Cardiovascular System Flashcards
Lec 21, 22, 23, 24, 25, 26, 27
1
Q
What are the parts of the cardiovascular system?
A
- heart - dual pump with valves, has 4 chambers. contractile cardiac mm cells connected by gap junctions. 2. conduction system - non-contractile cardiac mm cells modified to initiate and distribute impulses throughout the heart (conduction cells). and autorythmic cells that produce aps spontaneously (dont need stim), but at different rates.
2
Q
What are the parts of the conduction system? (list)
A
sinoatrial node, atrioventricular node, bundle of His (av bundle), purkinje fibres.
3
Q
What does to sinoatrial node do?
A
SA node in the right atrium is the pacemaker of the conduction system bc it produces aps faster than other areas at 100 aps/min. the PSNS fxns to slow the rate of aps to 75 a min during rest.
4
Q
What is the atrioventricular node?
A
AV node is in the right atrium and produces aps 50 a min.
5
Q
What is the bundle of His?
A
allows transmission of signals from one area to another. originates at AV node. the only route for electrical activity to go from atria to ventricles and bundle branches (right and left). rate = 30 aps/min.
6
Q
What are the purkinje fibres?
A
terminal (end) fibres, stimulate contraction of the ventricular myocardium. rate= 30 aps/min
7
Q
What is the pathway of APs in the heart?
A
Interatrial pathway; start at SA node –> aps go through atrial contractile myocardium (R and L) and contract as a unit bc of gap jxns. Internodal pathway; start at SA node –> AV node - delay of 0.1 sec to get through node due to small fibre size, allows ventricle to fill up with bl from atrial contraction –> bundle of His –> bundle branches –> purkinje fibres –> ventricular contractile myocardium - starts at apex, contracts as a unit bc of gap jxns
8
Q
What happens of the conduction system is damaged?
A
next fastest part becomes pacemaker. ie. if SA node damaged, AV node takes over (atria may not contract, and ventricles contract at AV speed - 50bpm). artificial pacemakers stimulate if SA or AV nodes damaged.
9
Q
What are the phases of APs in the SA and AV nodes, and what are the cells?
A
cells are non-contractile autorhythmic cardiac mm cells (self-excitable, produce APs). threshold -40 mV, NO RMP. 1. pacemaker potential 2. AP depolarization 3. AP repolarization 4. Na channels open at -50mV.
10
Q
What happens during phase 1 of APs in the SA and AV nodes?
A
Pacemaker potential= low K permeability (k voltage-gates closed) - so K staying in cell and making it pos. Na voltage gates are open and theres a slow inwards leak of Na, which causes slow depol toward thresh.
11
Q
What happens during phase 2 of APs in the SA and AV nodes?
A
AP depol= at threshold get AP. Na voltage gates close. Ca voltage gates open and influx of Ca into cell making it more pos. Ca gates close at peak of depol.
12
Q
What happens during phase 3 of APs in the SA and AV nodes?
A
AP repol= K voltage gates open and make cell more neg (k exiting cell). k gates close below the thresh
13
Q
What happens during phase 4 of APs in the SA and AV nodes?
A
Na channels open at -50mV= starts pacemaker potential again, continuous cycle.
14
Q
What are the phases of APs in the ventricular myocardium and what are the cells?
A
contractile cardiac mm. its a purkinje fibre AP, spread cell to cell by gap jxns. RMP= -90mV. 1. Depolarization 2. plateau 3. repolarization
15
Q
What happens during phase 1 of ventricular myocardium APs?
A
depol where Na voltage channels open (rlly fast) and MP gets to +30mV
16
Q
What happens during phase 2 of ventricular myocardium APs?
A
plateau where Na gates close and inactivate and we get a slight drop in the MP. Ca voltage channels open slowly which maintains depol
17
Q
What happens during phase 3 of ventricular myocardium APs?
A
repol where ca channels close and K voltage channels open and K going out of cell makes MP drop to resting
18
Q
What is the absolute refractory period in ventricular myocardium?
A
long - Na channels inactivated until MP is close to -70mV. plateau phase makes it take longer to get to repol and therefore near -70.
