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A&P 2 1st half > Lecture Exam 1- Blood and Respiratory System > Flashcards

Lecture Exam 1- Blood and Respiratory System Flashcards

1
Q

Three main functions of the circulatory system

A

transport
protection
regulation

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2
Q

Circulatory System Transport function

A

blood carries oxygen from lungs to body tissues picking up CO2 from tissues transporting to lungs, nutrients are picked up from digestive transporting to body tissues, metabolic wastes are taken from tissues to the kidney for removal, hormones are taken from endocrine cells to organs, and transports stem cells from bone marrow are moved to tissues where they lodge and mature.

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3
Q

Circulatory System Protection function

A

blood has roles in inflammation, limiting spread of infection (WBCs destroy microorganism and cancer cells removing tissue debris), and repair (platelets secrete factors to initiate clotting minimizing blood loss, contributing to tissue growth and blood vessel maintenance)

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4
Q

Circulatory System Regulation function

A

absorbing or giving off fluid under different conditions stabilizes fluid distribution, buffering acids and bases, stabilizing pH of extracellular fluid, cutaneous blood flow is also important in dissipating metabolic heat from body w/ shifts in flow helping to regulate body temperature by routing blood to skin for heat loss or retaining it deeper to conserve heat

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5
Q

Blood plasma and what it consists of

A

liquid matrix portion of blood (same as serum except serum doesn’t have fibrinogen), yellow fluid making up ½ of blood volume. Suspended in plasma are formed elements- cells and cell fragments ex. RBC, WBC, and platelets.

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6
Q

Function of and three major categories of plasma proteins

A

clotting, defense against pathogens, transport of other solutes aka iron, copper lipids, and hydrophobic hormones all produced by liver albumin and fibrinogen except globulin.

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7
Q

albumin

A

smallest most abundant and viscous contributor, responsible for colloid osmotic pressure, transports lipids, hormones, calcium, and other solutes, buffers blood pH. Affecting blood volume, pressure, and flow when changed.

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8
Q

globulin

A

(antibodies, alpha, beta, and gamma) produced by plasma transport and hemoglobin, copper, blood clotting, lipids, fat-soluble vitamins, and hormones, iron, defense and destroying pathogens, toxins, and microorganism

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9
Q

fibrinogen

A

forming blood clots by becoming fibrin

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10
Q

Other things found in blood

A

nitrogenous compounds-breakdown of free amino acids and toxic end product wastes are urea
Nutrients including Glucose, amino acids, vitamins, fats, cholesterol, phospholipids, and minerals
Dissolved O2, CO2, and nitrogen
Electrolytes: sodium makes up most of electrolytes and is most important for osmolarity affecting blood volume and pressure.

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11
Q

Viscosity what is blood’s viscosity and why? plasma?

A

resistance of a fluid to flow, resulting from the cohesion of its particles. Aka stickiness of a fluid. Blood is 4-5X as viscous as water because of RBCs, plasma is 2X more than water because of protein. If too viscous or not enough strains heart

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12
Q

osmolarity definition, important regulating substances and what happens if too high or too low?

A

the total molarity of dissolved particles that cannot pass through the blood vessel wall. Substance pass between bloodstream and fluid through capillary walls balancing filtration of fluid from capillarity and reabsorption by osmosis w/ sodium, protein, and erythrocytes playing big part. if too high blood absorbed too electrolytes and water w/ it, high volume and pressure strains heart. if osmolarity drops too low too much water in tissues becoming swollen dropping bp.

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13
Q

hemopoiesis

A

production of blood, especially its formed elements

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14
Q

hemopoietic tissues

A

produce blood cells. First RBCs form in yolk sac, then liver and spleen halting at birth. w/ spleen producing lymphocytes and storing blood throughout life
Red bone marrow produces all seven formed elements

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15
Q

Pluripotent stem cells (PPSC)

A

aka hematopoietic stem cells multiple to maintain small population in bone marrow becoming more specialized cells.

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16
Q

Colony-forming unit

A

more specialized cells that stem from PPSC destined to produce one of classes of formed elements

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17
Q

Myeloid hemopoiesis-

A

blood formation in bone marrow

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18
Q

Lymphoid hemopoiesis

A

blood formation in lymphatic organs (lymphocytes formed in thymus, tonsils, lymph nodes, spleen, and mucous membranes)

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19
Q

Erythrocytes two principal functions and hallmarks of cells

A

Carry oxygen from lungs to cell tissues. Does not have other organelles utilizes anaerobic fermentation to produce ATP doesnt use oxygen.
Pick up Co2 from tissues and bring to lungs. Resilient and durable can stretch, bend and fold squeezing through capillary

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20
Q

Hemoglobin what it consists of

A

gives RBC its red pigment carries oxygen and aids in transporting CO2 and buffering pH
Each Hb molecule consists of:
Four protein chains—globins alpha and beta chains bind to CO2
Four heme groups- binds oxygen to an iron atom w/ each carrying one molecule of O2
Heme groups
Nonprotein moiety that binds O2 to ferrous ion (Fe) at its center

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21
Q

Quantities of Erythrocytes and Hemoglobin determined by

A

RBC count and hemoglobin concentration indicate amount of O2 blood can carry
Hematocrit (packed cell volume): percentage of whole blood volume composed of RBCs
Men 42% to 52% cells; women 37% to 48% cells
Hemoglobin concentration of whole blood
Men 13 to 18 g/dL; women 12 to 16 g/dL
RBC count
Men 4.6 to 6.2 million/mL; women 4.2 to 5.4 million/mL. Lower in women than men because androgens stimulate RBC production w/ men have higher than woman, women have menstrual losses, hematocrit inversely proportional to body fat percentages higher in women than men woman blood vessels closer to surface

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22
Q

What is erythropoiesis production? How many are produced, how long do they last and how long does the process take?

A

RBC production
1 million RBCs are produced per second, Average lifespan of about 120 days
Development takes 3-5 days.

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23
Q

What are the three steps in erythrocyte production

A

Reduction in cell size, increase in cell number, synthesis of hemoglobin, and loss of nucleus and other organelles

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24
Q

Describe erythrocyte production?

A

Hemopoietic becomes erythrocyte colony-forming unit (ECFU) w/ receptors for EPO (erythropoietin from kidneys) stimulating ECFU to become erythroblasts, which build to synthesize hemoglobin. Once hemoglobin is completed nucleus shrivels and is discharged becoming reticulocytes. Reticulocytes leave bone marrow and enter blood ribosomes disintegrate becoming erythrocytes.

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25
Q

Iron metabolism

A

Fe2+ more absorbable converted from Fe3+ from stomach. Gastroferritin binds Fe2+ transporting to small intestine absorbed by blood transferred to transferrin traveling to bone marrow, liver, and other tissues. Bone marrow uses iron for hemoglobin synthesis, muscles use for myoglobin, and all cells make cytochromes in mitochondria. Liver binds surplus iron to apoferritin forming ferritin w/ iron to release when needed.

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26
Q

Erythrocyte Homeostasis

A

negative feedback control, kidney’s detecting low count increasing EPO output.

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27
Q

Hypoxemia caused by:

A

low RBC count

hemorrhage, high altitude, and exercise.

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28
Q

Erythrocyte death and disposal. What happen as they age? What are each of the components converted to and how are they disposed of?

A

as RBCs age membrane proteins (spectrin) deteriorate and become fragile, and cannot repair w/out cellular components. Narrow channels of spleen test ability of old, fragile RBCs to squeeze through where they become trapped, broken up, and destroyed. When rupture releases hemoglobin, macrophage separate heme from globin otherwise causes renal failure, leaving plasma membrane, digested by liver & spleen. iron released to blood, rest of heme turned into biliverdin>bilirubin by macrophage in spleen binds to albumin, liver separates and put bilirubin (green) in bile where it travels to to gallbladder then to small intestine converting to urobilinogen brown color of feces or urochrome yellow of pee.

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29
Q

Jaundice

A

yellowish cast of skin and whites of eyes as sign of rapid hemolysis, liver disease, or bile duct obstruction interfering w/ bilirubin disposal.

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30
Q

Enlarged and tender spleen indicates what?

A

diseases where RBCs rapidly breakdown

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31
Q

What is Polycythemia?

A

an excess of RBCs. Primary- cancer of erythropoietic line of red bone marrow, secondary- all other causes including: dehydration (less plasma more RBC concentration), smoking, air pollution, emphysema (lung tissue not available to oxygenate blood so RBC increase until polycythemia w/ blood still not being properly oxygenated), high altitude, excessive aerobic exercise.

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32
Q

What are the dangers of polycythemia?

A

Increased blood volume, pressure, viscosity

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33
Q

What can polycythemia lead to?

A

embolism, stroke, or heart failure

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34
Q

Anemia what are the three causes and what are the signs and symptoms of it in an individual

A

:lack of iron in blood 1) inadequate erythropoiesis or hemoglobin synthesis commonly because of kidney failure, 2) hemorrhagic anemia from bleeding, 3) hemolytic anemia from RBC destruction. Symptoms include: hypoxia of tisssues, blood osmolarity & viscosity reduced w/ lethargy, shortness of breath, pale skin, edema, faster heart beat, pressure drops, necrosis of brain, heart, and kidney tissues or cardiac failure

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35
Q

What is sickle cell disease?

