Human Structure & Function Ii - Exam I

Front 1

Function of Cardiovascular System

Back 1

-heart, vessels, blood (and sometimes the lymphatic system)
-adequately perfuse tissue to meet changing demands

Front 2

Closed System

Back 2

-vertebrates (and a few invertebrates) have a closed circulatory system
-Closed Circulatory System: have blood contained within elements of blood vasculature at all time

Front 3

Artery

Back 3

-conducting vessel
-takes blood away from the heart
-gets blood from point A to B

Front 4

Capillary

Back 4

-exchanging vessels
-exchange gases, nutrients, wastes, etc. with surrounding tissue through diffusion
-Endothelium: simple squamous epithelium surrounds blood vessels

Front 5

Veins

Back 5

-Capacitance Vessels --> relates pressure & volume
-return blood to heart
-highly compliant --> small changes in pressure cause large changes in volume

Front 6

Portal System

Back 6

-exception to rule of blood traveling from heart --> artery -->capillary --> vein
-when a capillary bed drains into another capillary bed through veins

Front 7

Venipuncture

Back 7

-blood is generally drawn from the median cubital vein

Front 8

Testing Blood

Back 8

-tells if organs are working correctly or not
-are glucose, gases, etc. at equilibrium
-venous blood has specific values that differ from arterial blood

Front 9

Plasma & Interstitial Fluid

Back 9

= exchanging fluids/environments

Front 10

Hematocrit

Back 10

-fraction of whole blood volume that contains RBC's
-average values:
males = 42-52%
females = 36-48%
-formed elements separated from plasma

Front 11

Buffy Coat

Back 11

very thin layer of white blood cells and platelets just above the thick layers of RBC's in the layer of formed elements after centrifugation

Front 12

Equation for Blood Volume

Back 12

BV = PV/(1-HC)
-BV = Blood Volume
-PV = Plasma Volume
-HC = Hematocrit

-78 mL/kg lean body weight, 9 pints in males
-56 mL/kg lean body weight, 6.5 pints in females

Front 13

Plasma (constituents)

Back 13

-92% water
-7% proteins (58% albumin, 37% globulins, 4% fibrinogen, 1% regulatory proteins)
-1% other solutes (electrolytes, nutrients, respiratory gases, waste products)

Front 14

Blood Proteins

Back 14

made by liver

Front 15

Plasma Proteins

Back 15

-serum albumin
-Globulins: made by liver; involved in transport of hormones; aplha, beta, and gamma bands
~alpha 1 --> alpha 1-antitrypsin, aplha 1-acid glycoprotein
~alpha 2 --> haptoglobin, alpha 2-macroglobulin, alpha 2 antiplasmin, ceruloplasmin
~beta bands --> transferrin, LDL, complement
~gamma bands --> immunoglobulins (IgA, IgD, IgE, IgG and IgM); made by plasma cells, not liver

Front 16

Clotting Factor

Back 16

Fibrinogen = most common clotting factor

Front 17

Erythrocyte

Back 17

-red blood cells
-average = 5 million RBC's (5 x 10^6)
-biconcave discs about 8 microns in diameter

Front 18

Leukocytes

Back 18

-white blood cells
-average = 5,000 - 10,000 (5 x 10^3)
-Neutrophils, Lymphocytes, Monocytes, Eosinophils, Basophils

Front 19

A1C Test

Back 19

-tests blood glucose; used for diabetes

Front 20

Platelets

Back 20

-sometimes called thrombocytes (not accurate in humans though)
-important in blood clotting

Front 21

Hemoglobin

Back 21

-made up of 4 polypeptide chains each with a heme group --> iron vital for transport of oxygen

Front 22

Hemoglobin Types (non-pathological variants)

Back 22

Embryo:
-Gower 1 (ζ2ε2)
-Gower 2 (α2ε2)
-Hemoglobin Portland (ζ2γ2)

Fetus:
-Hemoglobin F (α2γ2)

Adults:
-Hemoglobin A (α2β2) - The most common with a normal amount over 95%
-Hemoglobin A2 (α2δ2) - δ chain synthesis begins late in the third trimester and in adults, it has a normal range of 1.5-3.5%
-Hemoglobin F(α2γ2) - In adults Hemoglobin F is restricted to a limited population of red cells called F-cells.