19
Q
How does excitation-contraction coupling happen in myocardial cells?
A
AP ion sarcolemma of contractile cell triggers Ca voltage gates to open and Ca goes into cytosol (during plateau) but not enough to trigger contraction. but ca binds to chemically gated ca channels on SR and they open, releasing more ca into cytosol, producing a large increase. ca binds to troponin, moves troponin-tropomyosin complex exposing actin binding sites, crossbrigdges form, leads to contraction. contraction is the sliding filament mechanism which begins a few msec after ap begins.
20
Q
What is the timeline of ap and twitch/contraction in myocardial cells?
A
AP is around 250 msec and twitch is around 300 msec. so contraction is almost over by the time the ap ends. this contracts summation, and therefore keeps tetanus from occurring, so theres an alternation btwn contraction and relaxation.
21
Q
What are the 3 components of the cardiac cycle?
A
- electrical activity 2. mechanical activity 3.blood flow though heart
22
Q
What is electrical activity?
A
sum of electrical activity of all myocardial cells. small currents due to depol and repol of heart move through salty body fluids. potential difference (ionic mvmts) measured on body surface using electrode pairs, one pair = a lead. recording seen as waves.
23
Q
What are the different ECG waves? (list)
A
P wave, QRS wave, T wave.
24
Q
What happens during the P wave?
A
atrial depolarization followed by atrial contraction.
25
What happens during the QRS wave?
ventricular depolarization followed by ventricular contraction. atrial repolarization and relaxation also happening but wave created by this is masked by the ventricles since they have a larger mm mass.
26
What happens during the T wave?
ventricular repolarization followed by ventricular relaxation.
27
What are the ECG intervals?
P-Q interval= atria contracted, signals passing through AV node. S-T interval= ventricles contracted, atria relaxed. T-P interval= heart at rest atria and ventricles relaxed.
28
What is tachycardia?
when resting HR is more than 100 bpm (too fast)
29
What is bradycardia?
when resting HR is less than 60 bpm (too slow)
30
What is heart block?
when conduction through AV node is slowed, get an increased P-Q interval, and ventricles may not contract after each atrial contraction. ex. 3rd degree heart block - no conduction through AV node - atria fire at SA node rate 75 ap/m but ventricles use bundle/purkinje rate thats 30 ap/m
31
What are the 2 events in mechanical activity?
systole and diastole. both events initiated by electrical activity
32
What is systole?
contraction, emptying
33
What is diastole?
relaxation, filling
34
What is one complete heart beat?
diastole and systole of the atria and ventricles
35
What is the timing of mechanical events?
avg resting hr is 75 bpm which is 0.8 sec/beat. atria are in systole for 0.1 sec and then diastole for 0.7 sec. ventricles enter systole 0.1 sec after atria, in systole for 0.3 sec and diastole for 0.5 sec.
36
What does blood flow through the heart happen due to?
a. emptying pressure changes (high P --> low P) b. valves c. myocardial contraction (raises P)
37
What is the path of blood flow?
starts in large veins ie vena cava and pulmonary veins. P= 4.6 mmHg --> venous return (bl flowing into atria) --> atria relaxed (diastole; P less than 4 mmHg) --> 80% of bl into ventricle passively --> ventricles relaxed (diastole; P nearly 0) --> atria contract (systole; following P wave) --> atrial P increases - remaining 20% of bl delivered into ventr) --> ventricles contract (systole; increases ventr P to max) and atria relax (diastole) --> ventricles relax (diastole; P decreases to min)
38
What happens during ventricular systole?
1. higher P in ventricles than atria forces atrioventrcular valves to shut, and the turbulence from bl gives first heart sound (LUB) shortly after QRS wave starts. 2. P rises - higher in ventricle than aorta/pulmonary trunk pushes semilunar valves to open and bl enters the vessels.
39
What happens during ventricular diastole?
1. P drops in ventricles and is higher in the aorta/pulmonary trunk, causing semilunar valves to shut, bl turbulence causes 2nd heart sound (DUB) happens mid T wave. 2. AV valves open when P in ventricles drops below P of atria
40
What is turbulent flow?
noisy due to blood turbulence when valves shut. (so blood moving around in compressed area)
41
What is laminar flow?
no sound bc blood flowing smoothly in vessels.
