Exam 1 Flashcards
(189 cards)
1
Q
What is the #1 cause of death
A
CVD aka Cardiovascular disease
2
Q
What is the major underlying cause of CVD
A
Ischemia due to atherosclerosis
3
Q
What is atherosclerosis
A
Plaquing
4
Q
What is linked to high blood cholesterol
A
Atherogenesis
5
Q
Leukocyte recruitment and expression of pro-inflammatory cytokines characterize what
A
Early atherogenesis
6
Q
What promotes thrombosis
A
Inflammatory pathways
7
Q
What is Thrombosis is responsible for
A
MI and most strokes
8
Q
What can the nervous system modulate
A
Inflammation
9
Q
What is Hemostasis
A
Prevention of blood loss
10
Q
What are the Mechanisms of Hemostasis
A
Vascular Spasm, Form platelet plug, blood coagulation, and fibrous tissue growth to seal
11
Q
What is vascular constriction associated with
A
Trauma
12
Q
How do neural reflexes work in Hemostasis
A
SNS induced constriction from pain
13
Q
What is responsible for most of the constriction in hemostasis
A
Local myogenic spasm
14
Q
What is especially important in smaller vessels, and includes thromboxane A2 from platelets
A
Local Humoral factors
15
Q
What is the degree of spasm related to
A
Severity of the trauma
16
Q
What function as whole cells, but cannot divide
A
Platelets
17
Q
What do platelets contain
A
Contractile proteins, enzymes, calcium, ADP and ATP, Thromboxane A2, serotonin, growth factors
18
Q
What is the platelet cell membrane made of that makes it special
A
Glycoproteins that avoid the normal endothelium, but adhere to damaged area
19
Q
What do the phospholipids of a platelet cell membrane contain
A
Platelet factor 3
20
Q
What initiates clotting
A
Thromboplastin
21
Q
When platelets contact a damaged area they:
Select all that apply:
1) Swell
2) irregular form w/ irradiating processes protruding from surface
3) contractile proteins contract causing granule release
4) Secrete ADP, Thromboxane A2 & Serotonin
A
1,2,3,4
22
Q
What is a Vasoconstrictor and Potentiates the release of granule contents
A
Thromboxane A2
23
Q
What are these characteristics of 150,000-300,000; important in minute ruptures; half-life of 8-12 days
A
Platelets
24
Q
What prevents platelet aggregation, produces PGI2 (prostacyclin) and Factor VIII
A
Endothelium
25
What is factor VIII responsible for
Clotting
26
What is a Vasodilator, Stim platelet adenyl cyclase supressing the release of granules, and limits platelet extension
PGI2 (Prostacyclin)
27
What do Aspirin and Ibuprofen block
Fatty Acid Cyclooxygenase
28
What 2 things do Aspirin and Ibuprofen block production of by blocking fatty acid cyclooxygenase
Thromboxane A2 and Prostacyclin
29
What does FA cyclooxygenase convert ARA to
PGG2 and PGH2
30
What do anticoagulants do
Prevent clots from forming
31
What are the 3 types of anticoagulants
Chelators, Heparin, and Dicumarol
32
Which anticoagulant has complexes with Antithrobin III
Heparin
33
Which anticoagulant tye up calcium (citrate, oxylate)
Chelators
34
Which anticoagulant involves inhibition of Vit. K dependent factors
Dicumarol
35
What synthesizes factors II, VII, IX, X
Hepatocytes
36
Cumadin and Warfarin are what kind of anticoagulant
Dicumarol
37
What is the Lysis of clots used for
Dissolves colts that have already formed
38
What is required for the lysis of clots
Plasmin (from plasminogen)
39
What is plasminogen
Inactive form of plasmin
40
Where are endogenous activators of plasminogen found
Tissues, plasma, urine
41
What are Exogenous activators of plasminogen
Steptokinase and tPA (tissue plasminogen activator) 3 hour window for MI and stroke
42
When does most damage with reperfusion injury occur
Upon reperfusion
43
What specifically does the damage with reperfusion injuries
Formation of highly ROS w/ unpaired e- (free radicals)
44
What is the ability to open up alternate routes of blood flow to compensate for a blocked vessel
Collateralization
45
What may the SNS do in collateralization
Impede via vasoconstriction, or augment via release of neuropeptide Y (NPY)
46
What is a Thrombosis
Blood coagulation
47
What is the extrinsic mechanism of Thrombosis formation
Chemical factors released by damaged tissues
48
What is the intrinsic mechanism of Thrombosis formation
Requires only components in blood and trauma to blood or exposure to collagen
49
What 5 Clotting factors are synthesized in the liver
