BIOL 0800 Reading- Chapter 12 Flashcards
(263 cards)
1
Q
What are the two components of blood?
A
Formed elements and plasma
2
Q
What is hematocrit?
A
The percentage of blood volume that is erythrocytes
3
Q
At any given moment, what percentage of blood volume is in the capillaries?
A
Only about 5%, even though that’s the percentage that’s doing most of the work
4
Q
What is the pulmonary circuit?
A
Blood pumped from right ventricle to lungs to left atrium into systemic circulation
5
Q
What is the systemic circuit?
A
Blood pumped from the left atrium to the organs/tissues to the right atrium
6
Q
What is the aorta?
A
Where the blood leaves the left ventricle to go to systemic circulation
7
Q
What is microcirculation?
A
Arterioles, capillaries, and venules
8
Q
What is the inferior vena cava? And superior?
A
Brings all the veins together to bring the blood back to right atrium from below the heart; superior brings back all the blood from above the heart
9
Q
What is the pulmonary trunk?
A
Brings blood from the right ventricle to the lungs via two pulmonary arteries (one to each lung)
10
Q
What is the pulmonary vein?
A
Brings blood back from the lungs to the left atrium
11
Q
What pattern does the branching of the capillaries create, and why?
A
Delivers blood to peripheral organs and tissues in parallel so that each only receives a fraction of the bloodflow
12
Q
How does circulation to the liver and anterior pituitary gland differ from regular circulation?
A
Blood passes through two capillary beds in series connected by veins before returning to the heart (called a portal system)
13
Q
What is a portal system?
A
When blood passes through two capillary beds in series, connected by veins, before returning to the heart
14
Q
What is the equation relating flow rate, hydrostatic pressure, and resistance?
A
F = deltaP/R
15
Q
What is the equation for resistance?
A
(8Lviscosity)/(pi*r^4) = R
16
Q
How are blood viscosity and hematocrit related?
A
Increase in hematocrit increases blood viscosity
17
Q
How does flow change if the radius of the blood vessel is halved?
A
Decreases by 16x, since R = 16x
18
Q
What are the pericardium, epicardium, and myocardium?
A
The fibrous sac enclosing the heart; the inner layer of the pericardium; the wall of the heart
19
Q
What is the difference between the left and right AV valves?
A
LAB RAT: left is bicuspid, right is tricuspid
20
Q
How do pressure differences interact with AV valves?
A
If atrial pressure is greater, valve opens; If ventricular pressure is higher during contraction, valve is forced shut
21
Q
What is the pulmonary valve?
A
From the right ventricle to the pulmonary trunk
22
Q
What is the aortic valve?
A
From the left ventricle to the aorta
23
Q
What are the two semilunar valves?
A
From the ventricles to their respective vessels
24
Q
What is the conducting system of the heart?
A
The cells that don’t contract but control normal heart excitation; in electrical contact with cardiac muscle cells via gap junctions
25
How do sympathetic postganglionic fibers interact with the heart?
Innervate the entire heart: release epi/norepi to beta-adrenergic receptors in atria and ventricles
26
How do parasympathetic fibers interact with the heart?
Innervate only the atria: release acetylcholine to muscarinic receptors on the atria
27
Where does initial depolarization of the myocardium begin?
SA node: conducting system cells near the right atrium near the entrance of the superior vena cava
28
Where is the SA node?
Near the right atrium by the entrance of the superior vena cava
29
Describe the path of depolarization triggered by the SA node.
Travels to atria (contract at virtually the same time); then to AV node at base of right atrium, which propagates to the ventricle slowly; then down the interventricular septum through the bundle of His; then to Purkinje fibers, which depolarizes both ventricles from the apex up, squeezing blood out
30
What is the AV node?
Located at base of right atrium; depolarized after atrial contraction; propagates the action potential slowly, allowing the atria to finish contracting before the ventricles contract
31
Where does the action potential go after leaving the AV node?
To the bundle of His: AV bundle; separates into right and left bundle branches that separate at the apex of the heart (bottom) to enter the left and right wall
32
What are the Purkinje fibers?
Fibers that rapidly distribute the impulse through the ventricles and make contact with ventricular myocardial cells to depolarize the rest of the ventricle
33
In what direction does ventricular contraction occur?
