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Biol 1412 > Topic 11 > Flashcards

Topic 11 Flashcards

1
Q

2 major parts of the cardiac physiology

A
  • heart

- conduction system

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2
Q

Heart

A

dual pump with valves

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3
Q

Muscle cells of the heart connected by..

A

gap junctions

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4
Q

Conduction system produces

A

aps spontaneously (no stimulus) but at different rates

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5
Q

Conductions system is composed of…

A

non contractile cardiac muscle cells

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6
Q

Non contractile cardiac muscle cells are ..

A

modified to initiate and distribute impulses throughout the heart

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7
Q

4 parts of the conduction system

A
  • sinoatrial (SA) node
  • atrioventricular (AV) node
  • bundle of His (AV bundle) and bundle branches
  • purkinje fibres
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8
Q

Sinoatrial (SA) node

A

in right atrium. produces APs faster than other areas (pacemaker)

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9
Q

Sinoatrial node rate =

A

100 APs/min (modified by PSNS to be 75 aps/min at rest)

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10
Q

Atrioventricular (AV) node location and rate =

A

in right atrium . 50 aps/min

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11
Q

Bundle of His (AV bundle)

A

originates AV node. only route for electrical activity to go from atria to ventricles

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12
Q

Bundle branches

A

right and left. 30 APs/min

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13
Q

Purkinje fibres

A

terminal fibres stimulate contract of the ventricular myocardium

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14
Q

Purkinje rate

A

30 APs/min

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15
Q

Artificial pacemakers

A

stimulate if SA or AV node damaged

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16
Q

If conduction system damaged ..

A

next faster part becomes pacemaker (if SA damaged then AV node takes over)

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17
Q

Cells of the APs of SA and AV nodes

A

non contractile autorhythmic cardiac muscle cells (self excitable) and -40mV is threshold

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18
Q

Pacemaker potenital

A
  • low K permeability (K voltage gates closed).
  • slow inward leak of Na (Na voltage gates open)
  • causes slow depolarization toward threshold (-40mV)
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19
Q

AP depolarization for pacemaker potential

A
  • at threshold –> AP
  • Ca voltage gates open so Ca moves in and depol. (Na voltage gates close at threshold so not involved in AP)
  • Ca voltage gates close at peak
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20
Q

AP repolarization for pacemaker potential

A
  • K voltage gates open at peak so K out leads to repol.

- K gates close below thereshold

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21
Q

Na channels open at -50 mV for pacemaker potential then it..

A

starts pacemaker potential again. once K gates close so a continuous cycle.

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22
Q

Note for pacemaker activity

A

NO RMP!!

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23
Q

APs in ventricule myocardium

A
  • cells = contractile.
  • purkinje fibre AP –> ventricular (contractile) myocardial AP (spread cell to cell by gap junctions)
  • Resting MP= -90 mV
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24
Q

Depolarization of ventricular myocardial APs

A
  • Na voltage gates open fast = same gates as neuron, skel. muscle.
  • MP to +30 mV
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25
Q

Plateau of ventricular myocardial APs

A
  • Na channels close and inactivate (slight drop in MP)

- Ca slow voltage gates are open

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26
Q

Repolarization of ventricular myocardial APs

A
  • Ca channels close.

- K voltage gates open therefor K outflux and MP decreases to resting

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27
Q

Absolute refractory period of ventricular myocardial APs

A

LONG Na channels inactivated until MP to close to -70 mV

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28
Q

1st step in excitation contraction coupling in myocardial cells

A

open voltage gates Ca channels of AP = small increase cytosolic Ca (from ECF) so not enough trigger contraction

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29
Q

2nd step in excitation contraction coupling in myocardial cells

A

opens chemically gated Ca channels on SR so cytosolic Ca increases so it binds to troponin and leads to contraction

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30
Q

3rd step in excitation contraction coupling in myocardial cells

A

contraction. sliding filament mechanisms. begins a few msec after AP begins. duration of AP of 250 msec and duration of twitch is 300 msec therefor contraction almost over when AP ends. so NO summation and NO tetanus

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31
Q

Electrical activity (ECG)

A

small currents due to deploy/repol of heart move through salty body fluids. recording seen as waves which = sum of electrical activity of ALL myocardial cells (not AP)

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32
Q

Potential difference measured on body surface using..

