cardiovascular system Flashcards

1
Q

5 functions of blood

A
  1. transport of dissolved substances
  2. regulation of pH and ions
  3. restrictions of fluid losses at injury sites
  4. defence against toxins and pathogens
  5. stabilisation of body temperature
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2
Q

characteristics of blood

A

highly viscous
slightly alkaline
55% plasma
45% formed elements

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3
Q

what is hematopoiesis

A

the development of formed elements in red bone marrow

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4
Q

what do hematopoietic stem cells differentiate in to?

A

-myeloid stem cells (becomes blood cells)
-lymphoid stem cells (becomes lymphocytes)

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5
Q

Features of erythrocytes (RBCs)

A
  • biconcanve dics
  • no mitochondria
  • anucleate
    high SA to volume ratio
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6
Q

regulation of erythropoesis

A
  • regulated by erythropoetin, which is released by the kidneys
  • building RBCs requires amino acids, iron, vitamin B12, B6 and folic acid
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7
Q

4 basic blood types
Who can they give to and receive from?

A

Type A) has A antigens and antibodies to B. can receive A and O. can give to A and AB.
Type B) has B antigens and antibodies to A. can receive B and O. can give to B and AB.
Type AB) has A and B antigens and neither antibodies. can receive A, B or O. Can give to A, B or AB.
Type O) has neither antigens and has antibodies to A and B. can only receive O. can give to all.

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8
Q

Rhesus factor

A

refers to presence or absence of D surface antigen
presence of D antigen = Rh POSITIVE. can receive either + or - but can only give to +
absence of D antigen = Rh NEGATIVE. can only receive - but can donate to either.

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9
Q

Cross-reactions when determining blood type

A

normal cells ignored, blood is homologous
foreign cells attacked and will agglutinate

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10
Q

features of leukocytes (WBCs)

A

-nucleated cells
-do not contain hemoglobin
- short-lived
-play a role in inflammation and infection

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11
Q

function of leukocytes

A
  1. WBCs accumulate at sites of infection/inflammation
  2. WBCs ‘emmigrate’ from blood compartment into tissue site. WBCS stick to endothelium then move to site via chemotaxis
  3. Once at site, WBCs carry out functions in the imflammatory/immune response
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12
Q

Thrombocytes (platelettes)

A

-disc shaped
-anucleate
-come from bone marrow cells
-removed by spleen
-release important clotting chemicals to act as a patch in damaged vessel wall

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13
Q

what is hemostasis?

A

the cessation of bleeding
three phases
1. vascular phase
2. platelet phase
3. coagulation phase

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14
Q

hemostasis vascular phase

A

TRIGGERS PLATELETS
-vascular spasm
-contraction of smooth muscle in damaged blood vessel wall caused by activation of platelets
-reflexes initiated by pain receptors

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15
Q

hemostasis platelet phase

A

PLATELETS FORM A PLUG
-platelets contact each other and adhere to damaged tissue in the blood vessel wall
-platelets extend projections to one another
-positive feedback loop of aggregation (stuck together)
-activated platelets release clotting compounds, which stabilises platelet plug

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16
Q

hemostasis coagulation phase

A

FORMS MESHWORK TO WRAP AROUND THE PLUG TO MAKE IT STABLE
- clotting factors promote formation of prothrombinase
-converts prothrombin into thrombin
-thrombin converts soluble fibrinogen into fibrin
-fibrin forms threads which traps formed elements to form clots
-need calcium

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17
Q

Blood clot retraction and repair

A
  • platelets pull on each other
    -also pull on fibrin threads
    -clot contracts, pulling wound edges closer together
    -vessel lining is repaired
    -clot eventually dissolved through action of plasmin
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18
Q

pericardium

A
  • heart enclosed by fibrous network of collagen fibres
  • outer = parietal pericardium. lines inner surface of pericardial sac
  • inner = visceral layer. lines surface of the heart
  • pericardial cavity filled with fluid to reduce friction
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19
Q

three layers of the heart wall

A
  1. epicardium
  2. myocardium (cardiac muscle tissue, provides pumping action)
  3. endocardium
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20
Q

myocardium

A
  • cardiac muscle fibres
  • one central nucleus
  • connected via gap junctions
  • very high aerobic capacity (high mitochondria)
  • striated
  • intercalated discs
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21
Q

function of intercalated discs

A
  • maintain structure
  • enhance molecular and electrical connections
  • conduct action potentials
22
Q

sulcus of the heart (2)

A

coronary sulcus = divides upper atria from ventricles
interventricular sulcus = separates R and L ventricles

23
Q

Coronary circulation

A
  • circulation TO the heart
  • coronary arteries - fill upon diastole (relaxation). carry oxygenated blood to the myocardium
  • coronary sinus - carries deoxygenated blood back to the right atrium. thin walled vein with no smooth muscle to alter diameter.
24
Q

2 types of cardiac muscle fibres

A

Autorhythmic fibres
-specialised muscle fibres
-initiate and form an action potential

Contractile fibres
-provide mechanical work of the pump
-99% of all muscle fibres

25
Q

Components of conducting system (nodes)

A

SA node - pacemaker
-spontaneously depolarises 80-100 times per minute

AV node
-spontaneously depolarises 40-60 times per minute
-conduction slows at AV node (AV nodal delay)
- delay allows atria time to contract and fill the ventricles

26
Q

cardiac action potential

A

resting membrane potential is -90mV

  1. rapid depolarisation (NA+ ENTRY)
    - voltage gated ion channels open
    -rapid influx of sodium
  2. plateau (CA2+ ENTRY)
    - sodium channels close rapidly at 30mV
    -efflux of sodium
    -volatge gated slow calcium channels open
    -slow calcium influx
    -balances show sodium outflow
  3. repolarisation (K+ LOSS)
    - voltage gated slow calium channels close
    - voltage gated slow potassium channels open
    -potassium ellfux
27
Q

Sequence of electrical events

A
  1. SA node mass of cells, spontaneously generates an action potential
  2. stimulus spreads across atria and reaches the AV node
  3. AV nodal delay, atrial contraction begins
  4. action potential spreads across AV bundle, bundle fibres and Purkinje fibres
  5. AP relayed across ventricles, muscles of ventricle contract
28
Q

3 criteria for efficient pumping

A
  1. atria must contract before ventricles
  2. coordinate excitation so that each heart chamber contracts as a synctium
  3. two atria should contract together, two venrticles should contract together
29
Q

how is efficient pumping achieved?