A

hereditary hemoglobin defects because of recessive allele causing sickle cell shaped RBCs because of regular misbinding of hemoglobin to O2

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36
Q

what happens at low O2 w/ sickle cell disease?

A

At low O2 sickle cells are deoxygenated, and they polymerize to pointy shape at end causing it to become rigid, sticky, and clump together causing pain. Blockages can lead to kidney or heart failure, stroke, severe joint pain or paralysis.

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37
Q

why are the body’s attempt to counteract sickle cell blockages futile?

A

W/ breakdown of these causing anemia. Chronic hypoxemia causes fatigue, weakness, slow mental development, deterioration of heart and other organs, w/ overactive hemopoietic tissues (spleen become enlarged and fibrous) misshaping and block blood vessels, kidney, heart, stroke, joint pain, paralysis.

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38
Q

why is sickle cell anemia still prevalent?

A

Protective against malaria as if heterozygous as they have normal phenotype

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39
Q

Antigens

A

Complex molecules on surface of cell membrane such as proteins, glycoproteins, and glycolipids unique to each individual occur on all cells body to distinguish cells from foreign matter. When detects foreign that activate an immune response genetically unique to everybody used to distinguish cell from foreign matter.

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40
Q

Antibodies

A

Proteins (gamma globulins) secreted by plasma cells. Immune response to foreign matter binding to them, marking them for destruction.

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41
Q

Agglutination

A

Antibody molecule binding to antigens

Causes clumping of red blood cells can bind up to 10

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42
Q

agglutinogens

A

RBC antigens
Called antigen A and B and O (no antigens)
Determined by glycolipids on RBC surface

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43
Q

agglutinins

A

Antibodies. Found in plasma

Anti-A and anti-B

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44
Q

ABO blood type group is determined by? what is the most common type? least common?

A 
presence or absence of antigens (agglutinogens) on RBCs
Blood type A person has A antigens
Blood type B person has B antigens
Blood type AB has both A and B antigens
Blood type O person has neither antigen
Most common: type O
Rarest: type AB
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45
Q

What are the ABO group antibodies?

A

(agglutinins); anti-A (found in B or O blood type) and anti-B (found in A or O blood type)
Appear 2 to 8 months after birth; maximum concentration by 10 years of age. Produced in response to bacteria in intestines.
Antibody-A or antibody-B (or both or neither) are found in plasma
You do not form antibodies against your antigens

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46
Q

Agglutination of Erythrocytes ABO Group and the response if the transfusion is mismatched

A

Agglutination
Each antibody can attach to several foreign antigens on several different RBCs at the same time
Responsible for mismatched transfusion reaction
Agglutinated RBCs block small blood vessels, hemolyze, and release their hemoglobin over the next few hours or days
Hb blocks kidney tubules and causes acute renal failure

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47
Q

Universal donor blood type?

A

Type O: most common blood type
Lacks RBC antigens
Donor’s plasma may have both antibodies against recipient’s RBCs (anti-A and anti-B)

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48
Q

universal recipient blood type?

A

Type AB: rarest blood type

Lacks plasma antibodies; no anti-A or anti-B

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49
Q

How can you minimize transfusion reaction?

A

May give packed cells (minimal plasma), which reduces risk of transfusion reaction

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50
Q

What are Granulocytes?

A

granules containing azurophilic absorbing blue or violet dyes of blood stains and lysosomes visible w/ defense against specific pathogens neutrophils, eosinophils, basophils

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51
Q

What are leukocytes?

A

white blood cells, protect against infectious microorganism, other invaders, and diseases. Spend only few hours in bloodstream then migrate into connective tissue living there.

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52
Q

Agranulocytes

A

WBC w/out granules

lymphocytes, monocytes

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53
Q

Neutrophils

A

most abundant clearly visible but random shaped nucleus w/ 3-5 lobes Barely visible fine reddish to violet granules in cytoplasm containing lysosome and other antimicrobial; aggressively anti-bacteria, neutrophilia rise in # because of infection. Creamy color of pus disposed of by rupture of blister.

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54
Q

Eosinophils

A

found in mucous membranes of the respiratory, digestive, and lower urinary tracts. Two large lobes w/ coarse rosy to orange colored granules. Secrete chemicals that weaken or destroy parasites aka hookworms, tapeworms, disposing inflammatory chemicals, antigen-antibody complexes, and allergens. With allergies, parasites, and collagen, spleen and CNS diseases account for increases in their #s.

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55
Q

basophils

A

arest, have large abundant, blue-dark violet specific granules, nucleus is sometimes obscured but w/ a S or U shape. Secrete two chemicals: histamine and heparin. Release chemical signals attracting eosinophils and neutrophils to infection site.

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56
Q

histamine

A

vasodilator widens blood vessels, speeds flow of blood to injured tissue, makes blood vessels more permeable allowing blood components to enter quickly

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57
Q

heparin

A

anticoagulant inhibits blood clotting promoting mobility of WBCs to area

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58
Q

Lymphocytes

A

-second most common. Various types and sizes found in fibrous connective tissue (medium and large), and circulating blood (small). Uniform nucleus that look similar to basophils, clear cytoplasm w/ round, ovoid, slightly dimpled on side w/ dark violet staining nucleus. Variable amounts of bluish cytoplasm (scanty to abundant); Diverse infections and immune response, including destroy cancer, viral infection, foreign cells, secrete antibodies to coordinate actions of other immune cells and provide immune memory.

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59
Q

Monocytes

A

Usually largest WBC; large and clearly visible nucleus light violet ovoid, kidney or horseshoe shaped. Abundant cytoplasm w/ sparse fine granules angular and spiky shapes. Rise in inflammation and infections become macrophages. Become macrophages, phagocytize pathogens, dead neutrophils, and debris of dead cells, coordinate immune system by being antigen-presenting cells.

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60
Q

Leukopoiesis and the general differentiation groups

A

formation of leukocytes and its life cycle. Production of white blood cells and dead by macrophages. Hemopoietic stem cells, differentiate into 1) myeloblasts>neutrophils, eosinophils, and basophils, or 2)monoblasts > monocyte, or 3 )lymphoblasts> lymphocytes.

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61
Q

how do colony forming units for leukocytes determine what is needed?

A

Colony forming units each have receptors for colony-stimulating factors w/ several types to distinguish which cells needed infection vs. allergies.

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62
Q

Where does leukopoiesis occur?

A

These are all stored in red bone marrow, sometimes start in thymus too, release granulocytes and leukocytes when needed, lymphocytes start there but develop spleen, lymph nodes etc.

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63
Q

How long do these cells live for?

A

Granulocytes 8-9 hours in blood live 5 days, monocytes 10-20 hours then turn into macrophages living for several years. lymphocytes few weeks to decades leave bloodstream for tissues lymphatic back to blood stream.

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64
Q

leukopenia

A

low WBC count (lead, arsenic, and mercury poisoning, radiation sickness, measles, mumps, chicken pox, polio, influenza, typhoid fever, and AIDS or drugs) w/ elevated risk of infection.

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65
Q

leukocytosis

A

high white blood cell count. Indicates infection, allergy, or other diseases. Dehydration or emotional disturbances.

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66
Q

Complete Blood Count

Includes several values

A

Hematocrit
Hemoglobin concentration
Total count for RBCs, reticulocytes, WBCs, and platelets
Differential WBC count
RBC size and hemoglobin concentration per RBC

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67
Q

Differential white blood cell count and specifically which type

A

we have can help identify what kind of disease you have. Can specifically find: anemia by low RBC counts, size, shape, or HB content. Platelet deficiency- adverse drug reaction. High neutrophil- bacterial infection, eosiniophil- allergy or parasitic. WBC types- leukemia,

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68
Q

What is Leukemia? what kinds are there? What can happen if untreated? How do you treat?

A
  • cancer of hemopoietic tissue producing high number of circulating leukocytes and their precursors. Myeloid (uncontrolled granulocyte production), lymphoid (uncontrolled lymphocyte or monocyte production), acute(suddenly, rapidly, death w/in months) or chronic (slow over months, survival 3 years). Treat w/ chemo transplants control of anemia, hemorrhaging, and infection. Leukemic proliferate replacing normal marrow w/ deficiency of elements w/ high leukocytes w/ opportunistic infection or organisms that usually dont affect healthy people causing them to become anemic fatigued causing hemorrhaging and impaired blood clotting, bone and joint pain as cancer moves.
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69
Q

platelets what are they and what are their structure

A

play an important role in all three hemostatic mechanisms
small fragments of marrow cells (megakaryocytes) second most abundant formed element. W/ complex internal structure including lysosomes, mitochondria, microtubules, and microfilaments; granules w/ secretions and open canalicular system no nucleus w/ pseudopods and ameboid movement.

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70
Q

Platelet function

A

secrete vasoconstrictors (chemicals that stimulate constriction of broken vessels), stick together to form plugs sealing small breaks, secrete procoagulants (clotting factors), formation of clot-dissolving enzyme (dissolved blood clots once done), secrete chemicals attracting neutrophils and monocytes to inflammation, internalize and destroy bacteria, secrete growth factors stimulating mitosis in fibroblasts and smooth muscle.