42
What are the korotkoff sounds?
turbulence heard in the brachial artery during blood pressure measurements. begin at systolic pressure end at diastolic pressure. due to cardiac cycle events
43
What is cardiac output?
volume of blood ejected by each ventricle in 1 min (ml/min). CO = HR x SV.
44
What is end diastolic volume?
volume of blood in each ventricle at the end of relaxation/diastole. max ventricular volume ˜120 ml
45
What is stroke volume?
part of the calculation for CO. volume of bl ejected by each ventricle per beat. its equal to the difference btwn EDV and ESV. (EDV-ESV) so 120ml - 50ml = 70ml
46
What is end systolic volume?
volume of blood in each ventricle at the end of contraction/systole. so whats left after ejection ˜50 ml.
47
What is the calculation for CO?
CO = 75 (HR) x 70(SV) = 5250 ml/min per ventricle --> 5250/1000= 5.25 L/min per ventricle. total bl vol in body is 5L meaning the total bl vol passes through each ventricle each minute. CO may increase 5x or more during exercise.
48
What are the different kinds of control of CO?
1. Control of HR 2. control of SV
49
What are the 2 different ways HR are controlled?
intrinsically (built in) and extrinsically (modify)
50
What is the intrinsic control of the HR?
basic rate set by SA node.
51
How does extrinsic control effect the HR?
modifiers of HR which change the pacemaker potential not the AP.
52
What are the types of extrinsic control? (list)
1. Neural - sns and psns 2. hormonal 3. other factors - ions, fever, age, physical fitness
53
How does the SNS control the HR?
by the thoracic nerves which sends sympathetic signals that cause Na channels to open wider, resulting in an increase of Na permeability at SA node. this causes the slope of the pacemaker potential to increase which allows the MP to reach the threshold for depol faster, leading to increased HR bc getting APs faster.
54
How does the PSNS control the HR?
by the vagus nerve which keeps the resting HR lower than the pace set by the SA node alone (sends continuous impulses). parasympathetic signals increase K permeability at the SA node which causes the MP to become more neg during repol and the cells take longer to reach the threshold for the next AP (slower depol) which results in a longer time btwn heart beats and a decreased HR
55
What are the hormonal controls for HR?
epi and NE - increase HR using the same mech as SNS (so increasing Na perm). thyroid hormone - directly increase HR but slow, takes days. also increase the number of epi receptors, so more sensitive to epi.
56
What are some other factors that control HR?
1. ions - high K in ISF; Mp is more pos than normal so pacemaker Na channels may not open. also slows repol (bc more pos), decreased HR may lead to cardiac arrest. 2. fever - increased temp - increased resting HR 3. age - newborn - high resting HR 4. physical fitness - higher fitness = decreased RHR
57
What are the 2 different ways stroke volume is controlled?
intrinsically (hearts built-in ability to vary stroke volume and adjust to demands) and extrinsically.
58
What is the intrinsic controls for stroke volume?
increase venous return --> increases EDV --> increase stretch of heart --> increases force of contraction by getting cardiac fibres to approach the optimal length and form more crossbridges, therefore froducing more tension and force --> increases stroke volume (within physiological limits). so having more blood come in (increased venous return, means more blood is squeezed out (SV).
59
What is the relationship btwn EDV and SV?
Frank-Starling's Law of the Heart.
60
What is Frank-Starling's Law of the Heart?
describes how the force of ejection is directly proportional to length of ventricular contractile fibers. (ie if theyre close to optimal length or not, and how many crossbridges are forming). so how with increased stretch from more blood in ventricles during relaxation, we get i higher force of contraction because more crossbridges form, and with higher FoC we get more blood ejected out of ventricles and therefore a higher SV.
61
What increases venous return?
exercise - venous return speeds up. lower HR - has longer to fill (less of an effect than exercise).
62
What are the extrinsic controls of SV (list)?
1. ANS - SNS and PSNS 2. hormones 3. other factors
63
How does the SNS control SV?
