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Biol 233 > Exam 1: Cardiovascular > Flashcards

Exam 1: Cardiovascular Flashcards

1
Q

Clear, light yellow fluid that makes up a little over half of the blood volume

A

Plasma

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2
Q

Granulocyte Types (3)

A

Neutrophils, Eosinophils, Basophils

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3
Q

Agranulocyte Types (2)

A

Monocytes & Lymphocytes

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4
Q

Not cells, but fragments torn from megakaryocytes in the bone marrow

A

Platelets

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5
Q

What is Plasma made of?

A

water, proteins, nutrients, electrolytes, nitrogenous wastes, hormones, & gases

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6
Q

Categories of Plasma Proteins (3)

A

Albumin, Globulins, & Fibrinogen

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7
Q

What is the most abundant nitrogenous waste?

A

Urea

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8
Q

Which plasma protein is the smallest and most abundant

A

Albumin

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9
Q

Which plasma protein is divided into three classes and helps with transport, clotting, and immunity?

A

Globulins (alpha, beta, gamma)

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10
Q

Which plasma protein is a solute precursor to fibrin, is sticky, and helps to form blood clots?

A

Fibrinogen

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11
Q

Hematopoiesis

A

The production of blood, especially the formed elements (RBCs, WBCs, platelets)

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12
Q

What is the term for the type of cells that are the origin of all formed elements?

A

Hematopoietic Stem Cells

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13
Q

Hematopoietic Stem Cells become these specialized types of cells; each type produces a different class of formed element

A

Colony Forming Units

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14
Q

What is Hemoglobin?

A

A protein in the cytoplasm of all RBCs that can carry Oxygen and CO2

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15
Q

What is the structure of Hemoglobin?

A

2 alpha chains and 2 beta chains
Each chain has a nonprotein heme group that Oxygen binds to
Each chain also has a globin portion that CO2 binds to

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16
Q

What are some scenarios in which RBC production increases?

A

When bleeding, oxygen-rich blood is lost signaling the body to produce more

When training at high altitudes, the lack of O2 causes more RBCs to be produced so that more of the available Oxygen is captured and ready for use in the body

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17
Q

Erythropoiesis

A

Erythrocyte production, a process which takes 3-5 days

RBC count stays stable due to negative feedback. A lower count is detected by the Kidneys which in turn increases this process

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18
Q

What is the process of Erythropoiesis?

A

HSCs become erythrocyte CFUs that have receptors for erythropoietin (EPO), a hormone secreted by the kidneys that stimulates the CFU to become an erythroblast.

Erythroblasts multiply, build large populations, and synthesize hemoglobin

Erythroblast nuclei then shrivel and exit the cells, making the now brainless cells reticulocytes

Reticulocytes leave the bone marrow and enter the bloodstream where polyribosomes within the cells disintegrate until mature RBCs are made

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19
Q

This nutrient needs to be eaten so that erythropoiesis can occur and hemoglobin molecules can be made. It is lost mostly through urine. When in the body it is stored in the liver

A

Iron

When stored it is called Ferritin

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20
Q

Polycythemia (2 types) & its Dangers

A

An excess of RBCs

Primary - Cancer of the erythropoietic cell line in red bone marrow

Secondary - From dehydration, emphysema, high altitude, or physical conditioning

Dangers - Increased blood volume, pressure, and viscosity which can lead to embolism, stroke, or heart failure

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21
Q

Anemia (3 categories)

A

Too few RBCs:

Inadequate erythropoiesis or hemoglobin synthesis

Hemorrhagic anemias from bleeding

Hemolytic anemias from RBC destruction

Consequences - Tissue hypoxia and necrosis, Reduced blood osmolarity (causes edema), and Low blood viscosity (heart failure may follow)

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22
Q

Sickle Cell Disease

A

Caused by hereditary defects found in a recessive allele, mostly in African individuals

Sickled RBCs are sticky and prone to agglutination, blocking vessels and causing stroke, kidney failure, heart failure, joint pain, and paralysis