Front 23

Standard Blood Tests

Back 23

-report number of RBC's per microliter of whole blood called the red blood cell count
-or measured in mm^3

Front 24

Androgens Stimulate...

Back 24

RBC production --> more RBC's in hematocrit of men than women (estrogen does not stimulate RBC production)

Front 25

Blood Antigens

Back 25

-glycoproteins on the outside of RBC's
-A, B, AB, & O blood types
-O --> homozygous recessive
-AB --> codominant

Front 26

Blood Antibodies

Back 26

-Antigen A --> has anti-B antibodies
-Antigen B --> has anti-A antibodies
-Antigen AB --> has no antibodies
-Neither antigen A or B --> has anti-A and anti-B antibodies

Front 27

Universal Donor

Back 27

Blood type O (doesn't have antigens)

Front 28

Universal Recipient

Back 28

Blood type AB (can handle any antigens)

Front 29

What happens when someone receives blood with antigens that interact with antibodies?

Back 29

-antibodies & antigens combine --> agglutination
-have fever, chills, & hemolysis (lyse of RBC's)

Front 30

Hemolysis

Back 30

hemoglobin released in plasma, kidneys try to filter it out, but large molecules get stuck --> kidney failure

Front 31

Rh Factor

Back 31

-antigen responsible for + or - after blood type
-usually referred to as antigen D

Front 32

Cross Matching

Back 32

-take a sample of persons plasma & add some blood that will be transfused
-if agglutination occurs, it is not a match

Front 33

Rh- woman with Rh+ man

Back 33

-ok if baby is Rh-
-fetus with Rh+ blood = no reaction in first pregnancy
-2nd fetus with Rh+ blood --> maternal antibodies created during first pregnancy diffuse to child & attack fetal blood --> hemolysis in fetus
-Called Hemolytic Disease of Newborn of Erythroblastosis Fetalis
-Rhogam --> used to prevent HDN; cleans up left over RBC's before the mother can make antibodies against them

Front 34

Blood Islands

Back 34

-blood being produced in the yolk sac
-Blood Production --> eventually spreads to the liver & spleen as fetus develops

Front 35

Extramedullary Hematopoiesis

Back 35

-formation of blood cells outside of bone marrow in places like liver, spleen, and lymph nodes

Front 36

Erythroblasts

Back 36

fetal blood cells (blast = undifferentiated)

Front 37

Pleuripotent Stem Cells

Back 37

-can differentiate into many different things
-stem cells reproduce in undifferentiated state
-ex Bone Marrow transplanted --> reproduced in recipient --> normal function

Front 38

Myeloid Stem Cells

Back 38

make RBC's, platelets, & WBC's (except lymphocytes)

Front 39

Lymphoid Stem Cells

Back 39

make lymphocytes

Front 40

Hormones in Red Bone Marrow

Back 40

dictate which way pleuripotent stem cells will develop

Front 41

Red Bone Marrow regulated by...

Back 41

-negative feedback loops
-regulate number of each cell produced

Front 42

EPO

Back 42

-Erythropoetin
-determines rate at which RBC's are released into blood

Front 43

Reticulocytes

Back 43

-young erythrocytes with granular or reticular filamentous structures, constituting 0.5-2.0% of all RBCs.
-Proerythroblast --> Basophilic Erythroblast --> Polychromatic Erythroblast --> Orthochromatic Erythroblast --> Reticulocyte

Front 44

Decrease in Concentration of oxygen (efeedback loop of RBC's)

Back 44

decrease in O2 detected --> detected by peritubular fibroblasts in renal cortex of kidney --> increases release of EPO --> accelerates maturation of RBC's in red bone marrow --> increase in O2 concentration --> decrease in release of EPO

