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CVR lecture flashcards > CVR week 1: > Flashcards

CVR week 1: Flashcards

1
Q

valves- name and location?

A

R atrium to R venticle- tricuspid valve

L atrium to L venrticle- mitral valve

L ventricle to aorta- aortic valve

R ventricle to pulmonary artery- pulmonary valve

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2
Q

describe constituents of plasma?

A
  • plasma 55% of total blood :
  • 90% water (solvent)
  • 7-8% proteins e.g. albumin (blood volume), globulins (immune function), fibrinogen (blood clotting)
  • electrolytes: sodium, potassium, calcium etc.
  • nutrients: glucose, fatty acid, amino acid
  • gases: oxygen and carbon dioxide)
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3
Q

describe functions of the blood plasma?

A
  • transport nutrients
  • carries hormones and other signalling molcules
  • maintains blood pressure and volume
  • functional proteins e.g. antibodies, complement and clotting factors
  • temp and pH
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4
Q

what is normal oncotic pressure value?

A

30-50g/L

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5
Q

role of plasma in heat regulation?

A

plasma acts as a heat sink, circulating plasma removes excess heat from ‘hot’ organs and circulates heat to extremities, becomes the fluid for sweat

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6
Q

how does plasma act as a pH regualtor?

A

proeyiens act as H+ buffer through binding to amino acid side chain

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7
Q

role of plasma in inflammation and immunity?

A
  • contains and circulates immune cells and proteins produced by these
  • contains specialsied proteins that contribute to inflammatory response- complement system
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8
Q

How is complement activated?

A

3 different ways:
- classical: trigger by antibodies on pathogens
- alternative: activated directly by pathogens or damaged cells
- lectin pathway: initiated by specific sugars on microbe surfaces

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9
Q

Function of complement?

A

Opsonization/phagocytosis: complex bound to antigen antibody complex or on surface of pathogen activates phagocycotic cells.
Cell Lysis: Directly attacking and rupturing pathogen cell membranes through the formation of the membrane attack complex (MAC)
Inflammation: Complement proteins stimulate inflammation by attracting immune cells to the site of infection or injury
Aid production of antibodies: B cells have complement receptors and bind causing B cell to secrete more antibodies 9amplifies antibody production)

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10
Q

syntheis of plasma proteins- where does it occur?

A

produced in liver - liver disease levels of these are low leading to swelling, infection and bledding

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11
Q

Coagulation cascade - intrinsic pathway:

A

activated by damage to endothelial lining, slow and complex:
factor XII is activated by exposed collagen or other damage.
Activated Factor XIIa activates Factor XI
Factor XIa activates Factor IX, which, together with Factor VIIIa, activates Factor X in the common pathway.

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12
Q

Coagulation cascade - extrinsic pathway:

A

Triggered by external trauma that causes blood to escape from the vessel (e.g., tissue injury),
Faster than the intrinsic pathway

Key steps:
Tissue Factor (TF) is released from damaged tissue
TF combines with Factor VIIa, activating Factor X in the common pathway

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13
Q

Coagulation cascade: common pathway

A

Activated Factor X (Xa), with Factor Va, converts prothrombin (Factor II) to thrombin (Factor IIa)
Thrombin converts fibrinogen (Factor I) into fibrin, which forms a mesh that strengthens the platelet plug
Thrombin also activates Factor XIII, which cross-links fibrin to form a stable clot

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14
Q
A
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15
Q

regulation of coagulation cascade:

A
  • antithrombin III (Inhibits thrombin and Factors IXa, Xa, XIa, and XIIa)
  • Protein C and S (inactivate Va and VIIIa)
  • Tissue Factor Pathway inhibitor (TFPI) (blocks tissue factor VIIa complex formation in extrinsic pathway)
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16
Q

Fibrinolysis:
purpose?
how it happens?

A
  • breakdown of fibrin by proteolytic enzymes, example of use is given as a drug during stroke
  • plasminogen converted to plasmin (by XIa, XIIa, Kallikrein and Tissue plasminogen activator) which breaks down fibrin
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17
Q

Platelets - what they are? role? lifespan? avg platelet count?

A

fragments of megakaryocytes found in bone marrow, aid blood clot and wound healing, lifespan of 7-10 days, ranges from 150,000 to 450,000 per microlitre of blood.

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18
Q

platelet function-

A

Function:

  • adhere at site of injory to form plug
  • release chmicals to attract more platelest and coagulation factors
  • stabalize clot
  • relase growth factors to repair tissue
  • recruit leucocytes and release pro-inflammatory mediators
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19
Q

platelet activation? physical change that occurs after?