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71
Q

Hemostasis

A

—the cessation of bleeding
Stopping potentially fatal leaks
Hemorrhage: excessive bleeding

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72
Q

Thrombopoiesis-

A

megakaryoblasts w/ receptors stimulated by thrombopoietin (liver and kidneys) that replicate DNA w/out dividing forming big cells (megakaryocytes)
Platelets circulate freely for 5-6 days. 40% of blood in spleen are the megakaryocytes.

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73
Q

Megakaryocytes

A

live in bone marrow adjacent to blood sinusoids multiple lobe nucleus large collections of blood. Sprouting long tendrils proplatelets protruding through endothelium into sinusoid blood. Flow shears off proplatelets becoming platelets in small vessels of lungs.

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74
Q

Three hemostatic mechanisms

A

vascular spas, platelet plug formation, and blood clotting

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75
Q

Vascular spasm

A

prompt constriction of broken vessel. Injury stimulates pain receptors which innervate blood vessels causing short-term constriction, injury to smooth muscle of blood vessel causes long vasoconstriction w/ platelet releasing serotonin

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76
Q

Platelet plug formation

A

when vessel broken collagen fibers exposed to blood when platelets contact collagen/rough surfaces they grow long spiny pseudopods (Spider-man webs) adhering to vessel & platelets, which contract and draw walls of vessel together forming platelet plug loose and delicate (blot not wipe). w/ platelet aggregation degranulation/exocytosis of granules occurs releasing serotonin, ADP (attracts more platelets stimulating degranulation), thromboxane (promotes platelet aggregation, degranulation, and vasoconstriction)

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77
Q

Blood clotting

A

(coagulation)
process is to: convert plasma protein fibrinogen into fibrin (sticky protein adheres to walls of vessel). Blood cells and platelets stick to fibrin sealing break in vessel.
Use combination of both extrinsic and intrinsic for inside and outside. Use various procoagulants (clotting factors produced by liver) to help seal the break. Once factor X activated combines w/ others to form prothrombin activator, which acts on prothrombin converting to thrombin, which converts fibrinogen into fibrin, which covalently bond to each other. Platelet and endothelial cell them secrete platelet-derived-growth factor (PDGF) stimulating fibroblasts (invade clot producing fibrous connective tissue strengthening and sealing vessel) and smooth muscle cells to multiple and repair vessel

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78
Q

Extrinsic mechanism-

A

initiated by clotting factors released by damaged blood vessel and perivascular tissues from outside blood each activate part of pathway w/ a shortcut to coagulation. Pathway to activate factor X

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79
Q

Intrinsic mechanism-

A

platelets adhere to fatty plaque of atherosclerosis clotting factors in blood itself that each activate part of pathway. Pathway to activate factor X

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80
Q

Blood Clot Dissolution-

A

fibrinolysis. Factor 12 catalyzes formation of kallikrein converts plasminogen to plasmin, fibrin-dissolving enzyme which breaks up clot

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81
Q

Platelet repulsion

A

do not adhere to smooth prostacyclin-coated endothelium of healthy blood vessels

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82
Q

Dilution-

A

small amounts of thrombin form spontaneously in plasma w/ less flow can accumulate to cause clotting in circulatory shock

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83
Q

Antithrombin

A

-secreted by liver deactivated thrombin before acting on fibrinogens, heparin, interferes w/ formation of prothrombin activator blocking action of thrombin and fibrinogen, and promoting action of antithrombin.

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84
Q

What are clotting disorders causes by?

A

Deficiency of any clotting factor can shut down the coagulation cascade

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85
Q

hemophilia

A

Hemophilia—family of hereditary diseases characterized by deficiencies of one factor or another different types missing different factors w/ certain parts of cascade not properly clotting given specific factors. Physical exertion can cause bleeding into muscles and joints causing excruciating pain and joint immobility from hematomas (masses of clotted blood)

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86
Q

kinds of hemophilia

A

Sex-linked recessive (on X chromosome)
Hemophilia A missing factor VIII (83% of cases)
Hemophilia B missing factor IX (15% of cases)
Hemophilia C missing factor XI (autosomal)

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87
Q

Thrombosis

A

abnormal clotting in unbroken vessel often commonly found in older people’s leg veins and vessels because they don’t work as well and the people don’t move around as much and are inactive.

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88
Q

Thrombus

A

is a clot. Can grow large enough to obstruct small vessel or piece may break loose and travel in bloodstream as embolus (can lodge in small artery blocking blood flow) can cause infraction of downstream tissues.

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89
Q

Pulmonary embolism:

A

clot may break free, travel from veins to lungs can die of hypoxia

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90
Q

Embolus

A

—anything that can travel in the blood and block blood vessels

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91
Q

Infarction

A

(tissue death) may occur if clot blocks blood supply to an organ (MI or stroke)
650,000 Americans die annually of thromboembolism (traveling blood clots)

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92
Q

Clinical Management of Blood Clotting Goal

A

prevent formation of clots or dissolve existing clots

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93
Q

Preventing clots

A

Vitamin K is required for formation of clotting factors
Coumarin, warfarin (Coumadin)—vitamin K antagonists- making clot less readily
Aspirin suppresses thromboxane A2, factor in platelet aggregation
Other anticoagulants discovered in animal research
Medicinal leeches used since 1884 (hirudin)- secrete local anesthetic so bites painless ihbitting thrombin
Snake venom from vipers (arvin)- breaks down fibrinogen

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94
Q

Dissolving clots that have already formed

A

Streptokinase:enzyme made by streptococci bacteria
Used to dissolve clots in coronary vessels
Digests almost any protein
Tissue plasminogen activator (TPA): works faster, is more specific, and now made by transgenic bacteria. Converts plasminogen into clot-dissolving enzyme plasmin
Hementin:produced by giant Amazon leech. anticoagulatnt dissolving blood clots

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95
Q

Cardiovascular system-

A

heart (muscular pump keeps blood flowing through vessels) and blood vessels (deliver blood to all body’s organs and return it to the heart.)

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96
Q

Circulatory system-

A

consists of heart, blood vessels, blood, and lymphatic system

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97
Q

describe the pulmonary circuit

A

begins at the right side of the heart, which carries deoxygenated blood w/ CO2 and other waste to lungs for gas exchange receiving from circulated body (superior and inferior vena cava) that is pumped into the pulmonary trunk, which divides into right and left pulmonary arteries. This blood is carried to alveoli of lungs, where CO2 is unloaded and O2 is picked up where it then flows through pulmonary veins to left side of the heart

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98
Q

describe the pathway of the systemic circuit

A

Fully oxygenated blood arrives from lungs via pulmonary veins to left side of heart carrying blood through Aortic arch, U shaped, passes downward posterior to heart splitting off to the arteries that supply head, neck, and upper limbs, and splits and travels through thoracic and abdominal cavities into smaller arteries of organs to lower limbs. After circulation, systemic blood that is now deoxygenated returns to the right side of heart by superior vena cava (draining upper body) and inferior vena cava (draining everything below diaphragm) w/ major arteries and veins entering and leaving at great vessels.

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99
Q

Position, Size, and Shape of the Heart

A

size of fist. Heart lies w/in the thick partition mediastinum extending from broad base at the uppermost end, where major vessels attach, to bluntly pointed apex at lower end above diaphragm, tilting towards left. Right side has three lobes, left side two lobes.

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100
Q

Pericardium what is it? Where does it connect? What is it made of? What are its layers? what is its function?

A

double-walled cavity area or sac containing heart. Outer wall, pericardial sac (parietal pericardium) anchored by ligaments to diaphragm below and sternum above, w/ loosely anchored fibrous connective tissue connecting to mediastinal on posterior of heart. Made of tough superficial fibrous tissue of dense irregular connective tissue and a thin, deep serous layer. Serous layer turns inward at base of heart forming visceral pericardium, equivalent to epicardium w/ fluid exuded by serous layer lubricating membrane allowing heart to beat w/ minimal friction so it slides easier. Function: to isolate heart from other organs allow room to expand, but resisting excessive expansion.

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101
Q

What is the structure and significance of the framework of collagenous and elastic fibers in myocardium and what are its functions?

A

make up fibrous skeleton concentrating in walls between heart chambers in rings around the valves and sheets of tissue interconnecting rings. Functions: provides structural support for heart around valves and openings of great vessels holding oepn and preventing excessive stretch during blood surge 2) anchors cardiomyocytes giving them something to pull against 3) nonconductor of electricity serves as insulation between atria and ventricles not passing stimulation between the two 4) elastic recoil of fibrous skeleton may aid in refilling heart w/ blood after each beat.

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102
Q

Myocardial infarction and how are coronary ratios special in trying to prevent this? what symptoms present?

A

caused because of lack of blood supply such as a fatty deposit, not always cause by anastomoses, or blood clot in coronary artery. Coronary arteries protect against this by converging at various points combining blood flow to farther downstream (arterial anastomoses) alternative routes of blood flow supplying heart tissue w/ blood if primary is obstructed. Signs of heart attack- heavy pressure or squeezing pain into left arm, chest pressure, angina pectorosis- pain because of lost blood flow.