I, II, VII, IX, and X
50
How does Coumarin (warfarin or cumadin) depress liver formation of II, VII, IX, X
Blocking action of Vit. K
51
```
Name the Condition:
Sex linked on X chromosome
almost exclusively males
85% defect in factor VIII
15% defect in factor IX
Can range severe-mild
```
Hemophilia
52
What is the key step in clotting
Conversion of fibrinogen to fibrin which requires thrombin
53
What is an autoimmune disorder where the body makes antibodies against phospholipids in cell membranes causing abnormal clots to form
Antiphospholipid antibody syndrome
54
Increasing age, Male gender, Heredity (including race), Tobacco Smoke, High blood cholesterol, High blood pressure, Physical inactivity, Obesity/overweight, Diabetes Mellitus, High blood, homocysteine, are all Risk factors for what
Heart Disease
55
What AA in the blood may irritate blood vessels, promoting atherosclerosis
Homocysteine
56
What can cause cholesterol to become oxidized LDL
Homocysteine
57
T/F: Homocysteine is more likely to make blood clot
True
58
What can high levels of Homocysteine be reduced by
Increased intake of Folic Acid, B6 and B12
59
What antigen sets on RBCs are most likely to cause transfusion rxns if they are mismatched
A, B, O and the Rh factor
60
What are A and B antigens on RBCs known as
Agglutinogens
61
Why are A and B antigens known as Agglutinogens
When they are on RBCs, they cause most blood transfusion rxns
62
What is significant about the O antigen on a RBC
It is essentially functionless
63
Genetic locus has three alleles, IA, IB, IO that can combine into how many combinations
6
64
What determines if a person has one, none, or both surface antigens
Inheritance
65
When are Agglutinins produced
They arise spontaneously after birth (2-8 months)
66
What are Agglutinins
Soluble antibodies on RBCs
67
When are Agglutinins not produced
When the corresponding Agglutinogens are present on the RBC
68
When do antibodies peak, then decline for the rest of a persons life
Age 10
69
How common iss immediate hemolysis occur in mismatched transfusion
Uncommon/Less common
70
How common is delayed hemolysis in mismatched transfusions
Common/More common
71
Which antibody is primarily responsible for the lysis of RBCs
IgM
72
What is the most lethal effect of a mismatched transfusion reaction
Kidney failure
73
What blood type is the universal donor
O
74
What is the universal recipient
AB
75
Why does kidney failure occur in mismatched transfusion rxns
Toxic substances are released from the hemolysed RBCs
76
What potentially deadly effect can kidney failure lead to
Circulatory shock
77
What from lysed RBCs can precipitate and block renal tubules
Hemoglobin
78
T/F: Spontaneous Agglutinins can arise just like the A-B-O system
FALSE, Unlike the A-B-O system, Spontaneous Agglutinins CANNOT arise
79
What are the 6 Rh antigens (Rh factor)
C, D, E, c, d, e
80
What antigen is the most common and antigenic (85% of US pop)
D antigen (Rh +)
81
What is the Rh factor when the D antigen is missing
Rh-
82
What occurs when Rh+ blood is given to an individual with Rh- blood
Antibodies are created and slowly build until they reach max concentrations 2-4 months later
83
What is aka "Hemolytic disease of the Newborn"
Erythroblastosis Fetalis
84
Agglutination of fetal blood releases Hgb, which is converted by macrophages into bilirubin which causes
Jaundice
85
In most cases of Erythroblastosis Fetalis, the mother is RH(___) and the father is Rh(___), with the fetus being Rh(___) received from the father
Mom Rh-
Dad Rh+
Fetus Rh+
86
T/F: Erythroblastosis Fetalis is typically not seen in the firstborn, but more in the 2nd, and more again in the 3rd
TRUE
87
What can happen after birth in a newborn that had Erythroblastosis Fetalis
Mother's Rh Agglutinins can still circulate for 1-2 moths and destroy fetus RBCs leading to anemia
88
Erythroblastosis Fetalis can result in the enlargement of what in neonates
Liver and Spine
89
Bilirubin may precipitate in neurons of the brain causing what
Mental impairment (kernicterus)
90
What is the Tx for erythroblastosis Fetalis
Replacement of Neonate's blood with Rh- blood
91
What can be used to prevent Erythroblastosis Fetalis
Rh immunoglobulin globulin (RhoGAM), and anti-D antibody, given at 28-30 weeks of gestation
92
What is different about heart m.