A
  • activated by expose to collagen which they adhere to and release chemical signal to activate more platelts
  • undergo shape change to stellate (spiky) to increase SA and form plug to stop bleeding
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20
Q

haemocrit- what is it? percentage of blood volume?

A

part of blood that’s erythrocytes- 45%

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21
Q

feature of erythrocyte

A

biconcave shape, lacks nucleus(more haemoglobin), flexible to move through capillaries, 10 micrometers

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22
Q

features of haemoglobin

A
  • each molecule can carry 4 oxygen molecules
  • 2 alpha, 2 beta subunits
  • porphyrin ring with iron make up heme group (4 in 1 molecule)
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23
Q

what would cause a left shift in oxygen disocation curve? what about right?

A

Shift to left: (increased affinity)
- decrease temp, decrease 2,3-DPG, decrease H+, CO , feotal haemoglobin, myoglobin(very large shift left), lungs

Shift right (Bohr Shift): (decreased affinity)
- increased temperature, increase 2,3-DPG, increase H+, respiring tissues

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24
Q

What is 2,3-DPG?

A

2,3-diphosphoglycerate:

  • produced by erythrocytes during glycolysis by lumbering-rapoport pathway
  • reduces affinity of haemoglobin for oxygen, promoting release of oxygen to tissues
  • increased by factors associated with increase tissue oxygen demand e.g. hypoxia, anaemia, low pH
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25
Q

Transport of CO2 in blood:

A
  • CO2 binds to haemoglobin forming carbaminohaemoglobin
  • CO2 converted to bicarbonate by enzyme carbonic anyhdrase in RBC
  • bicarbonate is exchanged for Cl- in chloride shift
  • bicarbonate is carried in plasma to lungs where it enters RBC (reverse chloride shift) and is converted to CO2
  • small amount of CO2 dissolves directly in plasma
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26
Q

Erythropoiesis: where and reguated by what?

A

occurs in bone marrow, regulated by erythropoietin (produced in kidney by peritubular fibroblasts)

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27
Q

Erythrophagocytosis- where and what by?

A
  • at spleen and liver old rbc are removed, surface damage is detencted by macrophages which injest them
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28
Q

Buffer coat- what is it? percentage?

A

1%, white blood cells (also known as leucocytes)

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29
Q

Neutrophills:
amount? role? lifespan? innate or adaptive?

A
  • most abundant, first responders
  • phagocytose
  • neutrophil extracellar traps (use DNA to trap pathogens)
  • lifespace 5-90 hrs
  • part of innate response
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30
Q

B lymphocytes- innate or adaptive? purpose? produced? found where?

A

Lymphocytes: (2nd most common)
- when activated differnetiate: plasma cell and memory cell
- adaptive immunity

  • B cells: produce antibodies (immunoglobulins), produced and mature in bone marrow, migrate to lymph node system, found in germinal centres and follicles of lymph nodes
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31
Q

T Lymphocytes: innate or adaptive? purpose? produced? found where?

A
  • adaptive immunity, (2nd most common WBC)

T cells: mature in thymus gland, migrate to lymphoid organ:

  • Helper T cells - assist other immune cells e.g. stimulate B cells.
  • Cytotoxic T cells (CD8)- Directly kill infected or abnormal cells
  • Regulatory T cells-Help suppress inappropriate immune responses and maintain immune tolerance
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32
Q

Immunoglobins/antibodies:
some examples?
function?

A

immunoglobulin:

  • exist in different forms such as IgG and IgM
  • IgG- delayed prolongued response (day8), secondary response is larger
  • IgM- initial antibody produced (day4), secondary response is smaller (role in activating compliment)
  • IgE- allergic reaction
  • neutralisation- antibodies bind preventing them infecting cells or causing damage
  • opsonisation- tag pathogens for phagocytes e.g. macrophage, neutrophill
  • complement activation
  • agglutination- clump pathogens together
  • antibody dependent cellular cytotoxicity- triggered to destory virus and cancer cells
33
Q

Monocytes

A
  • large
  • differnetiate into macrophages and dendritic cells in tissue
  • phagocytose
  • role in chronic inflammation e.g atherosclerosis and immune surveilance
34
Q

Eosinophills

A

-2nd least common
- release toxic granules to kill parasites
- involved in inflammatory response e.g. asthama and allergy

35
Q

Natural killer cell:

A

type of lymphocyte

-no activation required
- release toxic granules to kill parasites
- involved in inflammatory response e.g. asthama and allergy

36
Q

Basophills

A

(least common)
release histamine during allegic reaction and inflammation

37
Q

Antigen presentation: MHC I vs II

A

APC- antigen presenting cells:

  • cells that present antigen to T cells
  • include B cells but also tissue cells e.g. macrophages and dendritic cells
  • MHC II involved in antigen presenting to T cells, MHC I used to recognise cell as self or non-self
38
Q

what is cooperative binding?