From apex to base, aka up the heart as if squeezing blood out
34
What two parts of the conducting system are the only conductive link between the aria and ventricles?
The AV node and Bundle of His
35
How do ion concentrations differ during cardiac action potentials from normal ones?
Na permeability up to depolarize and K permeability down; but then no repolarization: K permeability stays low and Ca permeability increases: stays depolarized around 0 mV
36
Why is there no rapid repolarization in cardiac action potentials?
K channels stay closed, and Ca permeability increases
37
Why does Ca permeability increase during cardiac action potentials?
Initial depolarization opens Ca channels and influx of Ca: L-type Ca channels
38
What are L-type Ca channels?
Channels in the myocardial cells that open during initial depolarization to allow an influx of Ca into the cell to balance the eflux of K out after Na influx; modified DHP receptors which were voltage-sensitive for skeletal muscle contraction
39
Which has a shorter plateau phase, atrial or ventricular cells?
Atrial
40
What is pacemaker potential?
The gradual depolarization from the plateau caused by Ca influx from L-type Ca channels
41
What are the three ion channel mechanisms that contribute to pacemaker potential?
K channels, F-type channels, and T-type Ca channels
42
What are F-type channels?
Funny channels: nonspecific cation channels that open at negative membrane potential values: conduct an inward depolarizing Na current
43
What are T-type Ca channels?
Ca channels that open briefly and contribute to inward Ca current to boost depolarization in pacemaker potential
44
Why do SA node cells initiate action potentials rather than AV node cells, if they're similar in shape?
Because pacemaker currents of SA node cells are brought to threshold more rapidly than AV node cells
45
Why is the AV node so slow at propagating cardiac excitation?
Because depolarization in nodal cells is caused by Ca influx from L-type Ca channels, which depolarize the membrane more slowly than voltage-gated Na channels do
46
What is the P wave?
Corresponds to atrial depolarization
47
What is the QRS complex?
Corresponds to ventricular depolarization
48
What is the T wave?
Ventricular repolarization
49
Why isn't atrial repolarization evident in an EKG wave?
Because it occurs at the same time as the QRS complex
50
What is Lead I?
Right hand (-) to left hand (+), ground at right ankle
51
What is Lead II?
Right hand (-) to left ankle (+), ground at right ankle
52
What is Lead III?
Left hand (-) to left ankle (+), ground at right ankle
53
How do augmented leads work?
Combine two electrodes into a single central electrode
54
What is Lead aVR?
Left arm and leg (-) to right arm (+); points up toward right shoulder [combines Lead III]
55
What is Lead aVL?
Right arm and left leg (-) to left arm (+); points up toward left shoulder [combines Lead II]
56
What is Lead aVF?
Right arm and left arm (-) to left leg (+); points down [combines Lead I]
57
What is the difference between partial block and complete block in EKG readings?
Partial block is when AV node damage permits only every other impulse to the ventricles; Complete block is when there is no synchrony between atrial and ventricular electrical activity and the ventricles are contracted by the slow bundle of His activity
58
How does excitation-contraction coupling with in cardiac muscle cells?
The Ca influx from L-type Ca channels during prolonger depolarization triggers greater release of Ca from ryanodine receptors in the SR, for standard thin filament binding and crossbridge cycling
59
Is ventricular muscle capable of contraction summation?
No: because of long absolute refractory period
60
What is the absolute refractory period of the heart?
The period during and following an action potential when the heart can't be re=excited: due to prolonger plateau of depolarization
61
What is systole?
The period of ventricular contraction and blood ejection
62
What is diastole?
The period of ventricular relaxation and blood filling
63
What are the two parts of systole?
IVC and ejection
64
What are the two parts of diastole?
IVR and filling
65
When is the only time during the cardiac cycle that all valves are closed?
IVC and IVR
66
What is EDV?
The amount of blood in the ventricle after ventricular diastole
67
What is ESV?
The amoutn of blood remaining after ejection
68
What is stroke volume?
EDV-ESV
69
What is a typical stroke volume for an adult at rest?
135-65 = 70 mL
70
How does the T wave correspond to action potentials?
Represents the end of the plateau phase of the action potential: onset of ventricular repolarization
71
What is the dicrotic notch?
