Exam 3: Ch 13 Blood Cardiac Cycle Flashcards
1
Q
Plasma Protein
A
Constitute 7-9% of plasma
2
Q
Three types of plasma proteins
A
- albumins
- globulins
- fibrinogen
3
Q
Albumin accounts for
A
- 60-80% of PP and smallest;
- made by liver
4
Q
Albumin Creates
A
colloid osmotic pressure that draws H20 from interstitial fluid into capillaries to maintain blood volume & pressure
5
Q
Globulins: 3 types
A
- alpha
- beta and
- gamma globulin
6
Q
Alpha and Beta globulins
A
made by liver and transport lipids and fat soluble vitamins
7
Q
Gamma globulins
A
antibodies produced by lymphocytes
8
Q
Fibrinogen
A
- (4% of PP);
- produced by liver;
- serves as clotting factor;
9
Q
Fibrinogen Converted to
A
- insoluble threads called fibrin during clotting process
10
Q
Anemia
A
any condition in which there is an abnormally low [hemoglobin] or RBC count
11
Q
Iron-deficiency Anemia
A
caused by deficiency of iron
12
Q
Pernicious Anemia
A
caused by inadequate [vitamin B12], which is needed for RBC production
13
Q
Aplastic Anemia
A
due to destruction of bone marrow
14
Q
Polycythemia
A
abnormal increase in RBC
15
Q
Antigens present on RBC surface specify
A
blood type
16
Q
Major antigen group is
A
ABO system
17
Q
Type A blood
A
- has only A antigens
- People with Type A blood make antibodies to Type B RBCs, but not to Type A
18
Q
Type B
A
- has only B antigens
- Type B blood has antibodies to Type A RBCs but not to Type B
19
Q
Type AB
A
- has both A & B antigens
- Type AB blood does not have antibodies to A or B
- Type AB is “universal recipient”
because does not make anti-A or anti-B antibodies; Won’t agglutinate donor’s RBCs
20
Q
Type O
A
has neither A or B antigens
- Type O has antibodies to both Type A and B
- Type O is “universal donor”
because lacks A and B antigens; recipient’s antibodies will not agglutinate donor’s Type O RBCs
21
Q
If different blood types are mixed
A
antibodies will cause mixture to agglutinate
22
Q
If blood types do not match
A
recipient’s antibodies agglutinate donor’s RBCs
23
Q
Rh Factor
A
Is another type of antigen found on RBCs
24
Q
Rh+ has
A
Rho(D) antigens; Rh- does not
25
Rh Factor Can cause problems when
- when Rh- mother has Rh+ babies
- At birth, mother may be exposed to Rh+ blood of fetus
- In later pregnancies mom may produce antibodies against Rh
26
Erythroblastosis fetalis
- mom may produce antibodies against Rh
| - antibodies cross placenta causing hemolysis of fetal RBCs
27
Hemostasis
cessation of bleeding
28
Hemostasis Promoted by
by reactions initiated by vessel injury
29
breakage of endothelial lining of vessels exposes
collagen proteins in subendothelial C.T. to the blood
30
breakage of endothelial lining of vessels Initiates
3 separate but overlapping hemostatic mechanisms
31
3 separate but overlapping hemostatic mechanisms
1. Vasoconstriction restricts blood flow to area
2. Formation of platelet plug
3. Production of web of fibrin proteins that penetrates and surrounds platelet plug, forming clot
32
Platelets
- smallest of formed elements
- lack nucleus
- are fragments of megakaryocytes
- amoeboid action
- constitute most of mass of blood clots
- last 5-9 days
33
Intact endothelium physically separates
blood from collagen and other clot forming factors
34
Endothelial cells secrete
prostacyclin (PGI2--a prostaglandin) and NO; that inhibit platelet aggregation and are vasodilators
35
Endothelial cell membranes have
enzyme = CD39 whose active site faces blood and converts ADP into AMP and Pi
36
Endothelial cell membranes inhibits platelet aggregation b/c
ADP is released by activated platelets and promotes platelet aggregation
37
Injured blood vessels =
= damage to endothelium;
| - allows platelets to bind to exposed collagen
38
von Willebrand factor
increases bond between collagen and platelets by binding to both
39
Platelets stick to
collagen randelease ADP and thromboxane A2 which recruit more platelets and = platelet release reaction occurs
40
= platelet release reaction occurs
= creates platelet plug in damaged vessel
41
Serotonin & thromboxane A2 stimulate
vasoconstriction, reducing blood flow to wound
42
ADP & thromboxane A2 cause
cause other platelets to become sticky & attach & undergo platelet release reaction; this continues until platelet plug is formed
43
Activation of platelets also causes
conversion of soluble PP fibrinogen into insoluble protein = fibrin