A

electrode pairs: 1 pair = a lead

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33
Q

3 ECG waves

A
  • p wave
  • QRS wave
  • T wave
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34
Q

P wave of ECG

A

atrial depol. which is followed by contraction

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35
Q

QRS wave of ECG

A

ventricular depol. which is the contraction but is also atrial repol which causes relaxation. (masked by larger ventricular electrical event/ larger muscle mass)

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36
Q

T wave of ECG

A

ventricular repol. followed by relaxation

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37
Q

3 ECG intervals

A
  • P-Q
  • S-T
  • T-P
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38
Q

P-Q interval for ECG

A

atria contracted, signals passing through AV node

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39
Q

S-T interval for ECG

A

ventricles contacted, ratio relaxed

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40
Q

T-P interval for ECG

A

heart at rest

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41
Q

3 abnormalities of heart beat

A
  • tachycardia
  • bradycardia
  • heart block
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42
Q

Tachycardia

A

resting HR more than 100 bpm

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43
Q

Bradycardia

A

resting HR less than 60 bpm

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44
Q

Heart block

A

when conduction through the AV node slowed. get increased P-Q interval and ventricular may not contract after each atrial contraction

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45
Q

3rd degree heart block

A

no conduction through AV node, atria fire at SA node rate (75 APs/min), ventricles at bundle/purkinje rate (30 APs/min)

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46
Q

2 main events of the mechanical activity of the cardiac cycle

A
  • systole= contraction/emptying

- diastole= relaxation/filling

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47
Q

1 complete heartbeat =

A

diastole and systole of atria AND diastole and systole of ventricles

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48
Q

Timing of mechanical events

A

average resting HR = 75 beats/min therefore 0.8 sec/beat

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49
Q

Blood flow through heart due to..

A
  • pressure changes
  • valves
  • myocardial contraction (raises P)
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50
Q

In diast. ventricules have..

A

lowest P and blood flows into them

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51
Q

In syst. ventricules have ..

A

highest P and blood flows out of them

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52
Q

2 steps during ventricular systole

A
  • higher P in ventricles than atria forces AV valves shut therefore turbulence of blood gives first heart sound (LUB) shortly after QRS wave starts
  • P rises so higher P in ventricle than aorta/pull trunk pushes semilunar valves open and blood enters vessels
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53
Q

2 steps during ventricular diastole

A
  • P drops, higher P in aorta/pulm trunk than ventricles forces semilunar valves to shut therefore turbulence into 2nd heart sound (=DUB). mid T wave
  • AV valves open when P in ventricle drops below P in atria
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54
Q

2 heart sounds

A
  • turbulent flow= noisy due to blood turbulence when valves shut
  • laminar flow= no sound
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55
Q

Sounds of Kototkoff

A

turbulence heard in brachial artery during blood pressure measurements.

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56
Q

Begin and stop of Kototkoff sounds

A
  • begin = systolic pressure

- stop = diastolic pressure

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57
Q

Cardiac Output (CO)

A

volume of blood ejected by EACH ventricle in 1 min (ml/min)

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58
Q

Equation for CO

A

CO= heart rate x stroke volume

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59
Q

Stroke volume (SV)

A

volume ejected by each ventricle per beat

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60
Q

Stroke volume is equal

A

to the difference between EDV and ESV

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61
Q

End diastolic volume (EDV)

A

volume of blood in each ventricle at end of ventricular diastole (preload). approx 120 mL

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62
Q

End systolic volume (ESV)

A

volume of blood in each ventricle at the end of the ventricular systole (whats left after ejection) approx. 50 mL

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63
Q

therefore SV =

A

120 mL- 50 mL = 70 mL

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64
Q

How often does the total blood volume (5L) pass through both ventricles

A

every minute

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65
Q

CO may increase ___ during exercise

A

5 times

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66
Q

Control of heart rate

A

basic rate set by SA node (intrinsic control so built in) modifiers of HR (extrinsic control) so a change (not AP)

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67
Q

3 types of extrinsic heart rate control

A
  • neural
  • hormonal
  • other
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68
Q

SNS (thoracic nerves) neural extrinsic controls

A

Na channels open wider therefore increase Na permeability at SA node and increases slop of pacemaker potential therefore each threshold faster and increases HR

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69
Q

PSNS (vagus nerve) neural extrinsic controls

A
  • keeps resting HR lower than pace set by SA node alone. (sends continuous impulses)
  • increase K permeability at SA node therefore more -‘ve on repol. and decrease HR so further to go to threshold and takes longer
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70
Q