The decrease and rebound of aortic pressure caused when the aortic valve closes (since aortic pressure is greater than the relaxing ventricular pressure), due to blood rebounding against the valve
72
How does typical pulmonary artery sys/dias differ from systemic?
Much lower: 25/10 vs 120/80
73
What is "lub?"
The first heart sound: closing of the AV valves, onset of systole
74
What is "dup?"
The second heart sound: closing of the pulmonary and aortic valves: onset of diastole
75
What is stenosis?
Abnormally narrowed valves
76
What is cardiac output?
The volume of blood each ventricle pumps, in L/min: volume of blood flowing through either the systemic or pulmonary circuit per minute
77
What is the formula for cardiac output?
CO = HR x SV
78
What is a normal cardiac output for a resting adult?
5.0 L/min
79
What is typical total blood volume?
5.0 L
80
Without any nervous system input, what is resting heart rate? Why is typical resting heart rate different?
100 bpm; but more parasympathetic input than sympathetic, so closer to 70 bpm
81
How does sympathetic NS increase heart rate?
Increases pacemaker potential slope by increasing F-type channel permeability: faster depolarization, SA nodal cells reach threshold faster, heart rate increases
82
How does parasympathetic NS decrease heart rate?
Decreases pacemaker potential slope due to reduction of inward current, so threshold is reached slowly and heart rate decreases; increased SA node cell permeability to K+
83
What are the three main factors that affect stroke volume?
Changes in EDV, changes in sympathetic NS input magnitude, and changes in afterload
84
What is preload?
The volume of blood in the ventricles just before contraction
85
What is afterload?
The arterial pressures against which the ventricles pump
86
What is the Frank-Starling mechanism?
Stroke volume increases as EDV increases
87
Why does the Frank-Staling mechanism work?
Because greater EDV stretches the ventricular sarcomeres before contraction, allowing a more forceful contraction later on, which puts out more SV
88
Why does cardiac muscle cell force increase more steeply as a function of sarcomere length than in skeletal muscle cells?
Because stretching the sarcomeres toward optimum length decreases spacing between thick/thin filaments (allows more crossbridge binding), and increases sensitivity of troponin for Ca and increases Ca release from the SR
89
What is the significance of the FS mechanism?
At any given heart rate, venous return increase forces an increase in cardiac output by increasing EDV and thus SV
90
How do epi/norepi increase contractility?
Act on beta-adrenergic receptors
91
What is ejection fraction?
SV/EDV = EF
92
What is standard EF?
Between 50% and 75%
93
What are the cellular mechanisms that regulate sympathetic myocardial contractility?
Adrenergic receptors activate G-protein coupled cascades (to produce cAMP and activate a protein kinase), which phosphorylates proteins to enhance contracility (L-type Ca channels, ryanodine receptors and proteins in the SR membrane, thin filament proteins (troponin), thick filament proteins, and Ca pump proteins)
94
Does parasympathetic NS activity affect ventricular contraction?
Not really: little parasympathetic innervation of ventricles
95
How does afterload affect stroke volume?
Greater load (increased arterial pressure) reduces stroke volume, because it's harder to push blood through against the pressure
96
What is echocardiography?
Beaming ultrasonic waves at the heart and electronically plotting the echoes
97
What is cardiac angiography?
Requires temporary threading of a thin flexible tube (catheter) through an artery/vein into the heart and injecting a radio-opaque contrast material for tracking
98
What is the formula for compliance?
Compliace = delta V / delta P
99
What is systolic pressure?
The maximum arterial pressure reached during peak ventricular ejection
100
What is diastolic pressure?
The minimum arterial pressure that occurs just before ventricular ejection begins
101
What is pulse pressure?
The difference between systolic and diastolic pressures
102
What are the three most important factors in determining pulse pressure?
Stroke volume, speed of ejection of stroke volume, and arterial compliance
103
How does SV affect pulse pressure?
Greater SV increases pulse pressure
104
How does speed of ejection affect pulse pressure?
Greater speed of ejection increases pulse pressure
105
How does arterial compliance affect pulse pressure?
Greater compliance decreases pulse pressure
106
What is mean arterial pressure?
The average pressure in the cardiac cycle
107
How do you calculate MAP?