A

when 1st oxygen moelcule binds there a shape change that makes it easier for more oxygen molecules to bind

39
Q

lubering rapoport pathway:

A

mechanism to produce 2,3-bisphosphoglycerate mediated by enzyme bisphophoglycerate mutase (activity increased at low pH and low oxygen etc.),

Other chain of pathway procuces ATP as side product

40
Q

Blood flow through different organs

A

liver 27%
kidneys 22%
muscle 15%
brain 14%
skin 6%

41
Q

what vessel has highest blood volume?

A

small vein and venules have pooling of blood which can sit and act as a reserve, capacitance vessels, - skeletal muscle/respiratory pump aids return
- SNS (sympathetic nervous system) mediated vasoconstriction maintains VR/VP

42
Q

arterioles

A
  • principal state of resistance to vascular flow (control flow of blood)
  • Total peripheral resistance- TPR = total arteriolar resistance
  • detremined by local neural and hormonal factors
  • distribute blood flow
  • vascular smooth muscle controls width of radius
  • VSM never completely relaxed = myogenic tone
43
Q

capillaries

A
  • large area so slow flow allowing time for nutrient/waste exchange
  • flow is determined by arteriolar resistance as well as number of open pre-capillary sphincters
44
Q

lymphatics:

A
  • specific ducts to return interstitiasl fluid to CV e.g. thoracic duct, left subclavian vein
  • uni-directional flow
45
Q

how to calculate cardiac output?

A

stroke volume times heart rate

46
Q

how to calculate blood pressure

A

cardiac output times total peripheral resistance

47
Q

how to claculate mean arterial pressure?

A

diastolic pressure + 1/3 pulse pressure

48
Q

how to calculate pulse pressure?

A

systolic - diastolic pressure

49
Q

What is the FrankStarling mechanism?

A

automatic response controlling how strong heart contracts each beat

As preload (end-diastolic pressure) of sarcomeres increases, stroke volume increases.

If preload goes to high (sarcomeres are streched too far) cannot contract properly therefore decreasing stroke volume.

50
Q

blood volume is an important factor of blood pressure. Things that affect blood volume:

A

albumin- oncotic pressure, sodium and water, renin-angiotensin-aldosterone system (RAAS), ADH/argenine vasopressin, Adrenal and kindeys

51
Q

how to take blood pressure?

A
  • blood pressure measured using sphymomanometer
  • use brachial artery (convenient and roughly level of heart)
  • systolic- fist tapping noise, diastolic pressure- when noise stops
52
Q

Ability to regulate blood flow- Myogenic auto-regulation? which organs have bettwr control than others?

A

arterioles stretch and vascular smooth muscles contract (myogenic tone) in response with goal of maintaining blood flow
ability varies around the body:
renal/cerebral/coronary have tight controll
skeletal muscle/splanchnic (abdominal) have moderate controll
cutaneous have little controll

53
Q

ability to regulate blood flow- balance of intrinsic and extrinsic controlls

A

brain and heart- rely on instrinsic controll to maintain blood flow
skin- important in general vasoconstrictor response and also in repsonse to temp (extrinsic)
skeletal muscle- dual effect:
at rest vasoconstrictor (extrinsic) tone is dominant, when excercise intrinsic predominates

54
Q

ability to regulate blood flow- local humoral factors: examples of vasodilators and vasoconstrictors

A

Vasocontriction:
- endothelian-1
-internal blood pressure (myogenic contraction)

Vasodilators:
-hypoxia
-adenosine
-bradykinin
-NO (L-Arg is converted into NO by No sythetase)
- K+, CO2, H+
- prostacyclin
- Tissue breakdown product

55
Q

ability to regulate blood flow- Hormonal factors:

A
  • vasoconstrictors: angiotensin II, ADH, Adrenaline (skin)
  • vasodilators: adrenaline (muscle), atrial natriuretic peptide
56
Q

ability to regulate blood flow- cardiopulmonary basoreceptors

A

stimulation of these causes a reduction in vasocontriction and reduces blood pressure
also reduced angiotensin, aldosterone and ADH production- lead to fluid loss, controll blood volume- controll blood flow

57
Q

ability to regulate blood flow- arterial baroreceptors

A

Short term
- detect pressure
- primarily located in carotid sinus and aortic arch
- afferent from glossopharyngeal nerve
- effernet from sympathetic and vagus nerve
- as BP increases, firing increases causing increase in Parasympathetic and decrease in sympathetic, decrease in cardiac output and reduced total peripheral resistance and decrease in blood pressure
- if change in pressure for a couple days baseline changes e.g. hypertension

58
Q

effect of chemoreceptors on blood pressure:

A
  • increase in pCO2 causes vasocontriction, increase in peripheral resistance, increase blood pressure
  • low pCO2 decrease medullary tonic activity and decrease bp
  • act similarly with pH
59
Q

Describe the electrical activation of the cardiac myocytes. Inculde the phase, what molecules move, whether its polarisation or depolarisation?