It is Specialized excitatory and conductive fibers (AS node, AV node, Purkinje fibers
93
What allows for the functional syncytium of the heart
The presence of intercalated discs
94
What are intercalated discs
Low resistance pathways connecting cardiac cells end to end with the presence of gap junctions
95
What is the duration of the AP in cardiac m.
.2-.3 sec
96
What are the types of channels in cardiac m.
Fast Na+, Slow Ca++/Na+, and K+
97
When do we see a sharp inc. in Na+ permeability
Onset of depolarization
98
When do we see an inc. in Ca++ permeability
During the plateau
99
When do we see an inc. in K+ permeability
During the resting polarized state
100
What does Tetradotoxin do to Na+ channels
Tetradotoxin blocks them selectively changing a fast response to a slow response
101
If ion channels are open, what will the ion seek
The nearest equilibrium potential
102
What does membrane permeability depend on
Ion channels (open or closed)
103
What is concentration gradient favoring ion movement in one direction offset by
Electrical gradient
104
What is Er
Resting membrane potential
105
During Er in cardiac m., what are the states of the channels (open/closed)
Fast Na+ and slow Ca++/Na+ are closed and K+ are open
106
What is the net charge change accomplished by the Na+/K+ pump
Net loss of one + charge from int. Of cell keeping the interior of cell negative
107
What can bind to and inhibit the Na+/K+ pump
Digitalis
108
What is an absolute refractory period, and when does it occurs
Inability to re-stim cardiac death cell, and occurs during the plateau
109
What is the relative refractory period, and when does it occur
It requires a supra-normal stimulus during repolarization
110
What is different about the refractory periods in a slow response cardiac m. Cell
Relative refractory period is prolonged and refractory period is ~25% longer
111
Why are refractory periods prolonged in slow cardiac m. Cells
AV node and bundle, serves to protect ventricles from supra-ventricular arrhythmias
112
What is the normal pacemaker of the heart
SA node
113
What structure has a self excitatory nature, Less neg. Er, Spontaneously depolarizes at fastest rate, and contracts feebly
SA node
114
If you drive a self-excitatory cell at a rate faster than its own inherent rate, what will happen
The cell's own automaticity will be suppressed
115
What is the job of the AV node
Delay the wave of depolarization from entering the ventricle
116
What does the AV node allow the atria to do
Contract slightly ahead of the ventricles (.1 sec delay)
117
What is the conduction velocity like in the AV node
Slow due to smaller diameter fibers
118
What can the AV node do in absence of the SA node
May act as the pacemaker, but at a slower rate
119
What happens to the Cycle length as HR Increases
CL decreases
120
Which is shorter at a resting HR, systole or diastole
Systole
121
At a high HR, what may not fill adequately
The ventricle
122
During systole perfusion of the myocardium, what may restrict reperfusion
Contracting Cardiac m. Compressing blood vessels (esp. LV)
123
Isovolumic Contraction and ejection describe what part of the cardiac cycle
Systole
124
What phase of the cardiac cycle involves, isovolumic relaxation, rapid inflow, diastasis, and atrial systole
Diastole
125
What is End Diastolic Volume (EDV)
Volume in ventricles at the end of filling
126
What is End Systolic Volume (ESV)`
Volume in ventricles at the end of ejection
127
What is stroke volume
EDV-ESV; volume ejected by ventricles
128
What is Ejection fraction
% of EDV ejected, normal is 50-60%
129
What is the stretch on the wall prior to contraction
Preload (proportional to the EDV)
130
What is the impedance that the heart has to pump against Asa blood is ejected
After load
131
What is the A wave associated with
Atrial Contraction
132
What is the C wave associated with
Ventricular contraction
133
What is the V wave associated with
Atrial filling
134
What do valves open with
A forward pressure gradient
135
What do valves close with
A backward pressure gradient
136
What are the AV valves of the heart
Mitral and Tricuspid
137
What are the Semilunar valves of the heart
Aortic and Pulmonic
138
What valves have a stronger construction
Semilunar (Aortic and Pulmonic)
139
What valves are thin and flimsy, have chorda tendinea, and papillary m.
AV valves (Mitral and Tricuspid)
140
What is the function of Chorda Tendineae
Prevent valve prolapse
141
What is the function of papillary muscles
Inc. tension on Chorda Tendineae
142
What is a stenotic valve
Valve not open fully
143
What is a valve that does not close fully
Insufficient/regurgitant/leaky
144
What is vibrational noise called with valvular dysfunction
A murmur
145
When are aortic/pulmonary stenosis and mitral/tricuspid insufficiency heard
Systolic
146
When are aortic/pulmonary insufficiency and mitral/tricuspid stenosis heard
Diastolic
147
What can be heard in both systolic and diastolic
Patent ductus arteriosis or combined valvular defect
148
What is the Law of Laplace
At a given operating pressure, as ventricular radius inc., developed wall tension inc.