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23
Q

Antigens

A

“Markers” found on RBCs

Type A has A-antigens, Type B has B-antigens, Type AB has both, Type O has none

These markers help to identify foreign objects in the bloodstream

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24
Q

Antibodies & Antigens

A

Proteins that defend the body

Antibodies attack the antigens that are DIFFERENT from those on the RBCs

Type A blood will have Anti-B Antibodies that attack B-antigens

Type AB has both antigens but no antibodies - Universal Receiver

Type O has no antigens but both antibodies - Universal Donor

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25
Rh Groups
Another set of antigens (C, D, & E) found in the Rhesus Monkey Antigen D individuals are Rh+ because it is highly reactive Those without Antigen D are Rh- Anti-D antibodies will not be present in any individuals, although they can form in Rh- individuals after exposure to Rh+ blood
26
Neutrophil
The most abundant WBCs (60-70%) that are aggressively antibacterial, have multi-lobed nuclei, and granules
27
Eosinophil
Makes up 2-4%, two lobes of granules connected by a thin band
28
Basophil
Rarest formed element (<0.5% WBC count), the cell appears to be full of granules
29
Monocyte
The largest WBC makes up 3-8% of the count. After leaving the cell, they turn into macrophages, cells that perform phagocytosis to consume dying and dead host cells
30
Lymphocyte
The second most abundant WBC (22-35%) but the smallest in diameter, they turn into immune cells
31
Leukopoiesis
The production of WBCs HSCs differentiate into CFUs, which then go on to produce precursor cells, each of which will become a different type of WBC CFUs are stimulated by Colony-Stimulating Factors (CSFs), each stimulates a WBC type - Myeloblast - Become granulocytes - Monoblast - Identical to Myeloblasts but they become Monocytes - Lymphoblasts - Produce all lymphocyte types The red bone marrow stores granulocytes and monocytes until they are needed
32
Leukopenia
Lower than normal WBC count Seen in lead, arsenic, and mercury poisoning; radiation sickness, and infectious diseases like measles, mumps, chickenpox, polio, influenza, typhoid fever, and AIDS
33
Leukocytosis
A WBC count above normal, usually indicates/is caused by infection, allergy, or disease
34
Leukemia
Cancer of the hematopoietic tissues that produce high numbers of circulating leukocytes and their precursors
35
Hemostatic Mechanisms (3)
Vascular Spasm - Prompt constriction of a broken vessel that provides immediate protection against blood loss. Not effective in larger vessels Platelet Plug Formation - Collagen fibers on the vessel walls are exposed to blood. This blood exposure causes platelets to grow long, tiny pseudopods that stick to the vessel and other platelets. The pseudopods then contract to bring the vessel together Blood Clotting/Coagulation - Clotting of the blood where the goal is to convert plasma protein fibrinogen into fibrin, a protein that adheres to the vessel walls
36
Thrombopoiesis
A division of hematopoiesis that produces platelets. The process is stimulated by thrombopoietin, a hormone from the liver and kidneys Megakaryoblasts are HSCs that developed receptors for Thrombopoietin and are committed to platelet production Megakaryoblasts duplicate DNA repeatedly without dividing, forming a megakaryocyte, a giant cell that lives in the red bone marrow and migrates to the lungs Long tendrils from the megakaryocyte protrude into the blood where the flow breaks off fragments
37
Platelet Function
Secrete vasoconstrictors Stick together to form the platelet plugs Secrete procoagulants (clotting factors) Chemically attract neutrophils and monocytes to sites of inflammation Phagocytize bacteria Secrete growth factors that stimulate mitosis to repair blood vessels
38
Vascular Spasm
The immediate constriction of a broken vessel reduces immediate blood loss Caused by pain receptors initially, then stimulated by serotonin released by the platelets
39
Platelet Plug Formation
When a vessel is broken, the collagen in the vessel wall (tunica media) is exposed to blood. The platelets, once in contact with the collagen, begin growing long spiny pseudopods that adhere to the vessel wall and other platelets to form a platelet plug
40
Coagulation
Clotting of the blood where the goal is to convert the plasma protein fibrinogen into fibrin, a protein that adheres to the vessel walls
41
Mechanisms of Coagulation (2)
Extrinsic Mechanism of Activation - Initiated by clotting factors released by the damaged blood vessels (thromboplastin from tissues) Internal Mechanism of Activation - Initiated by clotting factors in the blood itself (platelets releasing clotting factors)
42
Thrombosis
Abnormal clotting in unbroken vessels Clots are most likely to occur in the leg veins of inactive people Pulmonary embolism - a clot may break free and travel from the veins to the lungs
43
Pericardium Layers
Parietal (Fibrous) Layer - The outer, fibrous layer attached to the central tendon of the diaphragm and posterior sternum Serous (Visceral) Layer - The epicardium, the inner layer is made of simple squamous epithelium and covers the heart's surface. The outer layer lines the fibrous layer Pericardial Cavity - The space between parietal and visceral layers that is filled with fluid which reduces friction during heartbeats