A

-interatrial pathway
-internodal pathway
-AV nodal delay

30
Q

cardiac cycle

A

the period between the beginning of a heartbeat and the beginning of the next
-includes both contraction and relaxation/systole and diastole

31
Q

what is an electrocardiogram?

A

-represents the summed electrical activity of all cardiac cells recorded from the skin surface
-each peak represents a different component of electrical events during cardiac cycle
-mechanical events occur between each peak

32
Q

electrocardiogram peaks

A

During the P wave, atrial depolarisation occurs, corresponding with atrial contraction (systole), initiating the atria to empty their blood into the ventricles due to a build up of pressure.

During the QRS complex, ventricular depolarisation occurs, corresponding with ventricular contraction (systole), forcing the blood in the ventricles to be emptied into the arteries. Atrial repolarisation also occurs, corresponding with atrial relaxation (diastole), where the atria fill with blood from the blood vessels.

During the T wave, ventricular repolarisation begins, corresponding with ventricular relaxation (diastole), where the ventricles passively fill with blood from the atria.

33
Q

cadiac output

A

the volume pumped by the left ventricle in one minute
CO = HR x SV
factors effecting stroke volume and heart rate also effect cardiac output

34
Q

factors effecting heart rate

A
  1. autonomic innervation of the heart
    - ANS changes rate of spontaneous depolaristion of duration of repolaristion. this alters heart rate by changing the time required for cells to reach threshold
  2. hormones
    - adrenaline, noradrenaline and thyroid hormone
35
Q

factors affecting heart rate

A
  1. autonomic innervation of the heart
    - ANS changes rate of spontaneous depolarisation and duration of repolarisation
    -This alters heart rate by changing time required for cells to reach threshold
  2. hormones
    - adrenaline, noradrenaline and thyroid hormones,
36
Q

factors affecting stroke volume

A
  1. end-diastolic volume (blood ejected)
    - filling time
    - venous return
    - preload
  2. end-systolic volume (blood remaining)
    - preload
    - contractability
    - afterload
37
Q

5 major types of blood vessel

A

-arteries) thick, highly elastic walls, large radius
-arterioles) highly muscular, well innverated walls, smooth muscle, small radius
-capillaries) thin walled, highly permeable, high cross sectional area for nutrient exchange
-venules) thin walled
-veins) thin walls, large radius

38
Q

blood vessel structure

A

tunica interna
- endothelium
-basement membrane
- internal elastic lamina

tunica media
-elastic fibres
-smooth muscle
-external elastic lamina

tunica externa
-elastic and collegen fibres

39
Q

arteries

A

elastic/conducting arteries
-large
- carry blood away from the heart
- stores elastic energy

muscular/distributing arteries
-medium
-tunica media contains high proportion of smooth muscle
-distribute and regulate blood flow (constrict and dilate)

40
Q

Arterioles

A

-small almost microscopic
-deliver blood to capillaries
-key regulator of vascular resistance through vasoconstriction and vasodilation due to high innervation

41
Q

Capillaries

A

-microscopic
-walls consist of only endothelium layer and basement membrane
-extremely permeable
-exchange vessels

42
Q

3 types of capillaries

A
  1. continuous capillaries
    - uninterrupted solid lining
  2. fenestrated capillaries
    - many pores
  3. sinusoidal capillaries
    - large fenestrations and intracellular clefts
    - incomplete basement membrane
43
Q

venules

A

-small veins, venules merge to form veins

44
Q

veins

A
  • tunica externa is the thickest layer
    -may contain valves to prevent backflow
    -is a volume reservoir, holds 60% of blood volume
    -actively restricts and has blood ready to go to push through heart and increase cardiac output
45
Q

blood flow

A

-the volume of blood that flows through a tissue per unit of time
-determined by blood pressure and resistance
-proportional to pressure gradient
-inversely proportional to resistance

46
Q

vascular resistance

A

-opposite to blood flow
-depends on vessel length and vessel diameter
-increased length and decreased diameter increase resistance
-resistance is 1 over radius to the power of 4

47
Q

what happens if blood flow is too low or too high?

A

too low = hypotension = vessels collapse, blood flow stops, tissues die

too high = hypertension = vessel walls stiffen, capillary beds may rupture

48
Q

capillary exchange methods (3)

A
  1. diffusion
  2. transcytosis
  3. bulk flow
49
Q

cardiovascular regulation mechanisms (3)

A
  1. autoregulation
    - local vasodilators or vasoconstrictors
  2. neural mechanisms
    -neural control via cardiac and vasomotor centres in medulla oblongate
  3. hormonal mechanisms
    -adrenaline and noradrenaline increases CO
    -antidiuretic hormone increases BP
    -angiotensin II increased BP
    -erythropoietin from kidneys stimulates RBC production in bone marrow
50
Q

Baroreceptor reflex

A

-baroreceptors in sinus and aorta
-monitor degree of stretch
-sends impulses to cardiovascular centre to control cardioinhibitory centre, carioacceletory centre and vasomotor centre