A

Phase 0, initial depolarisation: voltage-gated Na channels open, large influx of Na+ into cell
Phase 1, small repolarisation: shutting of voltage gated Na+ channels, transient outward current of K+ ions leaving the cell
Phase 2, Maintain depolarisation/plateu: voltage gated calcium channels open causing calcium to enter the cell and maintain depolarised state, countered by continued transient K+ loss
Phase 3, repolarisation: calcium channels close, delayed outward K+ channel open causing repolarisaton back to resting potential
Phase 4, maintaining resting potential: Na/K ATPase moves 3 Na+ out cell, 2 K+ into cell. Na leak channels passively move very small na+ into cell (1:100). K+ leak channels allow large amounts of K+ to diffuse out the cell (down conc gradient)

60
Q

where in heart in action potential initiated? how does this action potential travel to and across cardiac myocytes?

A

action potential triggerd by pacemaker cell in SAN, action potential passes to other cells by movemnt of molcules through gap junctions between cardiac myocytes

61
Q

Describe the electrical activation of the pacemaker cells. Inculde the phase, what molecules move, whether its polarisation or depolarisation?

A

Phase 0, depolarisation: When membrane potential reaches -40 mV, voltage gated Ca channels open causing an influx of calcium
Phase 1+2: not present i pacemaker cells
Phase 3, Repolarisation: At peak depolarisation voltage gated K channels open causing efflux of K, Ca channels shut
Phase 4: Slow influx of Na through HCN channels until -40mV. Current created is called pacemaker/funny current.
(Do not have a resting potential)

62
Q

refractory period - what is it? ABSOLUTE VS RELATIVE?

A

when channels are closed and inactive- 0.25 seconds long

  • absolute- cannot
  • relative- can but very difficult, some Na channels still inactive and K channels still open, only strong stimuli can cause action potential here
63
Q

Normal ECG calibration?

A

25 mm/s and 10 mm/1mV

64
Q

What do P waves represent?

A

atrial depolarisation/contraction

65
Q

What does PR interval represent? how long should this take?

A

time taken for electrical activity to move from atria to ventricles (AVN delay), should be between 120-200 ms

66
Q

What does QRS complex represent? How long should this take?

A

depolarisation/ contraction of ventricles, should be less than 120ms

67
Q

What does ST segemnt show?

A

isoelectric line between depolarisation and repolarisation of ventricles

68
Q

what does T wave show?

A

ventricular repolarisation

69
Q

What does QT interval represent?

A

time taken for ventricles to depolarise and repolarise

70
Q

isolectric point?

A

no net current flow in any direction
- movement in negative direction is net current flow away from lead
- movent in positive direction is net movement toward the lead

71
Q

How should an ECG be set up?

A

10 electrodes (12 leads)

-1 electrode on each limb (4)
-6 chest leads- V1-V6 on chest

-right leg electrode is used as neutral lead

-Right arm (augmented vector right)
- left arm (augmented vector left)
- left leg (augmented ector foot)

Creates a triangle

72
Q

difference between bipolar and unipolar leads?

A

bipolar- measure differnce in voltage between 2 electrodes
unipolar- measure difference between elctrode to reference (calculated from many electrodes)

73
Q

Leads I and II - rule of thumb

A

if QRS are ‘leaving each other’ then theres left axis deviation
if QRS are ‘reaching towards each other’ then thats right axis deviation

74
Q
A

lead I uses RA as negative and LA as positive
lead II uses RA as negatve and LL as positve
lead III uses LA as negative and LL as positive

75
Q

which are the inferior leads? what area do they prepresent?

A

Leads II, III and AVF, right coronary artery

76
Q

which are the lateral leads? what area do they prepresent?

A

Leads I, AVL and V5, V6- left circumflex artery

77
Q

which are the anterior leads? what area do they prepresent?

A

V2, V3 and V4- LAD

78
Q

which are the septal leads? what area do they prepresent?

A

V1 and V2- interventricular septum

CVR lecture flashcards (16 decks)

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