Hormonal extrinsic controls of heart rate

A
  • epinephrine, NE increase HR (some as SNS)
  • thyroid hormone direct effect to increase HR (slow and takes days)
  • increase number of epi receptors so more sensitive to epi
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71
Q

Ions as a extrinsic factor of heart rate

A
  • high K in ISF: MP more +’ve than normal so pacemaker Na channels may not open and can’t reach threshold. slows repol. which decrease in HR can lead to cardiac arrest
  • low K in ISF: evidence that K channels in some cells change specificity and allow Na through instead of K so it depol. membrane and increase HR (feeble beat abnormal)
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72
Q

Fever as an extrinsic factor of heart rate

A

increase temp so increase HR

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73
Q

Age as an extrinsic factor of heart rate

A

newborn = high

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74
Q

Fitness as an extrinsic factor of heart rate

A

increase fitness = decrease HR

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75
Q

Intrinsic control of stroke volume is..

A

hearts built in ability to vary SV and adjust to demands.

76
Q

Intrinsic control of stroke happens by..

A

increase venous return so EDV increases so increase heart muscle stretch and force of contraction and increase SV within physiological limits

77
Q

Relationship between EDV and SV (frank starlings low of the heart)

A

force of ejection is directly proportional to length of ventricular contractile fibres

78
Q

In intrinsic control of stroke volume you get increase venous return due to..

A
  • exercise: venous return speeded up

- lower HR so had longer to fill and less of an effect than exercise

79
Q

Extrinsic controls of stroke volume

A
  • ANS - SNS
  • hormones
  • other factors
80
Q

ANS SNS extrinsic controls

A

-increase force of contraction (for given EDV) and increase SV. (SNS stimulation ⇑ opening of Ca channels ⇒ ⇑ Ca into cytosol ∴ more cross bridges ∴ ⇑ force)..
BUT SNS also ⇑ HR = less time to fill ∴ have ⇓ EDV at higher HR. However, ⇑ force ⇓ ESV - compensates for ⇓ in EDV
-by increase both force and HR allows at least maintenance of SV even at high HR

81
Q

Overall for extrinsic controls of stroke volume

A

SNS increase CO and PSNS decreases CO

82
Q

Hormones as an extrinsic control of stroke volume

A
  • Epi, NE - same mechanism as SNS - ⇑ force - thyroid hormone - ⇑ force (+ ⇑ epi receptor #)
83
Q

Force increase of stroke volume by..

A
  • ⇑ external Ca++ (more Ca++ moves in on AP) - digitalis (drug) - ⇑ Ca++ inside
84
Q

Force decrease of stroke volume by..

A
  • acidosis - ⇑ external K+ - Ca++ channel blockers (drugs) e.g. verapamil
85
Q

Blood flow

A

volume of blood flowing through any tissue/min (i.e. mL/min)

86
Q

Blood flow in a vessel determines by..

A

pressure and resistance

87
Q

Relationship for blood flow

A

F = ΔP

R

88
Q

Relationship for blood flow where F =

A

flow

89
Q

Relationship for blood flow where ΔP =

A

blood pressure gradient (difference) between 2 points

  • ⇓ blood pressure from: aorta ⇒ arterioles (resistance vessels) ⇒ large veins (capacitance vessels)
90
Q

Relationship for blood flow where R =

A

resistance. it opposes flow - friction of blood rubbing against vessel walls

91
Q

Resistance for blood flow depends on…

A

a) vessel length †
b) viscosity of blood: these normally do not change
c) radius of arterioles most important: - major resistance vessels
- controlled by smooth muscle innervated by SNS

92
Q

Vasodilation

A

increase radius therefore decrease R and increase F. P in arty is low and P in organs is high so more blood to capillaries

93
Q

Vasoconstriction

A

decrease radios therefor increase distance and decrease flow. P in artery is high so blood backs up. P in organ is low so less blood flow into organ capillaries

94
Q

Blood flow to organs controls by..

A
  • vasodilatation

- vasoconstriction

95
Q
  • If vasoconstriction/

dilation is local (i.e. to 1 organ)

A

no observable change in systemic (arterial) BP

96
Q

If vasoconstriction/dilation is systemic then ..

A

systemic BP will change

97
Q

Vasoconstriction/dilation (arteriolar radius) controlled by

A
  • intrinsic regulation

- extrinsic regulation

98
Q

Intrinsic regulation of vasoconstriction dilation allows..