149
What is anything that affects HR called (inc. or dec.)
Chronotropic
150
What is anything that affects conduction velocity
Dromotropic
151
What is anything that affects the strength of contraction called
Inotropic
152
What is the Frank-Starling Law of the Heart
W/in physiologic limits, the heart will pump all the blood that returns to it without allowing excessive damming of blood in veins
153
What does inc. venous return cause
Inc. stretch of cardiac m. Fibers
154
What are the intrinsic effects of Frank-Starling
Inc. cross-bridge formation, inc. Ca++ influx, and inc. stretch on SA node
155
What is Heterometric auto regulation
Within limits, as cardiac fibers are stretched, the force of contraction is increased
156
What is Homeometric auto regulation
Ability to inc. strength of contraction independent of a length change
157
What 3 factors can induce Homeometric autoregulatoin
Flow, Pressure, and Rate
158
What will direct stretch on the SA node cause
Inc. Ca++ and/or Na+permeability which will inc. HR
159
The autonomic nervous system, Hormonal, Ionic, and Temperature influences are all what kind of influences
Extrinsic
160
What effect does Sympathetic innervation have on the heart
+ HR, + strength of contraction, and + conduction velocity
161
What effect does Parasympathetic innervation have on the heart
- HR, - Strength of contraction, and - conduction velocity
162
How does the ANS effect SNS interaction with the heart
SNS effects are blocked using propranolol (beta blocker)
163
What effect does the ANS have on parasympathetic nervous system
Para effects are blocked using Atropine, blocking muscarinic receptors (inc. HR and strength of contraction dec.
164
What exerts a dominant inhibitory influence on HR
Parasympathetic NS
165
What exerts a dominant stimulators influence on strength of contraction
Sympathetic NS
166
Direct innervation of Cardiac cells accounts for most of what
The SNS effect. Norepinephrine actin on Beta-1 receptors (85%)
167
What causes indirect effects of SNS influence
Circulating Catecholamines from adrenal medulla find way to cardiac Beta-1 receptors (15%)
168
Stimulation of the left stellar ganglion does what
Dec. ventricular fibrillation threshold, and prolonged QT interval
169
What does stim. Of the right stellar ganglion do
Inc. ventricular fibrillation threshold
170
The Cardioaccelerator (Bainbridge) reflex, helps to prevent what
Damning of blood in the heart and central veins
171
The Benzold-Jarisch relex relates to what structures
Baroreceptors in ventricles
172
What does the Benzold-Jarisch reflex result in
Hypotension and Bradycardia
173
What stimulates the Benzold-Jarisch reflex
Occlusion of circumflex artery and Inc in LVP and LV volume (aka aortic stenosis0
174
What are the major thyroid hormone influences on the heart
+ Inotropic, + Chronotropic, and Inc. in CO by Inc. BMR
175
What ionic effect does elevated K+ have
Dilation and flaccidity of cardiac m. And dec. in resting membrane potential
176
What ionic effect can elevated Ca++ have on the heart
Spastic Contractions
177
What effect does inc. temp have on HR and strength of contraction
HR inc 10 beats beer 1 degree inc. and Temporary inc in strength of contraction
178
What effect does a dec. in temp have on HR and strength of contraction
Dec. HR and strength of contraction
179
What is the preferred energy substrate for cardiac m.
Fatty acids-70% preferred, can also use glucose, glycerol, lactate, pyruvate, and AAs
180
75% of the energy the heart uses is converted to what
Heat
181
The 25% of energy used as work is broken down into what
Pressurization of blood (>99%) and Acceleration of blood (
182
Pressurization of the blood is what kind of energy
Potential energy
183
What is the acceleration of blood to its its ejection velocity is what kind of energy
Kinetic
184
What does an EKG measure
Potential differences across the surface of the myocardium with respect to time
185
Give the ranges: Normal HR, Tachycardia, Bradycardia
N 60-80, T >100, and B
186
What does the P wave signify
Atrial Depolarization
187
What does the QRS complex signify
Ventricular Depolarization
188
What does the T wave signify
Ventricular Repolarization
189
Why can you not see the atrial Repolarization wave
It is buried in the QRS complex