44
Platelets have fibrin binding sites so
so platelet plug becomes infiltrated by meshwork of fibrin; clot now contains platelets, fibrin & trapped RBCs
45
Platelet plug undergoes
- plug contraction to form more compact plug:
| - fluid is squeezed from clot
46
- Note: serum =
plasma w/o fibrinogen
47
Anticoagulants
| Clotting can be prevented by
- Ca+2 chelators (e.g. sodium citrate or EDTA)
- Heparin
- Coumarin
48
Heparin
- which activates antithrombin III
49
antithrombin III
blocks thrombin, which directly converts fibrinogen into fibrin
50
Coumarin
blocks clotting by inhibiting activation of Vit K
51
Vit K works indirectly by
reducing Ca+2 availability
52
Cardiac cycle =
repeating pattern of contraction & relaxation of heart
53
Systole
refers to contraction phase (~0.3 second)
54
Diastole
- refers to relaxation phase (~0.5 second)
- Both atria contract simultaneously
- Both ventricles follow 0.1-0.2 sec later
55
End-systolic volume
amount of blood left in ventricles at end of systole
56
Stroke volume
is amount of blood ejected from ventricles during systole
57
End-diastolic volume
is amount of blood left in ventricles at end of diastole
58
As ventricles begin contraction
pressure rises closing AV valves = called isovolumetric contraction because all valves are closed
59
When pressure in ventricles exceeds that in aorta,
semilunar valves open & ejection begins and as pressure in ventricle falls below that in aorta, back pressure closes semilunar valves
60
When pressure in ventricles falls below atria
AVs open & ventricles fill
61
During ventricular diastole
ventricles fill ~ 80%
62
Atrial systole sends
~ 20 % of the total ventricular blood into ventricles
63
Closing of AV & semilunar valves produces sounds that can be heard thru stethoscope
- lub
| - dub
64
Lub
(1st sound) produced by closing of AV valves (between atria & ventricles)
65
Dub
(2nd sound) produced by closing of semilunars (between ventricles and aorta or pulmonary artery)
66
Heart Murmurs
Are abnormal sounds produced by abnormal patterns of blood flow in heart
67
Heart Murmurs
| Many caused by
- by defective heart valves
- can be of congenital origin
- rheumatic fever
68
in rheumatic fever,
damage can be from antibodies made in response to strep infection
69
In mitral stenosis
mitral (left A-V) valve becomes thickened and calcified
| impairing blood flow from left atrium to left ventricle
70
in mitral stenosis
| causes
accumulation of blood in left ventricle that can lead to pulmonary hypertension
71
Valves are incompetent when
when do not close properly
| - can be from damage to papillary muscles
72
Mumurs caused by septal defects are
- septal defects are usually congenital
due to holes in septum between left and right sides of heart
- pressure causes blood to pass from left to right
73
Myocardial cells are
short, branched, & interconnected by gap junctions
74
myocardium
Entire muscle that forms chambers
75
myocardium Works in
functional syncitium
| because APs originating in any cell are transmitted to all others
76
myocardium Chambers separated by
nonconductive tissue
77
In normal heart, SA node in
in R-atrium, near superior vena cava functions as pacemaker
78
pacemaker potential
Exhibits slow spontaneous depolarization to threshold
79
Membrane voltage begins at
at -50mV and gradually depolarizes to -40 threshold
80
Spontaneous depolarization is caused by
Na+ flowing through channel that opens when hyperpolarized (HCN (hyperpolarization cyclic nucleotide) channel)
81
At threshold V-gated Ca2+ channels
- open, creating upstroke & contraction
| - Repolarization is via opening of V-gated K+ channels
82
Ectopic Pacemakers
- Other tissues in heart are spontaneously active but are slower than SA node
- are stimulated to produce APs by SA node before spontaneously depolarize to threshold
- If APs from SA node are prevented from reaching these, they will generate pacemaker potentials
83
Myocardial APs
| - Myocardial cells have RMP of
- –90 mV; depolarized to threshold by APs originating in SA node
- Upstroke occurs as V-gated Na+ channels open
84
Myocardial APs
| - MP rapidly increases to
+15mV & stays there for 200-300 msec (plateau phase); Plateau results from balance between slow Ca2+ influx & K+ efflux
Repolarization due to opening of extra K+ channels
85
APs from SA node spread through
- atrial myocardium via gap junctions