DP + (1/3)(SP-DP)
108
Why is MAP the most important measure of arterial pressure?
Because it's the pressure driving blood into the tissues averaged over the entire cardiac cycle
109
Does compliance have a major influence on the MAP?
No: compliance affects SP and DP inversely, so it averages out to the same MAP
110
How does a sphygmomanometer work?
Increase pressure on arteries to greater than SP to cut them off, and slwoly opens up to allow spurts of blodo through at peaks of SP: when you hear the Korotkoff's sounds, you know that's the peak SP, and then when the sounds go away, there's continuous flow, signifying DP
111
What are the two major roles of arterioles?
Determining relative blood flow to organs at any given MAP, and determining MAP itself
112
What is the equation for blood flow through any organ?
F = (MAP- venous pressure)/ Resistance of organ
113
What does flow difference throughout the body depend on?
Relative resistance of respective arterioles, not MAP, because MAP is the same throughout the body
114
What is intrinsic tone?
The spontaneous contractile activity of ateriolar smooth muscle
115
What is the result of an increase in contractile force above the intrinsic tone?
Vasoconstriction (and the opposite would eb vasodilation)
116
What are the two mechanisms controlling vascon or vasodil?
Local controls and extrinsic (or reflex) controls
117
What are local controls?
Mechanisms independent of nerves or hormones by which organs/tissues alter their own arteriolar resistances and self-regulate their blod flows
118
What does self-regulation of blood flow by autocrine/paracrine substance through local control include?
Active hyperemia, flow autoregulation, reactive hyperemia, and local response to injury
119
What is active hyperemia?
When metabolic activity of organs/tissues is increased due to increased blood flow
120
What is active hyperemia a result of?
Arteriolar dilation in the more active organ or tissue
121
What are the factors that cause arteriolar smooth muscle to relax in active hyperemia?
Local chemical changes in the ECF surrounding the arterioles
122
What is one of the most obvious chemical changes when tissues become more active?
Decrease in local oxygen concentration
123
What chemical factors increase when metabolism increases?
Carbon dioxide, hydrogen ions, adenosine from ATP breakdown; K ions from repeated repolarization; eicosanoids from membrane phospholipid breakdown; bradykinin (peptide generated locally from kininogen by action of kallikrein enzyme); NO released by endothelial cells
124
What is flow autoregulation?
The change in resistance in the direction of maintaining blood flow as constant in the face of pressure change
125
What is the mechanism for flow autoregulation?
Arterial pressure decrease lowers blood flow and oxygen supply while increasing other chemical factors (carbon xioide, potassium, adenosine, etc.) just like in metabolic activity: results in vasodilation
126
Can flow autoregulation involve vasoconstriction? When?
Yes, when arterial pressure increases: removes local vasodilator chemical factors faster than they are produced, and increases oxygen concentration: causes constriction to maintain relatively constant local flow
127
What is the myogenic response?
The direct responses of arteriolar smooth muscle to stretch, caused y changes in Ca movements into smooth muscle cells through stretch-sensitive Ca channels
128
Describe myogenic responses to increased and decreased stretch.
Increased stretch: caused by increased arterial pressure, leads to greater contraction; Decreased stretch: caused by decreased arterial pressure, causes smooth muscle tone decrease
129
What is reactive hyperemia?
When organ/tissue has its blood supply completely occluded and causes a profound transient increase in blood flow as soon as occlusion is released
130
Reactive hyperemia is essentially an extreme form of what other local control mechanism?
Flow autoregulation
131
What happens during reactive hyperemia?
No blood flow causes dilation because of low oxygen and high vasodilator chemical factors, so blood flow increases greatly once occluson ends
132
What are the four main mechanisms of external control of vasocon/dil?
Sympathetic nerves, parasympathetic nerves, noncholinergic/nonadrenergic autonomic neurons, and hormones
133
How do sympathetic nerves affect arterial pressure?
Release norepi to alpha-adrenergic receptors on vascular smooth muscle to cause vasoconstriction
134
What is significant about the receptors for norepinephrine on the heart and on the arterioles?
Heart is beta-adrenergic, and arterioles is alpha-adrenergic: if you're going to block sympathetic nervous system activity on heart by beta-adrenergic blocking, then it won't affect the arteriolar constriction
135
What is the effect of the parasympathetic NS on arteriolar innervation?