44
Musculature of the ventricles
The right ventricle is only slightly muscular because it pumps blood through the pulmonary circuit The left ventricle is more muscular because it needs to pump blood through the systemic circuit, which requires a considerable amount of pressure
45
Atrioventricular valves
The AV valves control blood flow between the atria and ventricles Right AV valve - Tricuspid Left AV valve - Mitral/Bicuspid
46
Semilunar Valves
The semilunar valves control blood flow between the ventricles and vessels immediately outside of the heart Aortic valve Pulmonary valve
47
Coronary Circulation
5% of the blood pumped by the heart goes to the heart itself Flow through the coronary arteries is greatest when the heart relaxes because contraction causes the vessels to constrict
48
Cardiac Muscle Structure
Cardiomyocytes - muscle cells of the heart Striations - lines on the cells caused by myosin and actin filaments Intercalated Discs - End-to-end connections between cardiomyocytes Interdigitating Folds - The plasma membrane at the end of the cell is folded, increasing the surface area Mechanical Junctions - Fascia Adherins and Desmosomes that tightly join cardiomyocytes Electrical Junctions - Gap junctions that form channels, allowing ions to flow across the cells, causing electrical stimulation
49
Cardiac Conduction System
SA Node - Sinoatrial Node, a patch of modified cardiomyocytes in the right atrium. Acts as the pacemaker Gap Junctions in the Atria cause contraction AV Node - Atrioventricular Node, located near the end of the interventricular septum, an electrical gateway to the ventricles AV Bundle - The pathway by which signals leave the AV node Bundle Branches (R & L) - Enters the interventricular septum and descends to the apex Subendothelial conducting network - Bundles spread throughout the ventricles via gap junctions
50
Sympathetic Nerve Supply to the Heart
SNS increases heart rate and contraction strength
51
Parasympathetic Nerve Supply to the Heart
PNS nerves slow heart rate
52
Pacemaker Physiology
Prepotential - gradual depolarization Slow-opening Na+ channels begin depolarization Fast-opening Ca2+ channels then join in to depolarize quicker Ca2+ channels close slowly, slowing repolarization K+ channels open, K+ flows out - repolarizing SA Node fires, setting off a heartbeat
53
Timing of Conduction
The signal from the SA node stimulates the atria. From firing, the signal reaches the AV node in 50 ms. Through the AV node, the signal slows 100 ms, giving the ventricles time to fill The signal travels quickly through the AV bundle and Subendothelial Conducting Network
54
Electrocardiogram
P wave - ATRIAL DEPOLARIZATION, the signal produced due to a signal from the SA node QRS complex - Downward deflection (Q), Tall sharp peak (R), and another downward deflection (S) produced when the AV node causes VENTRICULAR DEPOLARIZATION ST segment - Ventricular systole T wave - VENTRICULAR REPOLARIZATION
55
Cardiac Cycle
One complete contraction and relaxation of all four heart chambers
56
Heart Sounds
S1 - The first heart sound, "Lubb," caused by the closing of the AV valves, louder and longer S2 - The second heart sound, "Dupp," caused by the closing of the semilunar valves, softer and sharper
57
Phases of the Cardiac Cycle
Ventricular Filling - during diastole, toward the end, the atria contract Isovolumetric Contraction - during systole, the ventricles contract, increasing pressure, closing the AV valves - Causes S1 Sound Ventricular ejection - during systole, the semilunar valves are forced open Isovolumetric relaxation - during diastole, ventricular expansion begins and the semilunar valves close - Causes S2 Sound
58
What Variables are on Wiggers Diagram
Pressure - Aortic, Left Ventricular, and Left Atrial Ventricular Volume (mL) ECG Heart Sounds Phases of the Cardiac Cycle
59
Cardiac Output
The amount ejected by each ventricle in 1 minute CO = HR x Stroke Volume
60
Stroke Volume
The amount of blood ejected by the heart in one contraction
61
Tachycardia
Resting heart rate above 100 bpm Causes: Stress, anxiety, drugs, heart disease, fever, loss of blood, or damage to the myocardium
62
Bradycardia
Resting heart rate below 60 bpm Causes: Sleep, low body temp, in endurance-trained athletes
63
Chronotropic Agents
Positive Agents raise heart rate Negative Agents lower heart rate
64
Variables that Govern Stroke Volume
Preload - The amount of tension in the ventricular myocardium immediately before it begins contraction Contractility - How hard the myocardium contracts for a given preload Afterload - The sum of all forces opposing the ejection of blood
65
Layers of the Vessel Wall
Tunica Interna - Lines the inner vessel, made of simple squamous epithelium, selectively permeable, secretes chemicals for dilation or constriction Tunica Media - The middle vessel layer, made of smooth muscle, collagen, and elastic tissue, is used to strengthen the vessel and prevent rupturing Tunica Externa - The outer vessel layer, made of loose connective tissue that merges with other vessels, nerves, and organs, is used to anchor vessels and provide passage for small nerves and lymphatic vessels
