • 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
Q

Identify major routes of blood flow

A
  • 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
Q

Describe the anatomical remnants of the foetal cardiovacular system after parturition

A
  • 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
Q

What is meant by “amount of substance” and what units should be used to describe an amount

A

Amount of substance can refer to the amount of things in a substance or can refer to the mass of a substance

87
Q

Give the conversions for commonly used lab units

A
  • Milli = 1/1000
  • Micro = 1/1000000
  • Nano = 10^-9
  • Pico = 10^-12
  • Kilo = x1000
88
Q

Describe how to perform dilution calculations

A
  • Find the dilution factor

- The total number of unit volume in which the material is dissolved

89
Q

Describe the anatomy of the vascular tree

A
  • 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
Q

Describe the structure and function of capillaries

A
  • 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
Q

Describe the struction and function of veins

A
  • 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
Q

Describe the importance of anastomoses

A
  • 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
Q

Describe the portal systems of blood flow

A
  • 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
Q

Describe the different types of capillaries

A
  • 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
Q

Describe the structure and function of arterioles

A
  • 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
Q

Describe how hydrophobic signalling factors can act directly at the nucleus

A
  • 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
Q

Describe the struction and function of veins

A
  • 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
Q

Identify the 3 main classes of cell surface receptors

A
  • G-protein linked
  • Ion channel/ligand gates
  • Enzyme linked
99
Q

Describe the cellular signalling mecahnism of endothelium derived hyperpolarising factor

A
  • 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
Q

Describe G-protein linked receptors

A

Pheromones, hormone, NTs, cAMP

- Receptor linked with G protein which carries out effect such as opening ion channels or activating an enzyme

101
Q

Describe enzyme linked receptors

A
  • Transmembrane element
  • Activates intracellular enzyme
  • Enzymes acitvated within cell
  • Causes chain reaction
102
Q

Describe how hydrophobic signalling factors can act directly at the nucleus

A
  • 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
Q

Lis examples of endothelial derived factors that influence vasomotor tone

A
  • Nitric oxide
  • INtracellular Ca
  • Angtiotensin II
  • Prostaglandins
  • Endothelin
104
Q

Describe the cellular signalling mechanism of PGI2 and its effect on the vascular system

A
  • 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
Q

Describe the cellular signalling mecahnism of endothelium derived hyperpolarising factor

A
  • 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
Q

Describe the cellular signalling mechanism of endothelins

A
  • 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

VetMed Year 1 (13 decks)

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