Front 45

Physiologic Polycythemia

Back 45

increase in RBC's due to cancer or some other abnormal source

Front 46

Blood Doping

Back 46

EPO increases RBC's --> more O2 in blood --> better performance

Front 47

RBC Lifespan

Back 47

100-120 days
-begin to display signs of senescence
-noticed by phagocytic cells in liver & spleen
-removed by macrophages --> recycle main parts of RBC's (cytoskeleton, membrane, etc.) as amino acids
-globin reused
-heme --> iron taken out
-iron picked up by protein (transferrin --> transport preotein for iron; feratin --> store iron in liver)
-non-iron heme --> transformed into bilirubin (yellow in color) which circulates in blood
-some removed by liver & used for bile salts --> secreted by liver, stored in gallbladder, released for breakdown of fats
-exit body in urine & feces

Front 48

Red Bone Marrow

Back 48

-hemopoetic material
-if it fails --> aplastic anemia

Front 49

Iron Deficiency

Back 49

-iron is needed for heme groups
-iron deficiency = iron deficiency anemia

Front 50

B12

Back 50

vitamin required for RBC synthesis

Front 51

Gastric Intrinsic Factor

Back 51

hormone produced by parietal cells in stomach

Front 52

Pernicious Anemia

Back 52

-B12 --> stomach with Gastric Intrinsic Factor --> distal portion of small intestine --> absorption
-if something doesn't function in this pathway = Pernicious Anemia

Front 53

White Blood Cells

Back 53

-Leukocytes
-no role in circulating blood, just use it as link between hemotapoetic tisue (red bone marrow) and body tissue
-function in immune processes
-Modal in tissue through amoeba motion --> attracted to some chemicals
-killing foreign invaders often require WBC's to kill themselves
-Nucleated
-polymorphonuclear --> varying nucleus shapes

Front 54

Diapededis

Back 54

White blood cells move out of blood vessels between endothelial cells

Front 55

Granulocytes

Back 55

-Neutrophils (60-70%): involved with bacteria
-Basophils (.5-1%): involved with allergies & autoimmune responses of asthma
-Eosinophils (2-4%): directed towards parasites

Front 56

Agranulocytes

Back 56

-Lymphocytes (20-25%)
-Monocytes (3-8%)

Front 57

All WBC's come from...

Back 57

red bone marrow

Front 58

Neutrophils

Back 58

-multiple lobes
-band cell --> young/early stage after release (confused with neutrophil)
-drumstick appendage --> represents heterochromatic X chromosome in WBC (only in females)

Front 59

Both mast cells and basophils contain special cytoplasmic granules which store mediators of inflammation. The extracellular release of the mediators is known as degranulation and may be induced by:

Back 59

(a) physical destruction, such as high temperature, mechanical trauma, ionising irradiation, etc.;

(b) chemical substances, such as toxins, venoms, proteases;

(c) endogenous mediators, including tissue proteases, cationic proteins derived from eosinophils and neutrophils;

(d) immune mechanisms which may be IgE-dependent or IgE-independent. The former is elicited by aggregation of IgE bound to high-afinity receptors (Fc RI) on the surface of these cells. Specific antigen (allergen) is responsible for the IgE aggregation. In the IgE-independent way, the anafylatoxins C5a, C3a and C4a are formed during activation of complement. Then, the degranulation is triggered through C5a-receptors on the surface of mast cells and basophils.

Front 60

Lymphocytes

Back 60

-nucleus takes up most of cytoplasm
-about same size as RBC

Front 61

B-lymphocytes

Back 61

turn into plasma cells & make circulating antibodies

Front 62

T-lymphocytes

Back 62

cell mediated immunity

Front 63

Megakaryocyte

Back 63

mother cell of platelets that never leave the Red Bone Marrow

Front 64

Monocyte

Back 64

-Biggest WBC
-the most phagocytic
-the most modal
-when it leave the blood --> called a macrophage