Basically none. Ha ha ha.
136
How do noncholinergic/nonadrenergic automatic neurons affect the vasocon/dil?
Release other vasodilator substances like NO, especially in GI system
137
How does epinephrine interact with arteriolar receptors?
Binds to alpha receptors for vasoconstriction, but also to beta-2 receptors for relaxation, especially in the skeletal muscle
138
What two hormones constrict most arterioles?
Angiotensin II and vasopressin (ADH)
139
What hormone is a potent vasodilator?
Atrial natriuretic peptide
140
What kind of cells near smooth muscle cells can also affect vasoconstriction/dilation?
Endothelial cells
141
What is an important paracrine vasodilator released by endothelial cells?
NO, which used to be called EDRF
142
What vasodilator is released by endothelial cells, especiall in response to blood clotting?
Prostacyclin, or PGI2
143
What is one of the most important vasoconstrictor paracrine agents released by endothelial cells?
Endothelin1 or ET-1
144
What is the effect of increased shear stress on release of NO, PGI2, and ET-1?
Increased release of NO and PGI2, but less ET (more vasodilation, less vasoconstriction)
145
What is flow-induced arterial vasodilation?
When shear stress changes the release of NO, PGI2, and ET-1 to result in vasodilation
146
What is angiogenesis?
Growth of new capillaries
147
What is angiostatin?
A peptide that inhibits vessel growth and can reduce tumor size
148
What are intercellular clefts?
The narrow water-filled spaced between the flat cells of endothelial capillary walls
149
What are metarterioles?
Vessels that connect arterioles to venules that also deliver blood to capillaries, instead of directly through arterioles
150
What is the precapillary sphincter?
The site at which a capillary exits from a metarteriole
151
How does flow velocity change from arterioles to capillaries?
Slows down: allows for diffusion of nutrients
152
How quickly can ions and small polar molecules move across the capillaries?
Quickly: water-filled channels in capillary walls
153
How quickly can lipid-soluble molecules move across capillary walls?
Very quickly: pass right through the membrane
154
How quickly can proteins cross the capillary walls?
Slowly: small amounts of specific proteins like some hormones can cross by vesciel transport
155
How do leakiness of brain and liver capillaries differ?
Brain is very tight and not leaky; liver is very leaky to allow for protein resorption
156
What is bulk flow in the capillaries?
The exchange of plasma and interstitial fluid (there's lots more interstitial fluid than plasma)
157
What is the direction of bulk flow between plasma and interstitial fluid? Why?
Plasma out of the capillaries into the interstitial fluid, because interstitial fluid hydrostatic pressure is lower than capillary blood pressure
158
Why doesn't all the plasma filter out into the interstitial space?
Hydrostatic pressure differences favoring filtration is offset by an osmotic force opposing filtration
159
What is filtration for capillaries?
In the presence of a hydrostatic pressure difference cross the capillary wall, the capillary wall acts like a porous filter that allows protein-free plasma to move by bulk flow from capillary plasma to interstitial fluid through water filled channels
160
Why is there an osmotic flow of water into capillaries?
Because capillary plasma has a lower osmolarity due to the presence of nonpermeable protein colloids
161
What is net filtration pressure?
NFP = capillary pressure + interstitial fluid protein concentration - interstitial hydrostatic pressure - plasma protein concentratioin
162
What are the four Starling forces?
Pc, piIF, Pif, piC
163
What is capillary hydrostatic pressure, Pc?
Favors fluid movement out of the capillary
164
What is interstitial hydrostatic pressure Pif?
Favors fluid movements into the capillary
165
What is osmotic force due to plasma protein concentration, pi C?
Favors fluid movement into the capillary
166
What is osmotic force due to interstitial fluid protein concentration, pi IF?
Favors fluid movement out of the capillary
167
What is the capillary filtration coefficient?
The measure of how much fluid will filter per mmHg net filtration pressure; major factor in kidney capillaries, whereas usually not under physiological control
168
How does pulmonary capillary fluid dynamics differ?
Low pressure, low resistance system: so normal pulmonary capillary hydrostatic pressure (movement out of capillary into interstitium) is less, and is offset by greater protein concentration in the lung interstitium: Starling forces facor filtratio, but have an active lymphatic system for drainage
169
Why is there swelling during injury?
