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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
Q

Rh Groups

A

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

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26
Q

Neutrophil

A

The most abundant WBCs (60-70%) that are aggressively antibacterial, have multi-lobed nuclei, and granules

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27
Q

Eosinophil

A

Makes up 2-4%, two lobes of granules connected by a thin band

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28
Q

Basophil

A

Rarest formed element (<0.5% WBC count), the cell appears to be full of granules

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29
Q

Monocyte

A

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

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30
Q

Lymphocyte

A

The second most abundant WBC (22-35%) but the smallest in diameter, they turn into immune cells

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31
Q

Leukopoiesis

A

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

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32
Q

Leukopenia

A

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

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33
Q

Leukocytosis

A

A WBC count above normal, usually indicates/is caused by infection, allergy, or disease

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34
Q

Leukemia

A

Cancer of the hematopoietic tissues that produce high numbers of circulating leukocytes and their precursors

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35
Q

Hemostatic Mechanisms (3)

A

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
Q

Thrombopoiesis

A

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
Q

Platelet Function

A

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
Q

Vascular Spasm

A

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
Q

Platelet Plug Formation

A

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
Q

Coagulation

A

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
Q

Mechanisms of Coagulation (2)

A

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
Q

Thrombosis

A

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
Q

Pericardium Layers

A

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
Q

Musculature of the ventricles

A

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
Q

Atrioventricular valves

A

The AV valves control blood flow between the atria and ventricles

Right AV valve - Tricuspid
Left AV valve - Mitral/Bicuspid

46
Q

Semilunar Valves

A

The semilunar valves control blood flow between the ventricles and vessels immediately outside of the heart

Aortic valve
Pulmonary valve

47
Q

Coronary Circulation

A

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
Q

Cardiac Muscle Structure

A

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
Q

Cardiac Conduction System

A

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
Q

Sympathetic Nerve Supply to the Heart

A

SNS increases heart rate and contraction strength

51
Q

Parasympathetic Nerve Supply to the Heart

A

PNS nerves slow heart rate

52
Q

Pacemaker Physiology

A

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
Q

Timing of Conduction

A

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
Q

Electrocardiogram

A

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
Q

Cardiac Cycle

A

One complete contraction and relaxation of all four heart chambers

56
Q

Heart Sounds

A

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
Q

Phases of the Cardiac Cycle

A

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
Q

What Variables are on Wiggers Diagram

A

Pressure - Aortic, Left Ventricular, and Left Atrial

Ventricular Volume (mL)

ECG

Heart Sounds

Phases of the Cardiac Cycle

59
Q

Cardiac Output

A

The amount ejected by each ventricle in 1 minute

CO = HR x Stroke Volume

60
Q

Stroke Volume

A

The amount of blood ejected by the heart in one contraction

61
Q

Tachycardia

A

Resting heart rate above 100 bpm

Causes: Stress, anxiety, drugs, heart disease, fever, loss of blood, or damage to the myocardium

62
Q

Bradycardia

A

Resting heart rate below 60 bpm

Causes: Sleep, low body temp, in endurance-trained athletes

63
Q

Chronotropic Agents

A

Positive Agents raise heart rate
Negative Agents lower heart rate

64
Q

Variables that Govern Stroke Volume

A

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
Q

Layers of the Vessel Wall

A

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
Q

Conducting Arteries

A

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
Q

Distributing Arteries

A

Also called Muscular/Medium Arteries, they distribute blood to specific organs

68
Q

Resistance Arteries

A

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
Q

Capillary Types (3)

A

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
Q

Capillary Bed

A

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
Q

Portal System

A

Blood flows through 2 capillary beds before exiting through the venules

72
Q

Vessel Blood Distribution

A

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
Q

Arteriosclerosis

A

Hardening of arteries primarily caused by free radicals gradually deteriorating tissues of the arterial walls

74
Q

Atherosclerosis

A

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
Q

Peripheral Resistance

A

The opposition to flow in vessels away from the heart due to resistance

76
Q

Variables that impact peripheral resistance

A

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
Q

Which types of vessels have the most significant point of control over peripheral resistance?

A

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
Q

Local Control

A

The ability of the arteries to control their own diameter via metabolic & myogenic controls

79
Q

Metabolic Local Control

A

When waste (CO2) accumulates, pH rises, causing vasodilation

80
Q

Myogenic Local Control

A

When arteries are stretched during movement, they constrict locally to prevent bulging or rupture

81
Q

Neural Control

A

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
Q

Hormonal Control & Specific Hormones (3)

A

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
Q

Blood Flow @ Rest vs Blood Flow During Exercise

A

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
Q

Capillary Exchange

A

The two-way movement of fluid into tissues from the capillaries and into the capillaries from tissues

85
Q

Filtration & Reabsorption Pressures Explained

A

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
Q

Colloid Osmotic Pressure

A

The concentration gradient between the blood and watery substances of the tissues

Biol 233 (4 decks)

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