A

organ to control its own blood flow

99
Q

Myogenic regulation

A

(intrinsic) when smooth muscle is stretched, it contracts ∴ if ⇑ systemic blood P ⇒ arterioles constrict.

100
Q

Example of myogenic regulation

A
  • on standing ⇒ high arterial bp in feet (gravity) ∴ arterioles constrict ⇒ ⇓ flow into capillaries
  • on standing ⇒ low arterial bp in brain (gravity) ∴ arterioles dilate ⇒ ⇑ flow to brain capillaries
101
Q

Metabolic regulation

A

(intrinsic) if blood levels of e.g. O2 ⇓, CO2⇑, pH ⇓ (⇑ metabolism in organ) - endothelial cells + hemoglobin release nitric oxide ⇒ vasodilation ⇒ ⇑ blood flow to organ

102
Q

Both myogenic regulation and metabolic regulation maintain..

A

blood gases, pH levels and very important in heart, skel. muscle and brian

103
Q

Extrinsic regulation of vasoconstriction and dilation

A

external control by nervous system and endocrine system

104
Q

Neural (SNS) regulation of vasoconstriction and dilation

A
  • arteriolar vasocon. (except in brain - intrinsic regulation only) - vasodilation due to ⇓ SNS signals (only important PSNS effect = dilation of arterioles of penis/clitoris) - also venoconstriction (vein constriction)
105
Q

Hormonal regulation of vasoconstriction and dilation (epinephrine)

A
  • vasocon: skin, viscera - reinforces SNS - vasodil: heart, skel muscle, liver - opposes SNS
106
Q

SNS causes release of epi - what is arteriolar response?

A
  • in skin, viscera: both ⇒ vascon (blood shifted away to where it’s needed) - in heart, skel. muscle, liver: opposite effects ⇒ response mainly determined by metabolic regulation
107
Q

What does angiotensin 11 and ADH do to arteriolar response

A

vasoconstriction

108
Q

What does histamine do to arteriolar response

A

vasodilation

109
Q

Blood pressure

A

hydrostatic P exerted by blood on wall of vessel (clinically on the walls of the arteries)

110
Q

Systolic pressure

A

arterial bp produced by ventricular contraction

111
Q

Diastolic pressure

A

arterial bp due to recoil of elastic arteries (when ventricles are relaxed)

112
Q

What we measure in an artery…

A

120/80 = syst./diast

113
Q

Pulse pressure

A

systolic - diastolic

114
Q

Mean arterial pressure (MAP)

A

regulated by the body i.e. what the body measures

= average blood P through cardiac cycle BUT diastole is longer than systole, so MAP = diast. P + 1/3 pulse P

115
Q

MAP regulation

A
  • F = ΔP/R ∴ ΔP = FxR

- ΔP = MAP - venous P (P in veins ~ 0 ∴ ΔP = MAP)

116
Q

MAP regulated by controlling ..

A
  • cardiac output
  • TPR (arteriolar radius)
  • blood volume (affects venous return ∴ SV; also MAP directly)
117
Q

Neural control of MAP contain

A
  • baroreceptors

- chemoreceptors

118
Q

Baroreceptors reflexes

A

short term changes (standing) stretch receptors that monitor MAP in carotid sinus (brain bp) and aortic arch (systemic bp)

119
Q

Chemoreceptors reflexes

A

peripheral chemoreceptors respond to pH, CO2 (and O2) and found in aortic arch and carotid sinus (called “bodies”)
-involved in regulation of respiration, but affect bp

120
Q

Epinephrine in MAP

A

⇑ HR, force of contraction ∴⇑ CO ⇒ ⇑ MAP

121
Q

Renin-Angiotensin system in MAP

A

plasma angiotensinogen to angiotensin 11.

122
Q

Angiotensin ll causes..

A
  • ⇑ vasocon, ⇑ venocon ∴ ⇑ MAP - ⇑ aldosterone, ADH ∴ ⇑ renal Na+, H2O abs; ⇑ thirst ∴ ⇑ blood vol ⇒ ⇑ MAP
123
Q

Atrial natriuretic peptide (ANP) in MAP causes..