SNS increases the force of contraction for a given EDV, which increases SV. SNS does so by stimulating the opening of more Ca channels which increases Ca entry into the cytosol and causes more crossbridges for form thereby increasing the force of contraction. BUT SNS also increases HR, which gives the ventricles less time to fill, therefore theres a decrease in EDV at a higher HR. however, the increased force also decreases ESV (less blood in ventricles after contraction) which compensates for decrease in EDV. so by increasing both force and HR theres at least maintenance of SV but usu an increase even at high HR.
64
How does the PSNS control SV?
no significant effect on force of contraction just HR. so doesnt have an effect.
65
How does the ANS overall effect the CO?
SNS increases CO by increasing both HR and SV, PSNS decreases CO by decreasing HR and has no effect on SV.
66
How do hormones control the SV?
epi and NE - use the same mechanism as the SNS (open more Ca channels) to increase force of contraction and therefore increase the SV. thyroid hormone - increases force of contraction and increases the number of epi receptors in cardiac mm cells.
67
How do other factors increase force of contraction?
having an increase in external Ca, so more ca moves in on AP. digitalis a drug - increases Ca inside.
68
How do other factors decrease force of contraction?
acidosis (acid build up), increase in external K, Ca channel blockers (drugs like verapamil).
69
What is blood flow?
volume of blood flowing through any tissue per minute.
70
What is blood flow in a vessel determined by?
pressure and resistance
71
What is the equation for blood flow?
F = ∆P/R. where F= flow ∆P = blood pressure gradient (difference) btwn 2 points. so change in pressure btwn points. R = resistance.
72
In what ways does blood pressure change during blood circulation?
decrease in bp from aorta --> arterioles (resistance vessels) --> large veins (capacitance vessels - not stretchy)
73
What is resistance?
opposes flow - friction of bl rubbing against vessel walls.
74
What does resistance depend on?
1. vessel length 2. blood viscosity 3. radius of arterioles (major resistance vessels) controlled by smooth mm innervated by SNS. vasodilation - increases radius therefore increasing F and decreasing R. vasoconstriction - decreases radius therefore decreasing F and increasing R.
75
What is blood flow to organs controlled by?
1. vasoconstriction - P in artery increases bc bl backs up, while P in organ decreases bc less bl flows into organ capillaries 2. vasodilation - opposite, so P in artery decreases and flows without obstruction, while P in organ increases bc more bl flows into organ capillaries.
76
What is the difference btwn systemic and local vasocon/dil?
local means in 1 organ, where we dont get any observable changes in systemic bp. whereas systemic has an effect on systemic bp.
77
What is vasocon/dil controlled by? (list)
intrinsic regulation - allows organ to control its own bl flow 1. myogenic regulation 2. metabolic regulation. extrinsic regulation - ext control by NS and ES 1. neural regulation 2. hormonal regulation
78
What is myogenic regulation?
when smooth mm is stretched it contracts therefore if bp increases, arterioles constrict. ex. standing; high arterial pressure in feet so arterioles constrict, decreasing flow into capillaries. at same time, have low arterial pressure in brain so arterioles dilate to increase or maintain blood flow into capillaries.
79
What is metabolic regulation?
if bl lvls of O2 decrease, CO2 increase, pH decrease (meaning increase in metabolism in organ), endothelial cells and hemoglobin release nitric oxide causing vasodilation to increase bl flow to organs. oppo; if bl lvls of O2 increase, CO2 decrease, pH increase (meaning low metabolism), endothelial cells release endothelins which cause vasoconstriction and decrease bl flow to organs.
80
What is neural regulation (SNS) of vaso?
arteriolar vasoconstriction caused by SNS (except in brain which is only controlled intrinsically). vasodilation due to decrease in SNS signals - only NB OSNS effect is dilation of arterioles in penis/clit. venoconstriction (veins).
81
What is hormonal regulation of vaso?
epi - vasocon; skin, viscera - reinforces SNS. vasodil; heart, skel mm, liver - opposes SNS. other hormones - angiotensin II, ADH; vasocon, histamine; vasodil
82
What is blood pressure?
the hydrostatic pressure of blood pushing up against the walls of vessels. results when flow is opposed by resistance.