Front 65

Thrombocytopenia

Back 65

not enough circulating platelets

Front 66

Layers of blood vessels

Back 66

-Tunica Interna --> endothelium
-Tunica Media --> smooth muscle & elastin
-Tunica Externa --> collagen

Front 67

Hemostasis

Back 67

1) Maintain Blood in a fluid state while circulating (Anticoagulation Activity)
2) Arrest bleeding at site of injury by formation of hemostatic plug (Procoagulation Activity)
3) Ensure the removal of the hemostatic plug when healing is complete
-Normally pro- and anti-coagulant activities exist in a delicate balance
-Pre-exist to quickly stop bleeding (balance shifts/outnumbers towards one the is needed at time)

Front 68

Virchow's Triad

Back 68

-Injury in Vascular Epithelium
-Alteration in normal blood flow
-Alteration in constitution of blood
(all 3 can lead to thrombosis)
*endothelial integrity is the single most important factor in maintaining a normal balance between pro- and anticoagulants

Front 69

Hemostasis prevented by...

Back 69

-under normal physiological circumstances, hemostasis is prevented by endothelium
-This provides a physical barrier and secretes platelet inhibitory products (prostacyclin & Nitric Oxide)

Front 70

Nitric Oxide

Back 70

promotes vasodilation

Front 71

Endothelin

Back 71

-protein that causes blood vessel constriction & raise blood pressure
-normally kept in balance by other mechanisms, but when over-expressed --> high blood pressure & heart disease

Front 72

Stages in hemostasis

Back 72

1)Vascular Phase
2)Platelet Phase (platelet plug formation)
3)Plasma Phase (clotting or coagulation)

Front 73

Vasulcar Spasm

Back 73

-local vasoconstriction at site of injury
-directly related to intensity of trauma
-clean cut (razors/glass) --> cause more bleeding than crushing injuries
-hemostat --> braod clamp used to close off blood vessels cut by scapula

Front 74

Platelet Phase (platelet plug formation)

Back 74

With endothelial cell injury, platelets adhere to vWf in the subendothelium via the platelet membrane receptor GPIb-IX.

Front 75

Von Willenbran Factor

Back 75

-vWf is needed for adherence, but there is also circulating vWf that is bound to a clotting factor
-keeps platelets from sticking together & keeps clotting factor VIII from degrading
-if this fails = Von Willenbran disease

Front 76

Release Reaction

Back 76

-Adhesion activates platelets, causing shape change and release reaction
-Platelets release ADP, TXA2, and seratonin, which promote platelet aggregation & increase cascular spasm (positive feedback)
-Ca2+ is released --> necessary for coagulation
-Platelet membrane intergrin receptor, GPIIb-IIIa, is activated
-Fibrinogen binds to this receptor, cross-linking platelets to form platelet plug
-phosphatidylserine is moved to the outer layer of the platelet membrane.
-Phosphatidylserine (which used to be called PF3) provides an essential binding site for activated coagulation factors.
-The platelet plug thus formed is able to stop the blood until the clotting mechanisms start operating.

Front 77

Clotting Phase (Plasma Phase)

Back 77

-Plasma proteins associated with the intrinsic and extrinsic pathways are activated which initiate the clotting process.

Front 78

Clotting Factors (13 of them)

Back 78

-made in liver & need vitamin K for synthesis
-vitamin K --> fat-soluble, we get half from diet & half from bacteria in large intestine

Front 79

Reaction Cascade

Back 79

-Good --> amplifies response
-Bad --> hard to stop; if one step gets screwed up it effects entire cascade

Front 80

Coagulation (Clotting)

Back 80

-formation of prothrombinase (Factor X, staurt-prower factor)
-conversion of prothrombin --> thrombin (Factor II)
-conversion of fibrinogen --> fibrin & clot formation (Factor I)

Front 81

Intrinsic Pathway

Back 81

-something pre-existing in blood vessels comes into contact with something outside of blood vessel
-Factor XII sets off pathway
-Fibrin forms meshwork & captures platelets/blood cells to form clot (thrombus)