Histamines dilate arterioles and increase capillary pressure and filtration; endothelial cells distort and widen intercellular clefts which increases plasma protein interstitium concentration
170
What is the average driving pressure from the peripheral veins to the right atrium?
10-15 mmHg
171
What is the major function of veins?
To act as low-resistance conduits for blood flow from the tissues to the heart
172
Why is venous pressure important?
Determines venous return to the heart, which is a major determinant of EDV and SV
173
What does smooth muscle on veins do?
Innervated by sympathetic neurons that release norepinephrine to contract the venous smooth muscle: increases pressure and drives blood towards the heart
174
What three factors affect venous pressure?
Venous constriction, skeletal muscle pump, and respiratory pump
175
What is the skeletal muscle pump?
During skeletal muscle contraction, the veins in the muscle are partially compressed
176
What is the respiratory pump?
The diaphragm lowers during inspiration, increasing abdominal pressure and intraabdominal vein pressure; while the thorax pressure decreases intrathoracic vein and right atrium pressure: enhances venous return during inspiration
177
What are lymphatic capillaries?
Like capillaries, but are permeable to all interstitial fluid constituents, including protein
178
What is the main function of lymphatic vessels?
To carry interstitial fluid back into cardiovascular system
179
Where does the lymph fluid come from?
When blood moves through the capillaries, filtration is larger at the arterial end and lower at the venous end, but more large at the arterial end, so there's a net loss of about 4 L of fluid per day.
180
What is the formula for mean arterial pressure?
Cardiac output times total peripheral resistance
181
What is total peripheral resistance?
The sum of the resistances to flow offered by all the systemic blood vessels
182
Which is lower, total pulmonary vascular resistance, or total peripheral resistance?
Pulmonary!
183
What are baroreceptor reflexes?
Reflexes that bring about homeostatic adjustments to MAP
184
How do baroreceptor reflexes generally work?
Changes in autonomic nerve activity, and secretion of hormones (epinephrine, angiotensin II, and vasopressin)
185
What is the carotid sinus?
The branching nerve endings of the carotid arteries that are highly sensitive to stretch/distortion
186
What are the arterial baroreceptors?
The carotid sinuses and aortic arch baroreceptors
187
How is the rate of discharge of the carotid sinus related to the MAP?
Directly proportional
188
What is the medullary cardiovascular center?
The primary integrating center for the baroreceptor reflexes: interconnected neurons in the medulla oblongata
189
What does the medullary cardiovascular center do?
Receives input from baroreceptors to determine the rate of action potential firing of parasympathetic neurons to the heart and sympathetic neurons to the heart/arterioles/veins
190
How are concentrations of angiotensin II and vasopressin affected by decreased arterial pressure?
Increased concentrations
191
How is arterial baroreceptor discharge related to medullary cardiovascular center activity?
Increased baroreceptor discharge leads to decreased sympathetic outflow; decreased baroreceptor discharge (lower pressure) leads to increased sympathetic outflow
192
What is the single most important long-term determinant of blood pressure?
Blood volume
193
What happens to stroke volume, heart rate, cardiac output, total peripheral resistance, and mean arterial pressure during hemorrhage?
SV, CO, and MAP are restored to near-normal levels, and HR and TPR are increased to pre-hemorrhage levels
194
What is autotransfusion?
When, during hemorrhage, there is net flux of interstitial fluid into the capillaries because of blood loss and decreased blood volume, to restore blood volume to near-normal levels
195
What is erythropoeisis?
Maturation of immature red blood cells to restore blood volume
196
What are the three types of shock?
Hypovolemic (decrease in blood volume), low-resistance (decrease in T{R), and cardiogenic (extreme decrease in cardiac output)
197
Why do you feel faint upon standing up quickly?
Reduced venous return causes a drop in EDV and decreased ventricle stretch, reducing stroke volume and cardiac output and blood pressure
198
What happens to the heart during exercise?
MAP increases, pulse pressure increases, stroke volume increases, cardiac output increases, heart rate increases, TPR DECREASES
199
What are four factors promoting venous return during exercise?