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103
Q

Compare the blood flow peak in systemic arteries versus coronary arteries

A

Organs other than heart, blood flow peaks when heart contracts and ejects blood into systemic arteries, diminishing when ventricles relax and refill.
In coronary arteries- Flow peaks when heart relaxes in coronary arteries 1) contraction of myocardium squeezes coronary arteries and obstructs blood flow 2) when ventricles contract, aortic valve is forced open and cusps covering openings to coronary arteries, blocking blood from flowing into them 3) when they relax, blood in aorta briefly surges back toward heart fills aortic valve cusps and flows into coronary arteries

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104
Q

Structure of Cardiac Muscle-

A

muscle fibers striated w/ short, thick, branched cells contacting several other cardiomyocytes through branches or intercalated discs, thick connections. forming network throughout each chamber. Cardiomyocyte single, centrally placed nucleus ⅓ have more than one nuclei surrounded by glycogen. Less developed sarcoplasmic reticulum then skeletal muscles, lacks cisterns, large T tubules not organized as nicely as skeletal and not as smooth as smooth muscle.

105
Q

Repair of damaged cardiac muscle

A

or fibrosis- undetected heart attack body repairs heart but it can only scar losing full function of muscle only repairing breaks

106
Q

Metabolism of Cardiac Muscle what does it use for fuel what fuel sources does it use what is the drawback?

A

Cardiac muscle depends almost exclusively on aerobic respiration to make ATP
Adaptable to different organic fuels most fatty acid, glucose and little other
Fatigue resistant because it makes little use of anaerobic fermentation or oxygen debt mechanisms. Myoglobin and glycogen rich big high concentrations of mitochondria. More vulnerable to lack of oxygen than other nutrients.

107
Q

The heart Conduction System what is it and how is it different than the nervous system?

A

heart beats rhythmically contracting at regular intervals around 75 beats/minute. Heart beat is myogenic- signal originates w/in heart itself. Heart is autorhythmic- does not depend on nervous system own built in pacemaker and nerve conduction pathway through cardiac.

108
Q

Sinoatrial node (SA)

A

pacemaker initiating each heartbeat determining heart rate consists of a patch of modified cardiomyocytes in right atrium, under epicardium near superior vena cava from where they spread throughout atria.

109
Q

Atrioventricular (AV) node

A

located at lower end of interatrial septum near right AV valve. Node acts as electrical gateway to ventricles w/ fibrous skeleton acting as an insulator to prevent currents from getting to ventricles by any other route.

110
Q

Atrioventricular (AV) bundle (bundle of His)-

A

pathway by which signals leave AV node. Bundle forks into right and left bundle branches entering interventricular septum descending toward apex

111
Q

Subendocardial conducting network/purkinje fibers

A

on lower end of bundle branch, cardiomyocytes not nerves but specialized for electrical conduction. At apex go up through ventricle form elaborate network more in left than right. Once electrical signal delivered signal passed through gap junctions

112
Q

Nerve Supply to the Heart

A

both sympathetic (changing strength and heart beat sometimes) and parasympathetic more strongly changes heart beat

113
Q

Sympathetic portion where are they from? where do they innervate? what do they do?

A

preganglionic starts in lower cervical region and upper thoracic. Postganglionic in cervical ganglia go through cardiac plexus in mediastinum continuing to cardiac nerves to heart terminating in SA and AV nodes and atria, ventricular, myocardium, aorta, pulmonary trunk, and coronary arteries. Sympathetic nerves increase heart rate but more so contraction strength

114
Q

Parasympathetic nerves where are they from? where do they innervate? what do they do?

A

begins in medulla oblongata through vagus nerve to cardiac plexus mingling w/ sympathetic fibers continuing via cardiac nerves to epicardial surface w/in heart walls right vagus nerve to SA node and left to AV node. No parasympathetic in myocardium but does inhibit some sympathetic. Functions to reduce heart rate than strength

115
Q

Systole

A

contraction refer to ventricular action, which ejects blood from the heart.

116
Q

Diastole

A

relaxation refer to ventricular action, which ejects blood from the heart.

117
Q

Cardiac Rhythms:

A

sinus rhythm, ectopic focus, and nodal rhythm

118
Q

Sinus rhythm

A

normal heartbeat triggered by the SA node

Adult at rest is typically 70 to 80 bpm(vagal tone)

119
Q

Ectopic focus

A

a region of spontaneous firing other than the SA node

May govern heart rhythm if SA node is damaged

120
Q

Nodal rhythm

A

if SA node is damaged, heart rate is set by AV node, 40 to 50 bpm
Other ectopic focal rhythms are 20 to 40 bp and too slow to sustain life too little flow to brain

121
Q

Pacemaker Physiology

A

SA node does not have stable resting membrane potential w/ potential starting at -60 mV and drifts upward, showing gradual depolarization called pacemaker potential (prepotential) resulting from slow inflow of Na+ w/out compensating outflow of K+ reaching threshold of -40 mV, when reached voltage-gated calcium channels open Ca2+ flows in from extracellular fluid. Depolarizing cells, peaking above 0 and repolarizing w/ each depolarization of SA node equating to a heartbreat then exciting other components firing every 20 seconds setting it at 75-80 bpm.

122
Q

Describe the impulse conduction through nodes to the myocardium describing timing and synchronistic.

A

Signal from SA node stimulates two atria to contract almost simultaneously reaching AV at 50 ms
Signal slows down through AV node thin cardiocytes w/ fewer junctions once hits signal has to slow down 100 ms allowing ventricles to fill w/ blood and allow it to synchronize decreasing pump.
Signals travel very quickly through AV bundle and Purkinje fibers because of lots of gap junctions, entire ventricular pumps together in tandem.
Ventricular systole begins at apex of heart, which is first stimulated progressing upward pushing blood toward semilunar valve twisting slightly

123
Q

Electrical behavior of the Myocardium. What are the three phases? Describe the nerve stimulation pathway of a cardiocyte?

A
  • Cardiocytes stable resting potential -90 depolarize only when stimulated, unlike SA node. Three phases to cardiac action potential, depolarization, plateau, and repolarization. Cardiac cycle complete contraction and relaxation of the heart
    1. Na+gates open
    2. Rapid depolarization
    3. Peaks at +30 Na+gates close
    4. Slow sarcoplasmic reticulum opening, closing, and reuptake Ca2+channels open Plateau phase for 30-40 ms to allow blood to flow. Binds to troponin for contraction for entire length of action potentia (w/ prolonged compared to skeletal) .
    5. Ca2+channels close, K+channels open (repolarization) stops premature pumping of heart by 250X w/ absolute refractory period preventing wave summation and tentanus unlike skeletal
124
Q

Describe the cardiac cycle in relation to pressure gradients and flow.

A

Ventricle expands (relaxing) w/ internal pressure falling, causing AV valve that hangs limply to open as blood flows into ventricle from atrium above, as ventricles fill the cusps float upward toward closed position. When ventricle contract internal pressure rises sharply w/ blood surging against AV valve pushing cusps together sealing them preventing blood flowing backward w/ papillary muscles contracting slightly before rest of ventricle tugging on cords preventing them from bulging excessively into atria or turning inside out. Rising pressure in ventricles become above arterial pressure forcing valves open w/ blood ejected from heart. Ventricles relax again and the ventricular pressure is below those in arteries so the blood flows backward filling and closing the semilunar valve shut preventing blood from reentering heart.

125
Q

Two main variables govern fluid movement:

A

pressure causes flow and resistance opposes it
Fluid will only flow if there is a pressure gradient(pressure difference)
Fluid flows from high-pressure point to low-pressure point
Pressure measured in mm Hg with a manometer (sphygmomanometer for BP)

126
Q

Auscultation

A
  • listening to heart made by sounds of body. First heart sound longer and louder lub closure of AV valves turbulent in bloodstream and movement of heart wall, dup-closure of valves semilunar valves
127
Q

Phases of the Cardiac Cycle list them

A 
Ventricular filling (during diastole)
Isovolumetric contraction (during systole)
Ventricular ejection (during systole)
Isovolumetric relaxation (during diastole)
The entire cardiac cycle (all four of these phases) are completed in less than 1 second.
128
Q

Blood Volume distribution by the heart

A

right and left ventricle pump same amount of blood even though pressure is less in right than left because bp in pulmonary trunk is low

129
Q

congestive heart failure

A

Congestive heart failure- fluid accumulation in either pulmonary or systemic circuit from inadequacies in one side of amount of blood pumped. Common causes- myocardial infarction, chronic hypertension, valvular defects, and congenital birth defects.

130
Q

pulmonary edema

A

If the left ventricle pumps less blood than the right, the blood pressure backs up into the lungs causing pulmonary hypertension etc. shortness of breath or suffocation

131
Q

systemic edema

A

If the right ventricle pumps less blood than the left, pressure backs up in the systemic circulation, causing hypertension and edema in multiple places such as organs like liver, abdominal cavity, and limbs, w/ possible distention of jugular veins leading to stroke or kidney failures.

132
Q

Cardiac Output (CO)

A

amount ejected by each ventricle in 1 beat= heart rate x stroke volume

133
Q

Cardiac reserve

A

the difference between a person’s maximum and resting CO people w/ heart disease may have little to none left w/ little tolerance to physical exertion.

134
Q

heart rate/pulse what is it? what are the abnormal rates and what causes them?

A

surge of pressure produced by heart beat that can be felt by palpating a superficial artery. Adult: 72-80 bpm, higher in older individuals. Tachycardia- resting heart rate above 100 caused by stress, anxiety, stimulants, heart disease, fever, or hemorrhage, bradycardia- persistent, resting adult heart rate below 60 bpm, common in sleep, endurance athletes, hypothermia (cardiac surgery).