Front 82

Extrinsic Pathway

Back 82

-Something outside blood vessel contacts something inside
-Tissue Factor: interacts with inactive pre-existing clotting factor
-Thrombin produced primarily for positive feedback on both intrinsic & extrinsic pathways (accelerant)

Front 83

Embolysm

Back 83

clot that breaks free into circulation

Front 84

Hemophilia A

Back 84

-don't make factor VIII
-very similar to von willenbran disease

Front 85

Hemophilia B

Back 85

issue with factor IX

Front 86

Timing of Clot Formation

Back 86

1)Vascular Spasm --> immediate reaction; lasts for 30 mins or more
2)Platelet Phase --> begins within 15-30 secs
3)Plasma Phase --> Begins after 30 secs
-Time to clot completion in a controlled setting:
in capillary tube = 8-18 mins (coagulation time
small controlled wound = 1-4 mins (bleeding time)

Front 87

Clot Retraction/Syneresis

Back 87

-serum --> plasm w/o clotting factors
-Factor XIII (clot stabilizing factor)
-Actin & Myosin --> pull edges of wounds together & squeeze fluid out

Front 88

Factors Limiting Clot Growth

Back 88

-Dilution
-Fibrin formed feedsback negatively on thrombin (self-limiting)
-Plasminogen - produced in liver; anticoagulant

Front 89

Plasminogen

Back 89

-produced in liver; anticoagulant
-clot forms with inactive plasminogen in it
-Tissue plasminogen activator --> causes plasminogen to go to active form of plasmin --> break down fibrin strands & blood clot

Front 90

Endogenous Inhibitors of Clotting

Back 90

-Thrombin plays a pivotal role in coagulation
-Antithrombin is present in the plasma in significant concentrations (~2-3 mM). Antithrombin primarily neutralizes factor Xa and thrombin, in addition to inhibiting most active serine proteases of the clotting system.
-Protein C is another plasma protein that limits clotting by being activated by thrombin to proteolytically inactivate proaccelerin (V) and antihemophilic factor (VIII).
-Thrombomodulin, a cell membrane bound glycoprotein lining the vascular endothelium, specifically binds thrombin so as to convert it to a form with decreased ability to catalyze clot formation but with a >1,000-fold increased capacity to activate protein C.

Front 91

Anticoagulants

Back 91

1)Caumarines
2)Heparin & derivatives
3)Direct Thrombin Inhibitors
4)Ca2+ sequestering Agents (ex EDTA)

Front 92

Order of Clotting Factors I, II, III, XIII, IV, Ca2+ in hemostasis

Back 92

Review

Front 93

Heart

Back 93

-pumps blood
-blood flows from high to low pressure
-heart --> about 90 mm/Hg
-arteries --> 20 mm/Hg
-Capillaries --> 5-10 mm/Hg
-Veins --> 1-5 mm/Hg

Front 94

Equation for Force

Back 94

F=P/R

Front 95

Heart Location

Back 95

-lies in pericardial cavity
-also lies in mediastinum (includes veins & arteries going into the heart

Front 96

Mediastinum

Back 96

-Superior Mediastinum --> no serous membrane; includes vessels & trachea
-Inferior Mediastinum:
~Anterior Mediastinum --> thymus
~Middle Mediastinum --> pericardial cavity (only serous membrane in mediastinum)
~Posterior Mediastinum --> trachae, esophagus

Front 97

Heart Positioning

Back 97

-lies on right side touching diaphragm
-base lies between inferior & superior mediastinum

Front 98

Parietal Pericardium

Back 98

Outer layer

Front 99

Visceral Pericardium

Back 99

Inner Layer

Front 100

Dense Fibrous Layer

Back 100

inelastic connective tissue of parietal pericardium limits how much heart can expand

Front 101

Pericardial Space

Back 101

-contains pericardial fluid (basically H2O & protein)
-fluid reduces friction

Front 102

Epicardium

Back 102

-Visceral Pericardium
-contains fat & blood vessels that supply heart

Front 103

Intercalated Disc

Back 103

-fascia adherons hold everything together
-gap junctions: occur between all cardiac cells
-functional syncichium