Increased skeletal muscle pump activity, increased respiratory pump, sympathetic increase in venous tone, greater ease of blood flow from arteries to veins through dilates skeletal muscle arterioles
200
What is the main difference between prolonged cardiac activity and exercise like weight-lifting?
At a certain point, blood flow to the muscle decreased with weight-lifting, since the contraction cuts off blood flow
201
What are some factors limiting increase in cardiac output during reaching VO2 max?
Rapid heart rate which reduces diastolic filling time, inability of peripheral factors factoring venous return to increase ventricular filling further in the short time
202
What is diastolic dysfunction?
When ventricle walls have reduced compliance and can't fill normally, leading to reduced EDV and stroke volume
203
What is systolic dysfunction?
Myocardial damage results in a decrease in cardiac contractility, lowering stroke volume at any given EDV: manifested as decrease in ejection fraction
204
What is pulmonary edema?
Accumulation of fluid in the interstitial spaces of the lung due to left ventricular failure
205
What is hypertrophic cardiomyopathy?
Increase in thickness of the heart muscle and disruption of the myocytes and conducting cells in the cardiac walls: interferes with ejection and may cause arrhythmias
206
What is ischemia?
Insufficient blood flow
207
What is nitroglycerin?
Used as a vasodilator because breaks down into NO
208
What are the three main classes of plasma proteins?
Albumins, globulins, and fibrinogen
209
What is the most abundant class of plasma protein?
Albumins: synthesized by the liver
210
What is the site of erythrocyte production?
Bone marrow
211
What are reticulocytes?
Young erythrocytes that still have a few ribosomes that produce a weblike appearance
212
What characterizes unusually high erythrocyte production?
A higher percentage of reticulocytes in the blood stream, since they usually get broken down pretty quickly
213
Do RBCs have nuclei or most organelles?
Nope!
214
What is the major breakdown product of hemoglobin?
Bilirubin, which is returned to circulation and gives plasma its yellowy color
215
Which element in hemoglobin does oxygen bind to?
Iron
216
What is ferritin?
A protein that binds the iron store, mainly in the liver
217
What does transferrin do?
Delivers almost all plasma iron to bone marrow to be incorporated into RBCs
218
Why is folic acid necessary?
Required for synthesis of thymine, so for DNA formation and cell division, especially of RBCs
219
What is intrinsic factor, and what is it necessary for?
Protein that allows absorption of vitamin b12, which is required for folic acid actioin
220
Why do men have a higher hematocrit than women?
Testosterone stimulates erythropoeitin
221
What is polycythemia?
When there are more RBCs than normal; increases blood viscosity
222
What are polymorphonuclear granulocytes?
The three classes of WBCs with multilobed nuclei and abundant membrane-surrounded granules
223
What are the three classes of polymorphonuclear granulocytes?
Eosinophils, basophils, and neutrophils
224
What are the two other classes of leukocytes?
Monocytes (larger, one nucleus, less granules) and lumphocytes (large nucleus)
225
Where are WBCs produced?
Bone marrow
226
What are pluripotent hematopoietic stem cells?
Undifferentiated cells that can give rise to any kind of blood cell in the bone marrow
227
What is a megakaryocyte?
Large bone marrow cells that form platelets when their cytoplasm pinch off
228
What ate hematopoeitic growth factors?
Protein hormones and paracrine agents that proliferate and differentiate various progenitor cells and inhibit apoptosis
229
What is hemostasis? And hematoma?
Stoppage of bleeding; accumulation of blood in the tissues that occurs as a result of bleeding from vessels
230
What is the immediate inherent response when a blood vessel is injured?
Constriction: slows blood flow, glues cells closer together
231
What does staunching of blood flow during injury depend on?
Formation of a platelet plug and blood coagulation (clotting)
232
What is the von Willebrand factor?
A plasma protein secreted by endothelial cells and platelets that helps platelets adhere to collagen fibers to forma bridge between damaged vessel walls and the platelets
233
What is platelet activation during injury?
When the binding of platelets to collagen triggers the platelets to release their vesicle contents that induce changes in the platelets to result in platelet aggregation
234
What is platelet aggregation?
When platelet activation causes new platelets to adhere to old ones to create a platelet plug in the damaged vessel
235
What is thromboxane A2?