A

⇓ renin (∴ angio II), ⇓ aldosterone, ⇓ ADH = ⇑ urine production ∴⇓ blood vol. and ⇓ vasoconstriction
SO overall = ⇓ MAP

124
Q

Capillary exchange is between…

A

blood and ISF

125
Q

Capillary exchange is when solutes enter and leave capillaries by

A
  • diffusion
  • vesicular transport
  • mediated transport
126
Q

Diffusion of solute from capillary

A 
major route (except brain). includes CO2, O2, ions, aa, glucose, hormones etc
-usually between endothelial cells
127
Q

Vesicular tranport of solute from capillary

A

includes large proteins (e.g. antibodies)

  • occurs via transcytosis
  • endocytosis from blood into endothelial cell, then exocytosis from endothelial cell into ISF
128
Q

Mediated transport of solute from capillary

A

requires membrane carrier protein and important in the brain

129
Q

Fluid (h2o) enters (absorption) or leaves (filtration) capillaries by..

A
  • osmosis

- bulk flow (pressure differences)

130
Q

4 pressures involved with bulk flow in capillaries

A
    • blood hydrostatic P (BHP) = blood pressure
    • blood osmotic P (BOP) – due to plasma proteins
    • ISF hydrostatic P (IFHP) = 0 mmHg
    • ISF osmotic P (IFOP) - due to ISF proteins
131
Q

Net filtration pressure (NFP)

A

sum of hydrostatic and osmotic pressures acting on the capillary

132
Q

Bulk flow in capillaries in the body

A
  • 90% of filtered fluid reabsorbed to blood

- 10 % enters lymph ∴ ISF vol. remains relatively constant

133
Q

Edema

A

accumulation of fluid in the tissue (ISF) causing swelling

134
Q

Edema due to..

A

1) high blood pressure (⇑ BHP) 2) leakage of plasma proteins into ISF ⇒ inflammation (⇑ IFOP) 3) ⇓ plasma proteins (malnutrition, burns) (⇓BOP) 4) obstruction of lymph vessels - elephantiasis, surgery

135
Q

Circulatory shock is..

A

inadequate blood flow (⇓ O2, nutrients to cells)

136
Q

3 types of circulatory shock

A
  • Hypovolemic
  • Vascular
  • Cardiogenic
137
Q

Hypovolemic shock

A

decrease blood volume. due to blood loss, severe burns, diarrhea, vomiting

138
Q

Vascular shock

A

blood volume normal but vessels expanded. due to systemic vasodilation of blood vessels (decrease bp)

139
Q

2 example of vascular shock

A
  • anaphylactic shock (allergic reaction/ histamine)

- septic shock (bacterial toxins)

140
Q

Cardiogenic shock

A

pump failure so decrease CO and heart cannot sustain blood flow

141
Q

1st stage of shock: Compensatory

A

mechanisms can restore homeostasis by themselves. trigger SNS

    • ⇑ HR, generalized vasocon. (except to heart, brain) = ⇑ bp
    • ⇓ blood flow to kidneys triggers renin release - get angio II + aldosterone, ADH release ∴ vasocon., ⇑ Na+, H2O retention (maintain blood vol.), ⇑ thirst
142
Q

Compensatory stage includes..

A
  • baroreceptors
  • chemoreceptors
  • ischemia (lack of O2) of medulla
143
Q

2nd stage of shock: Progressive

A
    • mechanisms inadequate to restore homeostasis - requires intervention
    • CO ⇓ ∴ ⇓ bp in cardiac circ ∴ ⇓ cardiac activity
    • ⇓ blood to brain ⇒ ⇓ cardiovascular control
    • damage to viscera due to ⇓ blood flow, especially kidneys (can lead to renal failure)
144
Q

3rd stage of shock: Irreversible

A

⇓ CO ⇒ too little blood to heart ⇒ ⇓ CO. self-perpetuating cycle and leads to death

145
Q

Blood contains what 2 things

A

plasma and formed elements

146
Q

Plasma contains..

A
  • H2O
  • proteins
  • electrolytes
  • other solutes (nutrients, wastes, gases, hormones)
147
Q

H2O in plasma

A

transport medium and carries heat. (90.5%) of plasma is water

148
Q

Proteins in plasma

A
  • albumins (58%)
  • globulins (38%)
  • fibrinogen (4%)
149
Q

Protein functions in plasma

A
  • produce osmotic pressure (albumins
  • buffer pH (7.35-7.45)
  • α, β globulins: transport lipids, metal ions, hormones
  • γ (gamma) globulins = antibodies
  • clot formation
150
Q

Electrolytes (ions) in plasma

A

functions are membrane excitability and buffers HCO3

151
Q

Formed elements of blood include

A
  • RBC
  • WBC
  • platelets
152
Q

RBC functions

A
    • transport - O2 on iron (Fe) of heme; CO2 on globin
    • buffer - globin binds to H+ reversibly
    • carbonic anhydrase (CA) important for CO2 transport in blood
153
Q

Hemoglobin

A

Hb = 4 hemes + 4 globins (protein)

154
Q

1 iron (Fe)/heme =

A

4 Fe/Hb

155
Q

Hemeglobin brown down by macrophages into..