135
Q

factors (chronotropic effects) that enlist the autonomic nervous system to change heart rate

A

factors that raise the heart right (positive chronotropic) and lower (negative chronotropic) heart rate. Does Not start heartbeat but regulates it. Excessively heart rate diastole too brief cardiac output reduced.
Autonomic nervous system does not initiate the heartbeat, it modulates rhythm and force
Cardiac centers in the reticular formation of the medulla oblongata initiate autonomic output to the heart doesn’t initiate heartbeat

136
Q

Cardiostimulatory effect

A

some neurons of the cardiac center transmit signals to the heart by way of sympathetic pathways ex. Vagus to Adrenergic releasing norepinephrine activating cAMP accelerating SA node and sarcoplasmic reticulum uptake of Ca2+ increasing contraction and relaxation. Vagal tone- steady background firing rate of vagus nerve 70-80 bpm, instrinsic rate 100 bpm

137
Q

Cardioinhibitory effect

A

others transmit parasympathetic signals by way of the vagus nerve, cholinergic inhibitory on SA and AV nodes w/ acetylcholine K+ route hyperpolarization faster than sympathetic.

138
Q

Chronotropic Effects of Chemicals:

Several chemicals affect heart rate

A

Autonomic neurotransmitters (Norepinephrine and Acetylcholine)
Blood-borne adrenal catecholamines (norepinephrine and epinephrine) are potent cardiac stimulants same effect as norepinephrine from sympathetic nerves.
nicotine
thyroid hormone
caffeine
potassium
calcium

139
Q

Nicotine

A

stimulates catecholamine secretion accelerating heartbeat

140
Q

Thyroid

A

hormone increases number of adrenergic receptors on heart so it is more responsive to adrenergic stimulation.

141
Q

Caffeine

A

inhibits cAMP breakdown, prolonging adrenergic effect accelerating heart rate
Potassium potassium- greatest chronotropic effect, hyperkalemia K+ diffuses into cardiomyocytes keeping membrane voltage elevated, inhibiting cardiomyocyte depolarization, less excitable heart rate slow and irregular possible arrest in diastole. Hypokalemia- k+ diffuses out of cardiomyocytes hyperpolarizing harder to stimulate
Calcium- excess hypercalcemia- slow heart beat. Hypocalcemia- elevates heart rate

142
Q

Three variables govern stroke volume

A

preload
contractility
after load

Increased preload or contractility increases stroke volume
Increased afterload decreases stroke volume

143
Q

Preload-

A

amount of tension in ventricular muscle layer before it begins to contract. Increased causes increased stroke volume, increased contraction. The more ventricles stretched (by having increased activity pumping more blood to heart at once) the harder they contract on the next beat matching both sides of the heart.

144
Q

Contractility-

A

how hard muscle contracts for a given preload. Indicating increase in the number of factors making cardiomyocytes responsive to stimulation (inotropic agents positive or negative). Calcium increases strength of each contraction of heart, hypercalcemia- strong prolonged contractions, and can cause cardiac arrest in systole. Hypocalcemia- lose Ca2+ to extracellular, weak, irregular heartbeat and cause cardiac arrest in diastole. Ex. norepinephrine (positive), glucagon (positive), hyperkalemia (negative-reduces strength of action potential and release of Ca2+ dilating and flaccid), vagus nerve (negative not significant)

145
Q

Afterload-

A

sum of all forces a ventricle must overcome before it can eject blood including blood pressure in aorta and pulmonary trunk distal to semilunar valve. Hypertension increasing afterload opposing ventricular ejection w/ increased opposing forces muscles become larger and actually weaken then fail. Increased afterload opposes emptying of ventricles reducing stroke volume

146
Q

Exercise and Cardiac Output

describe the pathway of stroke volume and cardiac output during and for high endurance athletes.

A

proprioceptors in muscles transmit to cardiac centers to increase flow, sympathetic increase output for demand w/ exercise increasing venous return, which increases preload on right ventricle copied to left w/ heart rate and stroke volume rising so cardiac output rises compensating for increased venous return. High endurance athletes have high stroke volume beating more slowly maintaining resting cardiac output w/ sustained exercising hypertrophy of ventricles w/ greater cardiac reserve tolerating more exertion.
•Exercise makes the heart work harder and increases cardiac output
•Increased muscular activity increases venous return
•Increases in heart rate and stroke volume cause an increase in cardiac output
•Exercise produces ventricular hypertrophy

147
Q

Coronary Artery disease what is it how does it progress

A

Bulging Mass grows to obstruct arterial lumen
Causes Angina pectoris,intermittent chest pain, by obstructing 75% or more of the blood flow
Immune cells of atheroma stimulate inflammation
Cause coronary artery spasms due to lack of secretion of nitric oxide (vasodilator)
Inflammation transforms atheroma into a hardened complicated plaque

148
Q

Treatment for CAD

A

Coronary bypass surgery
Uses great saphenous vein from leg or small thoracic arteries constructing detour around obstruction
Balloon or laser angioplasty- inflate widening lumen . can grow back months later
Insertion of a stent to prevent restenosis

149
Q

Unavoidable risk factors of CAD.

Preventable Risk factors:

A

unavoidable: heredity, aging, being male

Preventable risk factors: obesity, smoking, lack of exercise, anxious personality, stress, aggression, and diet

150
Q

Aneurysm what is it? where does it tend to occur?

what does it stem from?

A

weak point in artery or heart wall can rupture ex. thin wall bulging sac, each heart beat pushes against weak part causing rupture and bleed out.
Most common sites:abdominal aorta, renal arteries, and arterial circle at base of brain
Result from Congenital weakness of blood vessels, infections, trauma atherosclerosis and hypertension.

151
Q

Dissecting aneurysm:

A

blood accumulates between tunics of artery and separates them, usually because of degeneration of the tunica media. Pressure from bulges and if ruptures bleed out quickly.

152
Q

Capillaries what are they? how closely do they connect to cells? where are they absent or scarce?

A

exchange vessels: site where gasses, nutrients, wastes, hormones, and leukocytes pass between the blood and tissue fluid through walls of vessels smaller than RBC so they have to squeeze w/ each cell 4-6 cells wide away from capillary
The “business end” of the cardiovascular system Composed of endothelium and basal lamina
Absent or scarce in tendons, ligaments, epithelia, cornea, and lens of the eye

153
Q

Three capillary types and what are they distinguished by?

A

based on how easily things pass through walls and permeability.
continuous
fenestrated
sinusoid

154
Q

Continuous Capillary

A
  • found in most tissues endothelial cells have tight junctions forming continuous tube w/ basal lamina separating from adjacent connective tissues and endothelial cells have intercellular clefts that allow for glucose to pass through but not larger proteins, platelets or, parasites. Brain’s continuous capillaries lack these w/ tight junctions instead. Pericytes w/ elongated tendrils wrapping around capillary contains same contractile proteins as much regulating flow through capillaries and repair cells by becoming either time.
155
Q

fenestrated capillary

A

endothelial cells have filtration pores (fenestrations) by glycoprotein membrane, thinner than plasma membrane, allow for rapid passage of small molecules retaining larger proteins and cell. In organs w/ rapid absorption or filtration: kidneys, endocrine glands, small intestine, and choroid plexus of brain.

156
Q

sinusoid capillary

A

(discontinuous capillaries)- irregular blood-filled spaces in liver, bone marrow, spleen etc. twisted passages conforming to surrounding tissue shape, wide gaps w/ no basal lamina, large fenestrations throughout even allowing proteins and blood cells to pass through site where clotting factors and blood cells enter blood w/ macrophages

157
Q

Capillary Beds

A

capillary beds are 10-100 network of capillaries supplied by single artery or metarterioles funneling into more venules. Controlled upstream by precapillary sphincters controlling blood flow at opening to each capillary, sphincters contract restricting blood flow and opening up channel for blood to flow through bypassing to venule when closed. 90% of beds off at one time

158
Q

Varicose veins what do they result from? who are they commonly found in? hemorrhoids?

A

found in superficial veins not surrounded by supportive tissue, w/ stretching of vessels (people who stand for long periods) pulling cusps of venous valves farther apart until incapable of sealing vessel and preventing backflow of blood, weakening walls w/ irregular dilations and twisted pathway. Hereditary weakness, obesity, and pregnancy obstructing drainage from lower limbs. Hemorrhoids are varicose veins of the anal canal.

159
Q

Portal system

A
  • blood flows through two consecutive capillary networks before returning to heart ex. flowing through hypothalamus and pituitary, kidneys, and liver, intestine and liver.
160
Q

Anastomosis

A
  • point of convergence between blood vessels other than capillaries
    (shunts-artery to vein bypass capillary occur when cold in extremities).
161
Q

Vein anastomosis

A
  • one vein empties directly into another, providing different route of drainage for veins from an organ so blockage is not life-threatening adding extra or alternative paths for blood occuring around heart or joints because of extra blood supply w/ secondary pathway reaching final destination
162
Q

arterial anastomoses routes

A
  • two arteries merge, provide collateral (alternative) routes ex. coronary circulation, joints in limb movement.
163
Q

Blood supply to a tissue can be expressed in terms of

include an example

A

flow and perfusion ex. Femur has greater flow but less perfusion

164
Q

Blood flow:

A

the amount of blood flowing through an organ, tissue, or blood vessel in a given time (mL/min.)