83
How is systolic pressure produced?
by ventricular contraction against vascular resistance
84
How is diastolic pressure produced?
by elastic arteries recoiling against vascular resistance when ventricles are relaxed.
85
What is pulse pressure?
systolic pressure - diastolic pressure.
86
What is mean arterial pressure and its equation?
MAP is regulated by the body/what the body measures, so systemic blood pressure. avg bl pressure through cardiac cycle. MAP= diastole P + 1/3 pulse P
87
What is the MAP regulation calculation?
MAP= CO x TPR (total peripheral resistance). ∆P = MAP
88
How is MAP regulated?
by controlling; 1. CO 2. TPR (arteriolar radius) 3. blood volume (affects venous return which affects, and also MAP directly). regulated extrinsically and intrinsically.
89
What is the extrinsic regulation of MAP (list)?
1. Neural control 2. hormonal control
90
What are the types of neural control of MAP? (list)
a. baroreceptor reflexes b. chemoreceptor reflexes
91
What do baroreceptor reflexes do?
short term changes to MAP ie standing. stretch receptors monitor MAP/bl flow in the; carotid sinus (brain bp) and the aortic arch (systemic bp).
92
How is MAP controlled when it increases?
Increased MAP --> increase baroreceptor impulses --> medulla (cardiovascular control centre) --> send signals to increase the PSNS which decreases CO, and at same time decreases SNS --> decreases epi secretion, decreases vasoconstriction, decreases venoconstriction so bl pools on veins and venous return decreases --> decrease CO --> decrease in MAP
93
How is MAP controlled when it decreases?
decreased MAP --> decrease in baroreceptor impulses --> medulla --> decreases PSNS which increases CO. at same time medulla --> increases SNS --> increases epi secretion, increases vasoconstriction, increases venoconstriction --> increases CO --> increases MAP.
94
What do chemoreceptor reflexes do?
peripheral chemoreceptors respind to change in pH, CO2, and O2. they are found in the aortic arch and carotid sinus. involved in regular respiration but affect bp.
95
What do the chemoreceptors do when CO2 increases, pH decreases, and O2 decreases?
increase chemoreceptor impulses to medulla cardiovascular centre --> sends signals to increase SNS and epi output --> causes increased vasoconstriction (increased TPR), increased HR, force of contraction 9increased CO) --> increased MAP.
96
What are the types of hormonal control for MAP? (list)
a. epi b. renin-angiotensin system c. atrial natriuretic peptide (ANP)
97
What does epi do to MAP?
increases Hr, FoC, which increases SV and therefore CO, leading to an increase in MAP.
98
What is the Renin-Angiotensin System?
plasma antiotensinogen --> activated by renin --> angiotensin I --> angiotensin-converting enzyme changes to --> angiotsensin II.
99
What does angiotensin II cause pertaining to MAP?
increases vasoconstriction and venoconstriction, therefore increasing MAP. increases aldosterone and ADH which act to increase renal Na, H2O absorption, and thirst which will increase bl vol and therefore MAP
100
What does ANP cause pertaining to MAP?
decrease in renin therefore a decrease in angiotensin II, decrease in aldosterone and ADH, so urine production decreases which decreases bl vol. decreases vasoconstriction. overall decreased MAP.
101
What is capillary exchange btwn?
blood in capillaries and interstitial fluid.
102
how do solutes enter and leave the capillary? (list)
diffusion, vesicular transport, mediated transport.
103
Explain diffusion at the capillaries.
mvmt of gases (O2, CO2), ions, aa, glucose, hormones. usually diffuse btwn endothelial cells along cap wall.
104
Explain vesicular transport at the capillaries.
large proteins ie antibodies. occurs via transcytosis which transports solutes from one side of the cell to the other. so have endocytosis from bl into endothelial cell, and then exocytosis from endothelial cell into interstitial fluid.
105
Explain mediated transport at the capillaries.
requires a memb transport prot. NB mainly in brain.
106
How does fluid enter or exit the capillaries?
entering is absorption and exiting is filtration. done by osmosis - due to conc difference, and bulk flow - due to pressure difference.