66
Conducting Arteries
Also called Elastic/Large Arteries, they are the largest. They expand during systole and recoil during diastole Ex. Aorta, Common Carotid, Subclavian, Pulmonary Trunk
67
Distributing Arteries
Also called Muscular/Medium Arteries, they distribute blood to specific organs
68
Resistance Arteries
Arterioles are the smallest arteries, they control the amount of blood to various organs Metarterioles are short vessels that link arterioles to capillaries, they contain muscle cells that form the precapillary sphincters which reduce blood flow and divert it to other tissues
69
Capillary Types (3)
Continuous - Endothelial Cells have tight junctions, allowing the passage of glucose and other solutes; they also contract to regulate blood flow Fenestrated - Endothelial Cells with many holes (fenestrations), typically found in organs that require rapid absorption and filtration (kidneys, intestines) Sinusoids - Irregular, blood-filled spaces with large fenestrations that allow proteins (albumin), clotting factors, and new blood cells to enter the circulation
70
Capillary Bed
A network of 10-100 capillaries, usually supplied by a single arteriole or metarteriole. At the distal end, capillaries transition into venules or drain into a thoroughfare channel
71
Portal System
Blood flows through 2 capillary beds before exiting through the venules
72
Vessel Blood Distribution
65% of the blood is in the veins 15% is in the arteries 9% in the pulmonary circuit 7% in the heart 5% in the capillaries
73
Arteriosclerosis
Hardening of arteries primarily caused by free radicals gradually deteriorating tissues of the arterial walls
74
Atherosclerosis
The growth of lipid deposits in the arterial walls which can become calcified, making arteries hard or crunchy Plaque growth causes turbulent flow, where blood circles back after passing a blockage, which can cause bulging
75
Peripheral Resistance
The opposition to flow in vessels away from the heart due to resistance
76
Variables that impact peripheral resistance
Blood Viscosity - "thickness" of the blood. Increased viscosity slows flow, and decreased viscosity speeds up the flow Vessel Length - The farther the blood travels along a vessel, the more cumulative friction it encounters. Pressure and flow decline with distance Vessel Radius - The most powerful influence over flow. Vasoconstriction & vasodilation change the radius. With laminar flow, the blood moves faster in the center because it encounters little to no friction from vessel walls.
77
Which types of vessels have the most significant point of control over peripheral resistance?
Arterioles They outnumber any other type of artery, providing numerous points of control. They are more muscular in proportion to their diameter (changes in radius) Arterioles provide half of the total peripheral resistance
78
Local Control
The ability of the arteries to control their own diameter via metabolic & myogenic controls
79
Metabolic Local Control
When waste (CO2) accumulates, pH rises, causing vasodilation
80
Myogenic Local Control
When arteries are stretched during movement, they constrict locally to prevent bulging or rupture
81
Neural Control
The brain's ability to control artery diameter. The sympathetic nervous system has vasomotor control where higher fire rates cause vasoconstriction and reducing the rate of fire allows for vasodilation. Baroreflex Chemoreflex
82
Hormonal Control & Specific Hormones (3)
Different hormones cause different effects on artery diameter Atrial Natriuretic Peptides - Secreted by the heart, they increase Na+ excretion by the kidneys, reducing blood volume and BP Antidiuretic Hormone - ADH promotes water retention but in high concentrations, it causes vasoconstriction and an increase in BP Epinephrine & Norepinephrine - Adrenal & Sympathetic catecholamines that bind to receptors on smooth muscles and cause vasoconstriction and dilation
83
Blood Flow @ Rest vs Blood Flow During Exercise
At rest, total CO is 5 L/min with the flow spread out across all systems (more in renal and digestive) During exercise, total CO is 17.5 L/min with the flow increased drastically to the muscular system and reduced in the others
84
Capillary Exchange
The two-way movement of fluid into tissues from the capillaries and into the capillaries from tissues
85
Filtration & Reabsorption Pressures Explained
Initially, as blood enters the capillary from the arterioles, blood hydrostatic pressure is much higher than the osmotic pressure pushing in from the tissues. As the process continues, however, solutes exit the capillary, decreasing the blood hydrostatic pressure. The concentration of wastes is still high, so the osmotic pressure from the tissues gradually overcomes the BP, pushing more wastes into the capillary before it exits via venules
86
Colloid Osmotic Pressure
The concentration gradient between the blood and watery substances of the tissues

Biol 233 (4 decks)

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