165
Q

Perfusion:

A

the flow per given volume or mass of tissuein a given time (mL/min./g)

166
Q

Blood pressure (BP)

A

the force that blood exerts against a vessel wall. hemodynamics- physical principles of blood flow based on pressure and resistance. With less the resistance equating to more flow.
Measured at brachial artery of arm using sphygmomanometer
A close approximation of pressure at exit of left ventricle
Normal value, young adult: 120/75 mm Hg

167
Q

systolic pressure

A

peak arterial BP taken during ventricular contraction (ventricular systole)

168
Q

diastolic pressure

A

minimum arterial BP taken during ventricular relaxation (diastole) between heart beats

169
Q

Blood Pressure in vessels varies across? what contributes to it?

A

Varies across the type of vessels and age.
w/ arteries spurting intermittently. Capillaries and veins steady speed. Pressure rises w/ age arteriosclerosis stiffening of arteries w/ elastic portion of arteries hardening from free radicals. Atherosclerosis- also causes because of buildup of fatty deposits w/in artery wall, complicated plaques creating hard, crunchy, or bone like consistency.

170
Q

Hypertension what is it and what causes it?

A

—high blood pressure
Chronic resting BP > 140/90
Consequences
Can weaken arteries, cause aneurysms, promote atherosclerosis, caused by age

171
Q

Hypotension what is it and what causes it?

A

chronic low resting BP

Caused by blood loss, dehydration, anemia

172
Q

BP determined by

A

cardiac output, blood volume (regulated by kidneys), resistance to flow. Kidneys greater influence than any on BP.

173
Q

Pulse pressure

A

is the difference between the two systolic and diastolic- force that drives blood circulation stress exerted on small arteries

174
Q

mean arterial pressure

A

taking measurements at several intervals add diastolic and ⅓ systolic influencing syncope, atherosclerosis, kidney failure, edema, and aneurysm.

175
Q

Peripheral resistance

A

—the opposition to flow that blood encounters in vessels away from the heart. Pressure affected by resistance, and flow is affected by both. Arterioles most significant peripheral resistance and flow outnumber any capillary more muscular in diameter change radius to affect flow

176
Q

Resistance hinges on three variables:

A

blood viscosity, vessel length, and vessel radius

177
Q

Blood viscosity

A

(“thickness”)- red blood cell counts and albumin concentrations Viscosity changes w/ anemia reducing it speeding up blood flow. Increased viscosity from dehydration decreasing flow.

178
Q

Vessel length

A

farther liquid travels more cumulative friction it encounters, pressure and flow decline w/ distance.

179
Q

vessel radius

A

Vessel radius- is the greatest indicator as the other two do not change easily. Changes w/ constriction of tunica media or dilation via relaxation of muscle mostly in arterioles controlling flow because of most amount of muscle- Vasomotion controlled by medulla oblongata vasomotor center. Laminar flow-flows in layers faster near center of vessel w/ less friction, and slower near walls dragging against vessel. W/ dilation greater portion in center faster flow, and constrict more close to wall slower average flow. Increase in radius causes major increase in flow, Flow fastest in aorta because of ventricular pressure.

180
Q

Describe how all three viscosity, length, and radius come together to infer changes in pressure and velocity in blood flow throughout body

A

Aorta to capillaries decreases greater distance because of friction over throughout, arterioles and capillaries have smaller radii more resistance, number of vessels and total cross-sectional area greater. From capillaries to veins rising again- veins larger so less resistance, w/ many capillaries converging into one venule from capillaries increasing velocity.

181
Q

Vasoreflexes and what are the three ways of controlling vasomotor activity?

A

are quick and powerful ways of altering blood pressure and flow
local, neural, and hormonal control

182
Q

Local control what do they secrete

A
  • autoregulation ability of tissues to regulate own blood supply based on metabolic waste levels causing vasoconstriction or dilation. at precapillary sphincters using vasoactives chemical (stimulate dilation), reactive hyperemia (overindulge for cutoff vessels), angiogenesis (growth of new blood vessels)
183
Q

Neural control what is it and what are its reflexes

A

remote control by central and autonomic nervous system vasomotor center of medulla oblongata exerts sympathetic control over vessel size depending on exercise, sympathetic nerve fibers stimulate most blood vessel to constrict, vasodilating by reducing sympathetic nerve firing rate. Vasomotor center integrates autonomic reflex, baroreflex (negative feedback response to changes in blood pressure), chemoreflex (changes respiration based on blood chemistry), and medullary ischemic reflex (reduced perfusion in brain response).

184
Q

Hormonal control list the hormones and their affects on BP

A

by angiotensin II (vasoconstrictor ↑ BP), aldosterone (salt and water retaining ↑ BP), natriuretic peptides (increase sodium secretion lower BP), antidiuretic hormone (promotes water retention, vasoconstrictor ↑BP), epiephrine and norepinephrine (vasoconstriction ↑ BP)

185
Q

Two Purposes of Vasoreflexes

A

1) general method of raising or lowering BP throughout the whole body control of BP and 2) Method of rerouting blood from one region to another for perfusion of individual organs by central or local control. If one constricts it is rerouted to another area that is less constricted based on priorities

186
Q

Capillary Exchange

A

two-way movement of fluid across capillary walls. The most important blood in the body is in the capillaries ex water, oxygen, glucose, ammonia, and carbon dioxide. Chemicals passing through capillary walls perfusion transcytosis filtration and reabsorption.
Only through capillary walls are exchanges made between the blood and surrounding tissues

187
Q

Diffusion

A

is the most important form of capillary exchange. Glucose and oxygen more concentrated in blood diffusing out to tissues. wastes more concentrated outside diffuse into blood. Steroid hormones, o2, co2 dissolve. Others need funnel filtration to get through large proteins can’t get through.
Capillary diffusion can only occur if:
The solute can permeate the plasma membranes of the endothelial cell, or
Find passages large enough to pass through
Filtration pores and intercellular clefts

188
Q

Transcytosis-

A

endothelial cells pick up material on one side of plasma membrane and transport across cell by exocytosis. Important for fatty acids, albumin, and some hormones (insulin).

189
Q

Filtration and Reabsorption

A

Fluid filters out of arteriole end because of low pressure of interstitial space and osmotically re enters at venous end delivering material to cells and rinsing away metabolic waste. Hydrostatic pressure-physical force exerted by liquid against surface such as capillary wall, high on arterial and low on venule. Osmotic pressure tends to draw water into capillaries by osmosis, opposing hydrostatic pressure at vein end capillary pressure lower causing osmotic pressure to push fluid in at larger surface area venule end

190
Q

Variations in Capillary Filtration and Reabsorption

A

Capillaries usually reabsorb most of the fluid they filter with certain exceptions. 85% 15% in lymphatic system.
Kidney capillaries in glomeruli do not reabsorb
Alveolar capillaries in lung absorb completely to keep fluid out of air spaces
Active Muscles capillary pressure rises so its only filtration no absorption accumulating in muscle increase bulk

191
Q

edema

Three primary causes-

A

Edema—accumulation of excess fluid in a tissue commonly face, fingers, abdomen, or ankles.
Occurs when fluid filters into a tissue faster than it is absorbed causes blockage, and pain
increased capillary filtration, reduced capillary absorption, and obstructed lymphatic drainage

192
Q

Increased capillary filtration

A

Kidney failure, histamine release, old age, poor venous return (right or left side heart failure)

193
Q

Reduced capillary absorption

A

Hypoproteinemia (reduced albumin), liver disease (albumin produced in), dietary protein deficiency, severe burns

194
Q

Obstructed lymphatic drainage

and end result of edema

A

Surgical removal of lymph nodes

Result in possible suffocation if pulmonary edema occurs, cerebral edema produces-headache, nausea, delirium, seizures, and coma; circulatory shock

195
Q

Mechanisms of Venous Return name the five and briefly describe them

A

Pressure gradient- Blood pressure is the most important force in venous return, increasing w/ blood volume and vasoconstriction
Gravity drains blood from head and neck
Skeletal muscle pump in the limbs- contracting muscles squeeze blood w/ valves closing pumping blood backwards
Thoracic and respiratory pump- inhaling thoracic cavity expands and internal pressure drops while diaphragm going down on exhale raises pressure in abdominal cavity squeezing blood toward heart when you exhale, but flowing faster when inhale.
Cardiac suction- valves and muscles work together pulling blood back to the heart.

196
Q

Venous Return in Physical Activity vs. stagnation

A

exercise increases venous return by muscular pump and increasing cardiac output
Venous pooling occurs with inactivity can lead to clots
Venous pressure not enough to overcome weight of blood forcing it upward
With prolonged standing, all blood in veins may cause CO2 to be too low causing dizziness
Prevented by tensing leg muscles, activate skeletal muscle pump
Jet pilots wear pressure suits

197
Q

Circulatory Shock what is it and what are the two main causes for it?

A

—any state in which cardiac output is insufficient to meet the body’s metabolic needs
cariogenic shock
low venous return

198
Q

Cardiogenic shock:

A

inadequate pumping of heart (MI)

199
Q

Low venous return and what are the three usual causes of this?

A

(LVR): cardiac output is low because too little blood is returning to the heart
hypovolemic
obstructed venous return shock
venous pooling

200
Q

Hypovolemic

A

loss of blood volume resulting from hemorrhage, trauma, bleeding, ulcers, dehydration and burns. Obstructed venous tumor or injury stops blood from being flowing back to heart.