107
What are the 4 pressures involved in fluid absorption and filtration by capillaries?
blood hydrostatic pressure (BHP) - which is BP, filtration bc p pushes fluid out of cap. blood osmotic pressure (BOP) - mainly due to plasma proteins which pull fluid back into cap bc of their high [solute] (absorption). interstitial fluid hydrostatic pressure (IFHP) - pushes fluid into cap (absorption). interstitial fluid osmotic pressure (IFOP) - mainly due to ISF proteins that pull fluid into ISF bc of high [solute] (filtration).
108
What is net filtration pressure?
sum of hydrostatic and osmotic pressures acting on the capillary. NFP= (BHP + IFOP) promotes filtration + (BOP + IFHP) oppose filtration
109
What is the value of the 4 pressures form arteriolar end to venous end in a capillary?
Arteriolar end: BHP = 35 (filtration) IFOP = 3 bc not lots of prots in bl so not lots of fluid moving (filtration) BOP = 28 bc lots of plasma prot so lots of fluid moving (absorption) IFHP = 0. Venous end: BHP = 16 drops bc less P IFOP = 3 BOP = 28 IFHP = 0
110
What is the net filtration pressure at the arteriolar end?
NFP= (35 + 3) - (28 + 0) = 10mmHg so get filtration.
111
What is the net filtration pressure at the venous end?
NFP = (16 + 3) - (28 + 0) = -9mmHg so get absorption
112
What is the overall result of NFP across the whole capillary?
10 = (-9) = 1mmHg = net filtration. so in the body get 90% of filtered fluid reabsorbed into bl. 10% enters lymph. therefore ISF volume remains relatively constant.
113
What is edema?
accumulation of fluid in the tissue (ISF) causing swelling.
114
What is edema caused by?
1. high BP (increased BHP which causes more filtration) 2. leakage of plasma prots into ISF leading to inflammation (increases IFOP so get more filtration bc now more solute in ISF). 3. decrease plasma proteins from malnutrition or burns (decrease in BOP bc less solutes and now less absorption). 4. obstruction of lymph vessel - elephantiasis, surgery.
115
What is circulatory shock and the types?
inadequate bl flow to cells, tissues, organs. (decreased O2 and nutrients to cells). hypovolemic, vascular, cardiogenic.
116
What is hypovolemic shock?
from low bl volume. due to; bl loss, severs burns, diarrhea, vomiting.
117
What is vascular shock?
bl vol normal but vessels expanded/dilated. due to; systemic vasodilation of bl vessels which decreases BP. ex: anaphylactic shock; allergic rxns, due to lots of histamine released from mast cells. septic shock; due to bacterial toxins spread through body and lead to release of histamine.
118
What is cardiogenic shock?
pump/heart failure results in decreased CO. heart cannot sustain bl flow.
119
What are the stages if shock (list)?
1. compensatory 2. progressive 3. irreversible
120
What happens during the compensatory phase of shock?
compensates for bl loss. mechanisms can restore homeostasis. involves baroreceptors, chemoreceptors, ischemia/lack of O2 of medulla. these all trigger the SNS which; increases HR and generalized vasoconstriction (except to heart and brain) to increase BP. decrease bl flow to kidneys to trigger renin release and get angiotensin II aldosterone and ADH release which causes vasocon, incerased Na and H2) retention, and increased thirst.
121
What happens during the progressive stage of shock?
mechanisms inadequate to restore homeostasis so need medical intervention. decreased CO therefore decreased BP in cardiac circulation which will decrease cardiac activity. decreased bl to brain will decrease the ability of the brain to exert cardiovascular control. damage to viscera due to decreased bl flow, especially in kidneys (can lead to renal failure).
122
What happens during the irreversible stage of shock?
lost too much bl. decreased CO means too little bl to heart which further decreases CO. self-perpetuating cycle, leads to death.
123
what does blood contain (list)?
plasma that has H2o, proteins, electrolytes., other solutes. formed elements such as RBCs, WBCs, and platelets.
124
What are the components of plasma?