An eicosanoid synthesized when platelets adhere together; released into ECF, acts locally; stimulates more platelet aggregation and release of their secretory vesicle contents
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What are platelet plugs for?
Sealing small breaks in blood vessel walls
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What happens to the blood vessels when there is a break and platelet plugs form?
Vasoconstrict to reduce blood flow to the damaged area
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Why doesn't the platelet plug continue to expand once started?
Because the arachidonic acid that's used by platelet cells to make thromboxane A2 to stimulate platelet aggregation is also used by normal endothelial cells to produce PGI2, which inhibits platelet aggregation
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What is PGI2?
Inhibits platelet aggregation; also called prostacyclin
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What is blood coagulation?
Clotting: the transformation of blood into a solid gel called a clot/thrombus; consists mostly of fibrin
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What is the make component of a blood clot?
A protein called fibrin
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What is the dominant hemostatic defense to vessel damage?
Clotting: supplements the platelet plug
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What is the first specific step in the clotting cascade?
Prothrombin is converted by an enzyme into thrombin (also an enzyme), which catalyzes the reaction of splitting peptides from fibrinogen until it turns into fibrin
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How is fibrin made?
Prothrombin is converted into thrombin, which detaches peptides from fibrinogen into fibrin
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What is factor XIIIa?
The enzyme that strengthens and cross-links the newly "carved" fibrin
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How is factor XIIIa made?
Formed from plasma protein factor XIII by thrombin
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What kind of feedback is thrombin involved in?
Positive feedback
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Why are activated platelets essential to clotting, even if the main component of clots is fibrin?
Because the cascade of enzymatic reactions occurs on the surface of platelets, and because once activated, they display "Platelet factor" (PF) phospholipids that act as cofactors in clotting
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What are the two pathways that make up the early half of the clotting cascade?
Intrinsic pathway and extrinsic pathway
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What are the steps in the intrinsic pathway of early clotting?
XII is converted to XIIa due to collagen contact; this catalyes the conversion of XI to XIa, then IX to IXa (which activates VIII into VIIIa as a cofactor for next step), then X to Xa, then prothrombin to thrombin
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What problem in the clotting cascade causes the majority of hemophilia cases?
Problems with VIII's conversion to VIIIa, which is a cofactor for converting X to Xa
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What are the steps in the extrinsic pathway of early clotting?
Tissue factor protein (in outer plasma membrane of tissue cells, exposed after damage) binds to VII, into VIIa. Then catalyzes X into Xa (and also IX into IXa as a cofactor for more X to Xa conversion at intersection with intrinsic pathway)
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Do intrinsic and extrinsic pathways occur simultaneously or serially?
Serially: usually always starts with activation of tissue factor from damage, no by XII into XIIa
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How are large amounts of thrombin created if only the extrinsic pathway really produces it?
Positive feedback on factors V, VIII, and XI in the intrinsic pathway: independently triggers intrinsic pathway without XII into XIIa
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Why is the liver important to clotting?
Produces many clotting factors, and produces bile salts that are necessary for absorption of Vitamin K to make prothrombin and clotting factors
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What two substances inhibit platelet aggregation?
Prostacyclin (PGI2) and NO
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What are the three main anticlotting mechanisms?
With TFPI, with thrombin, and with antithrombin III
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How does TFPI inhibit clotting?
Secreted by endothelial cells: binds to VII-VIIa to inhibit X-Xa
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How does thrombin inhibit clotting?
Thrombin binds to endothelial cell receptors (thrombomodulin) to cause thrombin to bind to protein C to inactivate VIIIa and Va; interesting because thrombin activates VIII and V if endothelium is damaged, but inhibits them if intact
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How does antithrombin III inhibit clotting?
Inactivates thrombin and clotting factors when it binds to heparin on endothelial cells
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What is the fibrinolytic system?
Removes clots: plasminogen activated into plasmin by plasminogen activating factors: the plasmin enzyme breaks down clots
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What is t-PA?
Tissue plasminogen activator: secreted by endothelial cells; binds to fibrin during clot formation; this allows tPA to generate plasmin from plasminogen
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How does aspirin affect clotting?
Inhibits platelet COX (generates prostaglandins and thromboxanes), but not endothelial: no impairment of PGI2