201
Q

Obstructed venous return shock

A
  • object such as growing tumor or aneurysm compresses vein impeding flow
202
Q

Venous pooling-

A

body has normal blood volume but too much accumulates in lower body ex. Long periods of standing or sitting or Neurogenic shock- form of venous pooling shock resulting from sudden loss of vasomotor tone and vasodilation resulting from brain stem trauma or emotional shock

203
Q

Septic & anaphylactic shock

A

can be classified under both cariogenic shock or low venous return as they cause both
bacterial toxins trigger vasodilation and increased capillary permeability.

exposure to antigen on allergen, releasing histamine and generalized vasodilation and capillary permeability.

204
Q

What are the two Responses to shock:

A

compensated- homeostatic mechanisms have spontaneous recovery aka faints and falls w/ gravity restoring blood flow to brain. Decompensated shock- life-threatening positive feedback loops w/ poor cardiac output result in MI weakening heart and output congesting clotted blood in vessel decreasing venous return hurting brain losing vasomotor tone- vasodilation, drop in BP and cardiac output.

205
Q

Anatomy and Physiology of of the Pulmonary Circuit describe the pathway

A

Pulmonary trunk (large vessels ascends diagonally from right ventricle branching into right and left pulmonary arteries to lungs at hilum.
Lobar branches for each lobe (three right, two left). Superior, medial, and lower. Right superior lobar, right medial, inferior lobar artery.
Branches to different parts of lungs w/ basketlike capillary beds surrounding alveoli, exchanging gases w/ air and blood, coming back to pulmonary veins and heart.
Pulmonary veins return to left atrium
Increased O2and reduced CO2 levels

206
Q

Portal Hypertension and Ascites caused by…?

A

Obstruction of hepatic circulation can cause blood pressure to back up in the hepatic portal system
Schistosomiasis—as liver venules are clogged with eggs of parasitic worms living in small veins of mesenteries and intestinal wall moving up to hepatic portal, inflammation results w/ scar tissue around each egg blocking lumen
Spleen enlarges because of lack of drainage
High pressure in vessels of abdominal viscera cause fluid leakage and ascites
Ascites—distension of abdomen

207
Q

Arterial Pressure Points-

A

some major arteries close to surface allow for palpation of pulse and serve as pressure points to reduce arterial bleeding aka femoral artery.

208
Q

Hypertension

A

—most common cardiovascular disease affecting about 30% of Americans over 50
“The silent killer”
Major cause of heart failure, stroke, and kidney failure
Damages heart by increasing afterload
Myocardium enlarges because increases afterload until overstretched and inefficient
Renal arterioles thicken in response to stress
Drop in renal BP leads to salt retention (aldosterone) and worsens the overall hypertension
Primary hypertension
Obesity, sedentary behavior, diet, nicotine
90% of cases
Secondary hypertension—secondary to other disease
Kidney disease, atherosclerosis, hyperthyroidism, Cushing syndrome
10% of cases

209
Q

Breathing represents

A

life!
First breath of a newborn baby
Last gasp of a dying person

210
Q

All body processes directly or indirectly

A

require ATP
Most ATP synthesis requires oxygen and produces carbon dioxide
Drives the need to breathe to take in oxygen, and eliminate carbon dioxide

211
Q

Respiration

A

is a term used to refer to ventilation of the lungs (breathing) or use of oxygen in cellular metabolism

212
Q

Functionsof respiration include:

A

Gas exchange- provides oxygen and CO2 exchange between blood and air
Communication- serves for speech and vocaliazation
Olfaction- provides sense of smell important for social, food, and danger
Acid-Base balance- eliminating CO2 helping to control pH of body fluids excess reacts w/ water generating acid
Blood pressure regulation- lungs carry out step in synthesizing angiotensin II regulating blood pressure
Blood and lymph flow- breathing creates pressure gradients between thorax and abdomen promoting flow of lymph and venous blood
Blood filtration- lungs filter small blood clots from bloodstream dissolving them, preventing clots from obstructing more vital pathways ex. Coronary, cerebeal, and renal circulation
Expulsion of abdominal contents- breath holding and abdominal contraction help expel abdominal contents during urination, defecation, and childbirth
Respiratory System: Nose, pharynx, larynx (last three upper respiratory), trachea, bronchi, lungs (lower respiratory

213
Q

Nose function

A

warms, cleanses, and humidfies inhaled air, detects odors, serves as resonating chamber to amplify voice

214
Q

Tracheostomy-

A

temporary opening in trachea inferior to larynx where a tube is inserted to allow airflow preventing asphyxiation, inhaled air bypassing nasal cavity humidifying it. Can cause mucous membranes to get dried out and encrusted interfering w/ clearance of mucus from tract promoting infection

215
Q

lamina propia-

A

connective tissue layer beneath epithelium where nasal mucosa contains mucous glands, by supplementing mucus produced w/ lymphocytes and plasma cells that can mount immune defenses against inhaled pathogens and w/ blood vessels warming air as it goes by

216
Q

Pleura and pleural fluid functions:

A

reduce friction (lubricant to move w/out friction pleurisy when friction), creation of pressure gradient lower pressure than atmospheric helping w/ lung inflation, compartmentalizing to prevent spread of infection w/ pleura, mediastinum, and pericardium preventing spread

217
Q

Pulmonary Ventilation what does breathing consist of? what is a respiratory cycle?

A

breathing (pulmonary ventilation) consists of a repetitive cycle of inspiration (inhalation) and expiration (exhaling)
Respiratory cycle- one complete inspiration and expiration
Quiet respiration: while at rest, effortless, and automatic
Forced respiration: deep, rapid, breathing, such as during exercise

218
Q

Normal muscular expiration

A
  • all muscles spring back when relax but slow process down so smooth.
219
Q

Forced muscular expiration-

A

rectus abdominis pulls down on sternum and lower ribs, internal intercostals and serratus posterior inferior and abdominal muscles (increase pressure in abdominal cavity forcing organs against diaphragm to expel more air) pull others down reduce chest dimensions expelling air more rapidly.

220
Q

Valsalva Maneuver how is it done what is it important for?

A

deep breath, held by glottis and the contraction of abdominal muscles to raise abdominal pressure and push organ contents out by squeezing them Using abdomen to expel air, excretion, and birth.

221
Q

Neural control of Breathing-

A

no autorhythmic pacemaker cells for respiration, as in the heart because use smooth muscles, and requires multiple muscles so coordinating mechanism needed. Exact mechanism for setting the rhythm of respiration remains unknown. Cease if spinal cord severed high in neck, require nervous stimulation/ respiratory muscles coordinating to breath properly.

222
Q

Respiratory Control Centers

A
  • automatic, unconscious cycle of breathing controlled by three pairs of respiratory centers in reticular formation of medulla oblongata and pons on each side of brainstem so muscles contract simultaneously. Controlled at cerebral and unconscious and Automatic unconscious cycle of breathing. Respiratory center- ventral respiratory group primarily generator of respiratory rhythm w/ inspiratory neurons firing for two seconds and expiatory for 3 seconds relax in time w/ breahting out breathing 12/min. Dorsal respiratory group modifies rate and depth from breathing from external sources. Pontine respiratory group PRG regulating rhythm for ventral and dorsal for sleep, exercise, vocalization, and emotional responses.
223
Q

Peripheral Receptors- provide an example of when this is important and the four kinds of receptors

A 
responding from other areas of nervous system based on body’s needs. Hyperventilation- anxiety triggered state w/ CO2 expelled causing a rise in pH causing cerebral arteries to constrict can cause dizziness or fainting. 
central chemoreceptors
peripheral receptors
stretch receptor
irritant receptors
224
Q

Central chemoreceptors

A

based on cerebral spinal fluid pH, regulating respiration to maintain stable CO2 levels and therefore a proper pH level.

225
Q

Peripheral chemoreceptors

A

located in carotid and aortic bodies responding to CO2, O2 and contents of blood mostly pH.

226
Q

stretch chemoreceptors

A

chemoreceptors
found in smooth muscle of bronchi, bronchioles, and visceral pleura responding to inflation of lungs and signal DRG via vagus. Inflation reflux- excessive inspiration stops respiration so aren’t doing it to much common in infants

227
Q

Irritant chemoreceptors-

A

nerve endings of epithelial cells of airways detecting: smoke, dus, chemical fumes, cold air, and excess mucus. Trigger protective reflexes such as bronchoconstriction, shallow breathing, breath holding, or coughing.

228
Q

Voluntary Control of Breathing

A
  • voluntary control over breathing originates in the motor cortex of frontal lobe of the cerebrum. Send down corticospinal tract to integrating center in spinal cord bypassing brain stem. Limits to when Co2 levels rise overriding ones will.
229
Q

Pressure, resistance, and airflow what are the rules of this?

A

Flow of fluid proportional to pressure difference between two points and inversely proportional to resistance.

230
Q

Intrapleural pressure describes how it changes in inhalation and exhalation

A

upon inspiration- end of expiration chest wall (parietal pleura) expand outward because of elasticity while lungs recoil inward pulling in opposite direction causing it ot be negative. The space is filled w/ watery fluid helping layers to stay together. Intrapleural pressure is kept through cohesion of water keeping two layers together during inspiration when ribs spring up and out visceral follows parietal pleura stretching alveoli decreasing alveolar pressure, and as it increases in volume internal pressure drops so air flows in.