1. H2O - 90.5% which is a transport medium and carries heat. 2. proteins - 7%; albumin (58% of prots), globulins (38%), fibrinogen (4%). fxns; a. produce osmotic pressure b. buffer pH to keep it from changing. c. alpha and beta globulins transport lipids, metal ions, hormones. d. y (gamma) globulins are antibodies. e. lotformation 3. electrolytes (ions) - fxn; membrane excitability in neurons and buffers (H2O). 4. other solutes - nutrients, gases, wastes, hormones
125
What are the components of red blood cells (formed elements)?
RBCs have no nuclei or mito, so only anaerobic resp. fxn; a. transport O2 on iron of heme and CO2 on globin. b. buffer - globin binds t =o H reversibly. c. carbonic anhydrase - NB for CO2 transport in bl. Hemoglobin: HB = 4 hemes and 4 globins, with 4 irons. Hb broken down by macrophages into; a. heme; Fe removed and stored in liver, mm, or spleen from stores or diet - bone marrow cells make heme --> RBCs. non-iron portion --> bilirubin --> excreted in bile. b. globin - converted to aas, recycled.
126
What is jaundice?
excess bilirubin in bl bc; excess rbc breakdown or liver dysfxn or blockage if bile excretion.
127
What are the different types of white blood cells (basic list)?
1. granulocytes 2. arganulocytes
128
What are the diff kinds of granulocytes and their fxn?
1. neutrophils - phagocytic so do phagocytosis. first to enter infected area. 2. eosinophils - attack parasites, break down chemicals released in allergic rxns (histamine). 3. basophils - secrete histamine (increases inflammation), secrete heparin (inhibits local clotting)
129
What are the diff kinds of arganulocytes?
1. monocytes - large eaters. enter tissues, enlarge and become phagocytic macrophages .2. lymphocytes - T lymphocytes; Helper T (Th) and cytotoxic T lymphocytes (CTLs). B lymphocytes; when activated give rise to plasma cells, secrete antibodies. natural killer cells; attack foreign bodies, abnormal cells.
130
What are platelets?
cell fragments from megakaryocytes. fxns; form platelet plug - prevents excess bl loss. contain granules - coagulation factors (prots/chemicals involved in clotting)
131
What is hemostasis?
process of stopping bleeding.
132
What are the 5 stages of hemostasis?
1. vascular spasm 2. platelet plug formation 3. clot formation 4. clot retraction and repair 5. fibrinolysis.
133
What happens during vascular spasm?
vasoconstriction (closing gap) of damages arteries and arterioles. decreases bl flow from minutes to hours.
134
What happens during platelet plug formation?
platelets stick to damaged bv and release chemicals/factors which; a. cause more platelets to stick (pos feedback). b. promotes clotting c. begin healing. neighbouring healthy endothelial cells release a chemical preventing the spread of plug. plug formation requires a prostaglandin (inhibited by aspirin).
135
What are the 3 stages of clot formation (list)?
1. production of prothrombin activator 2. prothrombin converted to thrombin 3. fibrinogen converted to fibrin.
136
How is prothrombin activator produced?
extrinsic pathway - tissues in surrounding area. uses factors released by damaged tissues. intrinsic pathway - uses factors contained in bl. usu both occur together, require Ca, tissue, platelet and/or plasma factors.
137
How is prothrombin converted to thrombin?
prothrombin --prothrombin activator--> thrombin.
138
How is fibrinogen converted to fibrin?
fibrinogen --thrombin, CA--> fibrin. fibrin forms insoluble web of threads on the plug - traps formed elements.
139
Where do the factors come from?
diet, liver (plasma prots), damaged tissue, platelets. vitamin K required for synthesis of 4 factors.
140
What happens during clot retraction and repair?
retraction - bv edges pulled together. repair - fibroblasts form new CT, new endothelial cells repair lining.
141
What happens during fibrinolysis?
clot dissolution. fibrin digesting enzyme plasmin. plasminogen --factors--> plasmin (breaks down clot). phagocytes then remove clot in clumps.
142
What is a thrombus?
a stationary clot in an undamaged vessel.
143
What is an embolus>
free floating clot
144
What is hemophilia?
clotting is abnormal or absent. about 83% of ppl with this have type A where they lack clotting factor VIII.