A
  • heme

- globin

156
Q

Heme

A
  • Fe removed + stored (liver, muscle, spleen)
  • from stores (or diet) ⇒ bone marrow cells make heme ⇒ RBCs
  • non-iron portion ⇒ bilirubin ⇒ excreted in bile from liver
157
Q

Jaundice

A

excess bilirubin in blood

158
Q

Jaundice is due to..

A
  • excess RBC breakdown; or
  • liver dysfunction (neonates ⇒ liver immature); or
  • blockage of bile excretion
159
Q

Globin

A

converted to amino acids (recycled)

160
Q

RBC have no..

A

nuclei/mitochondria so only anaerobic respiration

161
Q

WBC are either..

A

granulocytes or agranulucytes

162
Q

3 types of granulocytes

A
  • neutrophils
  • eosinophils
  • basophils
163
Q

Neutrophils

A

phagocytosis/ 1st to enter infected area

164
Q

Eosinophils

A

attack parasites. break down chemical released in allergic reactions

165
Q

Basophils

A

secrete histamine (inflammation) and secrete heparin (inhibits clotting)

166
Q

2 types of agranulocytes

A
  • monocytes

- lymphocytes

167
Q

Monocytes

A

enters tissues, enlarge to become phagocytic macrophages

168
Q

3 types of lymphocytes

A
  • T lymphocytes
  • B lymphocytes
  • Natrual killer cells
169
Q

T lymphocytes

A

helper T (Th) + cytotoxic T (CTLs) lymphocytes

170
Q

B lymphocytes

A

when activated give rise to plasma cells and secrete antibodies

171
Q

Natural killer cells (NKs)

A

attack foregone cells, normal cells

172
Q

Platelets

A

cell fragments from megakaryocytes in red marrow

173
Q

Functions of platelets

A
  • form platelet plug which prevent excess blood loss.

- contains granules (coagulation factors/ clotting)

174
Q

Hemostasis

A

process of stopping bleeding.

175
Q

Hemostasis involves

A
  • vascular spasm
  • platelet plug formation
  • clot formation
  • clot retraction and repair
  • fibrinolysis
176
Q

Vascular spasm

A

vasoconstriction of damaged arteries, arterioles. ⇓ blood flow (min. to hrs.)

177
Q

Platelet plug formation

A
    • platelets stick to damaged blood vessel, release chemicals (factors)
    • neighbouring healthy endothelial cells release a chemical, preventing spread of plug
    • plug formation requires a prostaglandin – PG formation inhibited by aspirin
178
Q

Factors of platelet plug formation do..

A

a) cause more platelets to stick (+ve feedback)
b) promote clotting
c) begin healing

179
Q

1st stage of clot formation: production of prothrombin activator by..

A

– extrinsic pathway - uses factors released by damaged tissues
– intrinsic pathway - uses factors contained in blood
→ usually both occur together - require Ca++, tissue, platelet and /or plasma factors

180
Q

2nd stage of clot formation ..

A

Prothrombin converted to thrombin

181
Q

3rd stage of clot formation

A

Fibrinogen converted to fibrin

182
Q

Thrombin

A

+ve feedback to ⇑ its own formation ⇒ thrombin trapped in clot, inactivated by plasma factors, washed away ∴ limits clot spread

183
Q

Clot retraction and repair

A

retraction: blood vessel edges pulled together
repair: fibrinoblasts from new CT, new endothelial cells repair lining

184
Q

Fibrinolysis

A

clot dissolution. fibrin digesting enzyme (plasmin). phagocytes then remove clot clumps

185
Q

Thrombus

A

stationary clot in an undamaged vessel

186
Q

Embolus

A

free floating clot

187
Q

Hemophilia

A

clotting abnormal/absent about 83% = type A and lack clotting factor Vlll

Biol 1412 (15 decks)

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