| - But need special pathway to ventricles because of non-conducting fibrous tissue
86
special pathway to ventricles
AV node at base of right atrium & bundle of His conduct APs to ventricles
87
In septum of ventricles
- bundle of His divides into right and left bundle branches
| - Which give rise to Purkinje fibers in walls of ventricles; these stimulate contraction of ventricles
88
Conduction of APs
- APs from SA node spread at rate of 0.8 -1 m/sec
- Time delay occurs as APs pass through AV node; has slow conduction of 0.03– 0.05 m/sec
- AP speed increases in Purkinje fibers to 5 m/sec and ventricular contraction begins 0.1–0.2 sec after contraction of atria
89
Excitation-Contraction Coupling
| - Depolarization of myocardial cells opens V-gated Ca2+ channels in sarcolema
- This depolarization opens V-gated and Ca2+ release channels in SR (calcium-stimulated-calcium-release)
- Ca2+ binds to troponin and stimulates contraction (as in skeletal muscle); During repolarization Ca2+ pumped out of sarcoplasm and into SR
90
Refractory Periods
- Heart contracts as syncytium and thus cannot sustain force; its AP lasts about 250 msec
- Has a refractory period almost as long as AP
- Cannot be stimulated to contract again until has relaxed; thus there is no summation
91
Electrocardiogram (ECG/EKG)
- Is a recording of electrical activity of heart conducted thru ions in body to surface and recorded by electrodes placed on the skin
92
NOTE: ECG is not recording of AP!! It is a
recording of the electrical activity of the heart
93
Changing position of ECG recording electrodes (leads)
a more complete picture
94
3 distinct waves are produced during cardiac cycle
- P wave caused by atrial depolarization
- QRS complex caused by ventricular depolarization
- T wave results from ventricular repolarization
- Atrial repolarization is hidden by the QRS complex
95
Correlation of ECG with Heart Sounds
- 1st heart sound (lub) comes immediately after QRS wave as AV valves close
- 2nd heart sound (dub) comes as T wave begins and semilunar valves close.
96
Is most common form of arteriosclerosis
- (hardening of arteries);
| - Accounts for 50% of deaths in US, Europe, and Japan
97
localized plaques
- (atheromas) reduce flow in an artery
| - and act as sites for thrombus (blood clots)
98
Plaques begin at
sites of damage to endothelium; from hypertension, smoking, high cholesterol, or diabetes
99
High blood cholesterol is associated with
- risk of atherosclerosis
| Cholesterol, is carried in blood attached to LDLs (low-density lipoproteins) and HDLs (high-density lipoproteins)
100
LDLs & HDLs are produced in
- in liver and taken into cells by receptor-mediated endocytosis
- in cells LDL is oxidized
101
Oxidized LDL
can injure endothelial cells facilitating plaque formation
102
Arteries have receptors for
for LDL but not HDL (only liver has HDL receptors), which is why HDL is not atherosclerotic
103
Ischemia
- occurs when blood supply to tissue is deficient
| - causes increased lactic acid from anaerobic metabolism
104
Myocardial ischemia is most commonly due to
atherosclerosis in coronary arteries and is often accompanied by angina pectoris (substernal pain) or left shoulder and arm pain
105
Myocardial infarction (MI)
= heart attack
- caused by prolonged (minutes) periods of ischemia resulting in necrosis
= leading cause of death in the world!!
106
```
Myocardial infarction (MI)
Diagnosed by
```
by high levels of creatine phosphate (CPK) & lactate dehydrogenase (LDH), and ↑plasma [troponin]
107
Arrhythmias are
- are abnormal heart rhythms are detectable by changes in ECG
- Heart rate <60/min is bradycardia;
- >100/min is tachycardia
108
Flutter
= coordinated contraction rates can be 200-300/min
109
Fibrillation
contraction of myocardial cells is uncoordinated & pumping ineffective
110
Ventricular fibrillation
is life-threatening
111
Electrical defibrillation
resynchronizes heart by depolarizing all cells at same time
112
AV node block occurs
when node is damaged
113
First–degree AV node block
is when conduction through AV node > 0.2 sec
| Causes long P-R interval
114
Second-degree AV node block
is when only 1 out of 2-4 atrial APs can pass to ventricles
| Causes P waves with no QRS
115
In third-degree or complete AV node block
- no atrial activity passes to ventricles
| Ventricles driven slowly by bundle of His or Purkinjes