Front 104

right & left halves of heart

Back 104

-function is parallel
-everything happens in equal proportions

Front 105

Right Atrium

Back 105

-receives blood from IVC, SVC, & coronary sinus

Front 106

Fossa Ovale

Back 106

-Remnant of Foramen Ovale --> connects two atria

Front 107

Chordae Tendinae

Back 107

connected to cusps of valves; keep them from flipping into Atria

Front 108

Trabeculae Carnae

Back 108

where chordae tendinae attach in left ventricle

Front 109

Left Coronary Artery

Back 109

left anterior surface of heart --> circumflex artery in coronary surface to posterior heart & left anterior descending artery

Front 110

Right Coronary Artery

Back 110

posterior heart --> posterior interventricular sulcus & right marginal artery

Front 111

anastomose

Back 111

all branches of coronay arteries eventually connect

Front 112

Common Place for Heart blockage

Back 112

Anterior interventricular artery & circumflex artery

Front 113

Myocardial Infarction

Back 113

-farther from origin = smaller effect

Front 114

Cardiomyocytes

Back 114

-cardiac muscle cells
-lie in subendocardial tissue

Front 115

Pacemaker Cells

Back 115

-part of intrinsic cardiac activity
-share presence of gap junctions & linked to contractile cells

Front 116

Twitch Summation & Tetanus

Back 116

Do not occur in cardiac muscle

Front 117

Contractile Cardiomyocytes

Back 117

-Ca2+ sustains depolarization
-Reach threshold --> influx of Ca2+
-Repolarization caused by K+ flowing out

Front 118

Bundle of His

Back 118

travels through interventricular septum

Front 119

Ectopic Focus

Back 119

pacemaker rhythm thrown off by outside source

Front 120

Tachycardia

Back 120

sustained increase in heart rate

Front 121

Bradycardia

Back 121

sustained decrease in heart rate

Front 122

EKG

Back 122

-P wave --> SA node firing = atrial contraction
-QRS complex --> vent depolarization
-T wave --> vent repolarization
-PQ segment --> AV nodal delay
-QT segment --> ventricular systole
-TQ interval --> vent. diastole

Front 123

Cardiac Cycle

Back 123

-Contraction followed by relaxation
-Systole & Diastole
-P wave to P wave

Front 124

Systole

Back 124

Contraction

Front 125

Diastole

Back 125

Relaxation

Front 126

Cardiac Cylce Calculation

Back 126

Beats per min./ 60 = 0.8 sec

Front 127

last 400 msec of cardiac cycle

Back 127

both atria & ventricles are relaxed

Front 128

During Increase heart rate...

Back 128

Diastole ventricular filling is shortened

Front 129

Atrial Contraction

Back 129

quickly adds small amount of blood to ventricle (tops it off)

Front 130

End Diastolic Volume

Back 130

-Volume after ventricles fill
-potential of what heart can do

Front 131

End Systole Volume

Back 131

Volume of blood in ventricles after contraction

Front 132

Stoke Volume

Back 132

-how much blood is pumped out of heart
-actual measure of work done by heart

Front 133

Lub-Dub sounds

Back 133

-First caused by blood hitting closed AV valves
-Second caused by blood hitting closed semilunar valves

Front 134

Isovolumetric Ventricular Contraciton

Back 134

pressure is there, but no movement of blood, all valves closed

Front 135

Ventricular ejection

Back 135

overcomes pressure of blood in aorta & pushed through semilunar valve

Front 136

Ejection Fraction

Back 136

stroke volume/end diastolic volume --> good read of hearts productivity/efficiency

Front 137

Athletes

Back 137

better at pumping blood --> lower end systolic volume

Front 138

Cardiac Output

Back 138

Stoke Volume x heart rate

Front 139

Isovolumetric Ventricular Relaxation

Back 139

all 4 valves closed during relaxation

Front 140

Turbulance

Back 140

backflow of blood, called a murmur