231
Q

charles- law and how that correlates w/ respiration

A

volume of a given quantity of gas is directly proportional to its absolute temperature. Air is warmed warmed by reaching alveoli expanding and causing expansion of lungs.

232
Q

Atelectasis

A
  • collapse lung from airway obstruction, aneurysm, swollen lymph nodes, or expired object, or blood absorbing gas distal to obstruction causing collapse.
233
Q

Pneumothorax

A

Air in pleural cavity, such as if punctured, inspiration when breathing sucks air in potential space will fill w/ air decreasing negative intraneural pressure collapsing. instead of moisture

234
Q

Quiet breathing volume pressure and flow and how Forced breathing is different

A

few mm in either way but increase volume significant to get enough in. Expiration relaxed breathing passive achieved by recoil of thoracic cage w/ volume of whole cage decreasing increasing intrapulmonary pressure out of gradient down lungs.

use accessory to raise pressure.

235
Q

Boyle’s law and what that means for respiration

A

at a constant temperature, the pressure of a given quantity of gas is inversely proportional to its volume
If the lungs contain a quantity of a gas and the lung volume increases, their internal pressure (intrapulmonary pressure)falls
If the pressure falls below atmospheric pressure, air moves into the lungs
If the lung volume decreases, intrapulmonary pressure rises
If the pressure rises above atmospheric pressure, air moves out of the lungs

236
Q

Resistance to Airflow what chemical helps decrease this problem in lungs? what happens if this goes wrong?

A

increasing resistance decreases airflow. Surfactant disrupts hydrogen bonds between molecules decreases surface tension, resisting compression halting collapse of airway that would unchecked collapse by surface tension w/ water. Ex. Infant respiratory distress syndrome- babies lack surfactant

237
Q

Two factors influence airway resistance

A

Diameter of the bronchioles
Bronchodilation (caused by epinephrine and sympathetic nerves norepinephrine increasing airflow)
Bronchoconstriction (caused by histamine, parasympathetic nerves (acetylcholine), cold air, and chemical irritants)

238
Q

Pulmonary compliance-

A

ease w/ which lung expands or change in lung volume relative to given pressure change. Ex. inspiratory effort same intrapleural pressure in two people but lungs expand less in person w/ poor compliance stiffer lungs.

239
Q

Alveolar Ventilation-

A

Air that enters alveoli is made available for gas exchange but not all air gets in there rest comprising anatomical dead space that is not exchanged. Can be altered by sympathetic (dilates airway increasing airflow) and parasympathetic (keeps airway constricted minimizing dead space more of inhaled air ventilates alveoli). Pulmonary diseases can have more dead space w/ alveoli unable to exchange gases because of lacking blood flow or membrane too thick etc.

240
Q

Alveolar ventilation rate (AVR)

A

If a person inhales 500 mL of air, and 150 mL stays in anatomical dead space, then 350 mL reaches alveoli
This measurement is crucially relevant to the body’s ability to get oxygen to the tissues and dispose of carbon dioxide
Residual volume—1,300 mL that cannot be exhaled with maximum effort

241
Q

Composition of Air

A

78.6% nitrogen, 20.9% oxygen, 0.04% carbon dioxide, 0% to 4% water vapor, depending on temperature and humidity, and minor gases argon, neon, helium, methane, and ozone

242
Q

Dalton’s Law

A

and ozone
Dalton’s law—total atmospheric pressure is the sum of the contributions of the individual gases
Partial pressure: the separate contribution of each gas in a mixture
At sea level 1 atm of pressure = 760 mm Hg
Nitrogen constitutes 78.6% of the atmosphere

243
Q

Spirometry-

A

measurement of pulmonary ventilation in order to assess the severity of a respiratory disease or monitor the patient’s improvement or deterioration allowing to distinguish between restrictive and obstructive disorders:

244
Q

Obstructive disorders

A

blocking airway harder to inhale or exhale air asthma and chronic bronchitis measured by forced expiratory volume amount exhaled in given time.

245
Q

Restrictive disorders-

A

pulmonary compliance limiting amount lung inflates, reducing vital capacity ex. pulmonary fibrosis ,black lung disease.

246
Q

Pneumonia

A
  • cant flow and exchange as fast because of a buildup of mucous making it farther to travel to lung and air can’t reach equilibrium as fast can’t breath as well when sick.
247
Q

Emphysema

A
  • alveolar walls breaking down exchange improperso not gas exchange and walls destroyed or damage w/ disruption in gas exchange.
248
Q

Alveolar Gas Exchange how do high altitudes affect this?

A

-Air in alveolus in contact w/ film of water covering epithelium, O2 has to dissolve in water and passing through membrane. CO2 diffuse out of water into alveolar air. Gases diffuse down own gradients O2 gradient much greater even though CO2 diffuse faster. partial pressures of all gases are lower causing less oxygen to diffuse into blood.

249
Q

Inspired air vs. alveolar-

A

warmed and residual air from previous cycles are mixed in w/ alveolar having a lot more CO2 exchange oxygen w/ gas exchange only occurs in alveoli area.

250
Q

Membrane thickness affected by things like

A

Membrane thickness affected by things like- Tuberculosis, emphysema, and lung cancer causing less CO2 exchanged because of dead and weak cell walls. Pulmonary edema and left ventricle creates thickening in heart and lungs also leading to longer and less exchange.

251
Q

Ventilation-perfusion coupling:

A

match airflow to blood flow. If part damaged changes flow to another part because not adequate. There would be a problem w/in this gas exchange perfusion of capillaries issue in either side causes problem in both

252
Q

Henry’s law—

A

at the air–water interface, for a given temperature, the amount of gas that dissolves in the water is determined by its solubility in water and its partial pressure in air
The greater the PO2in the alveolar air, the more O2the blood picks up
Since blood arriving at an alveolus has a higher PCO2than air, it releases CO2into the air
At the alveolus, the blood is said to unload CO2 and load O2 (involves erythrocytes)
Efficiency depends on how long an RBC stays in alveolar capillaries
Each gas in a mixture behaves independently
One gas does not influence the diffusion of others

253
Q

Respiration and Exercise what triggers changes in respiration during exercise

A

causes of increased respiration in anticipation of exercise not from any changes actually yet sense by body. Specific commands to muscle and different respiratory centers increases ventilation because of it. Proprioceptors Sending to brain stem w/ respiratory centers increasing breathing and inform a muscle of moving. Keep bodies values on normal levels
When the brain sends motor commands to the muscles
Exercise stimulates proprioceptors of muscles and joints

254
Q

Oxygen Imbalances what is it and what are two kinds that cause it? what is a sign of it?

A

Hypoxia—a deficiency of oxygen in a tissue or the inability to use oxygen- A consequence of respiratory diseases
Anemic hypoxia—due to anemia resulting from the inability of the blood to carry adequate oxygen
Histotoxic hypoxia—metabolic poisons such as cyanide prevent tissues from using oxygen
Cyanosis—blueness of the skin–Sign of hypoxia

255
Q

Chronic Obstructive Pulmonary Disease

A

Long term obstruction of flow and substantial reduction in pulmonary ventilation. Include: chronic bronchitis and emphysema as a result of cigarette smoking as well as air pollution, occupational exposure to airborne irritants, and hereditary.

256
Q

Chronic bronchitis-

A

severe, persistent inflammation of lower respiratory tract. Goblet cells enlarge and secrete more mucus than they should w/ cilia overloaded not moving like they are supposed to prime area for bacterial growth developing chronic cough because consistently trying to get mucus out/ sputum. Continued smoking kills macrophages that would defend against it. Ventilation-perfusion ratio reduced w/ patients exhibiting Hypoxemia and cyanosis. Inflamed and filled w/ mucous so not enough air and entire area for gas exchange too much for it to occur.

257
Q

Emphysema-

A

damaged alveoli w/ walls breaking down and less membrane for gas exchange less amount of space to travel and less surface area for gas to occur. Collapse and obstruct outflow of air w/ normal respiration leading them to be barrel chested as air is trapped in lungs. Alveolar wall and capillaries destroyed ventilation-perfusion ratio normal so no cyanosis, exhausted or emaciated expending three to four times normal amount of energy just to breathe by using using accessory. COPD reducing capacity lungs causes hypoxemia, hypercapnia, and respiratory acidosis. Stimulating kidneys to secrete erythropoietin increasing erythrocyte production and polycythemia leading to cor pulmonale- hypertrophy and failure of right heart due to obstruction of pulmonary circulation

258
Q

Smoking and Lung Cancer three types? how they develop? rates of survival?

A
  • Squamous Cell Carcinoma ciliated pseudostratified cells become Stratified squamous invade underlying tissues causes bleeding lesions, dense swirled masses of keratin swirls replacing functional tissue. Adenocarcinoma- mucous glands of lamina propria. old cell carcinoma clusters of cells originate in primary bronchi metastasizes quickly and spreads. 90% originate in mucous membranes compression airway and lung collapsion, coughing up blood because of damaging walls of heart and alveoli and bronchi. Metastasis quickly spreads super fast to everything else. Only 7% survive after 5 years.

A&P 2 1st half (3 decks)

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