BIO 202 Exam 1

functions and properties of blood

• transport

  • O2 from lungs → organs/cells

  • CO2 from cells → lungs

  • nutrients from digestive system & storage

  • wastes to liver & kidneys

  • hormones

• regulates temp

• immunity

• clotting

• stabilizes water balance

• stabilizes pH

Why is blood a connective tissue?

it has more matrix than cells (more plasma > cells)

How many liters of blood do adults have?

4-6 L

plasma

a clear extracellular fluid (55% of blood)

erythrocyte

red blood cells

• count = 4.2-6.2 million/microliter

leukocyte

white blood cells

• count = 5,000-10,000 per microliter

platelet

count = 130,000-400,000 per microliter

granulocytes

• white blood cells with cytoplasmic granules

  • Basophils

  • Eosinophils

  • Neutrophils

agranulocytes

• white blood cells with NO cytoplasmic granules

  • lymphocytes

  • monocytes & macrophages

hematocrit

percent of total volume that is cells

• erythrocytes are heaviest and settle first

• 37-52% total blood volume

• blood viscosity is dependent on hematocrit

buffy coat

• white blood cells and platelets

• 1% of total blood volume

plasma

47-63% of blood volume

• 92% water

• contains proteins, enzymes, nutrients, wastes, hormones, lipids, trace elements, gases

• serum = plasma minus the clotting proteins

viscosity

resistance to flow (thickness/stickyness)

• blood is 4.5-5.5 times more viscous than water

• too many or too few RBCs changes the viscosity of blood and puts a strain on the heart

osmolarity

total molar concentration of dissolved particles in 1L of solution due to transfer of nutrients and wastes between the blood & tissue fluids

• too high → bloodstream absorbs too much fluid from tissues, leading to hypertension

• too low → bloodstream transfers too much fluid to tissues, resulting in edema and hypotension

what is the most abundant solute in plasma?

proteins

• used for clotting, defense, and transport

3 categories of plasma proteins

1. albumins = most adundant plasma protein, made by liver, contribute to viscosity & osmolarity, influences blood pressure, flow, and fluid balance

2. fibrinogen = clotting

3. globulins = antibody = immune system defenses

hemopoietic tissues

produce formed elements

• red bone marrow produces RBCs, WBCs, and platelets

• hemopoietic stem cells multiply continually and are pluripotent (can differentiate into multiple cell lines)

• lymphatic organs produce some types of WBCs

stimulated by erythropoietin, thrombopoietin, and colony stimulating factors

erythropoiesis

production of erythrocytes, produced 2.5 million RBCs/second, dev takes 3-5 days

1. hemopoietic stem cell in red bone marrow

2. first committed cell = erythrocyte CFU (proerythroblast)

   1. has receptors for erythropoietin from kidneys

3. eryhtroblasts multiply and synthesize hemoglobin

4. nucleus degenerates to form a reticulocyte

5. erythrocyte (endoplasmic reticulum degenerates and cell is mature)

An erythrocyte does not have a nucleus and lives for _ days

120

nutrients required for erythropoiesis

• iron

• B12 & folic acid → for DNA synthesis and rapid cell division

• Vitamin C & copper → cofactors for enzymes and synthesizing RBCs

erythrocyte structure

• disc shaped, sunken center (no nucleus)

• outer surface of plasma membrance has glycoproteins and glycolpids for blood type

• inner surface of plasma membrane has actin & spectrin for resilience & durability

• performs anaerobic fermentation

  • no oxygen needed

erythrocyte function

• gas transport

  • increased surface area/volume ratio helps

• 33% of cytoplasm is hemoglobin

  • helps )2 delivery to tissues and CO2 transport to lungs

• carbonic anhydrase (CAH) in cytoplasm

  • produces carbonic acid from CO2 and water

  • important for CO2 gas transport and pH balance

hemoglobin structure

• 4 protein chains (globins)

  • 2 alpha and 2 beta

• each protein chain has a heme group that binds O2 to iron

• Hb molecule can carry 4 O2

  • 2.5% of adult Hb has delta globin chains instead of beta

  • fetal hemoglobin binfs O2 more tightly and has gamma instead of beta chains

hematocrit values by gender

women - 37-48% cells

men - 42-52% cells

hemoglobin concentration by gender

women - 12-16 g/dL

men - 13-18 g/dL

RBC count by gender

women - 4.2-5.4 million/microliter

men - 4.6-6.2 million/microliter

women have lower counts due to:

• androgens (male hormone) stimulate RBC production

• periodic menstrual losses

• counts are inversely proportional to body fat (women have more body fat)

men blood clot faster and fewer skin blood vessels

erythrocyte homeostasis

negative feedback control

1. hypoxemia (low oxygen in blood)

2. liver and kidneys sense this

3. secretion of erythropoietin (hormone calls for RBCs to be made)

4. stimulation of red bone marrow

5. accelerated erythropoiesis

6. increased RBC count

7. increases oxygen transport

causes of hypoxemia

• loss of blood (bleeding, donating blood)

• high altitudes

  • less O2 available

• sedentary person starts exercise program, which makes them require more O2

erythrocyte death & disposal

• RBCs live for 120 days

• spleen - RBC graveyard

  • macrophages in spleen digest membrane bits

  • separate heme from globin

  • hydrolyze globin into amino acids

  • remove iron from heme

  • convert heme to bilirubin

    • liver uses bilirubin to make bile

    • excess bilirubin leads to jaundice

polycythemia

erythrocyte disorder

• excess of RBCs (thick blood, blockages, strain on heart)

• primary __ = due to cancer of erythropoietic cell line

  • RBC count as high as 11 million/microliter; hematocrit 80%

• secondary __ = RBC count up to 8 million/microliter

  • dehydration - more RBCs/microliter due to less plasma

  • high altitude

  • physical conditioning (enduranced trained athletes)

  • emphysema (less lung tissue)

dangers = increased blood volume, pressure and viscosity lead to poor circulation, heart strain and clogged capillaries

→ embolism, stroke, heart failure

iron deficiency anemia

dietary iron deficiency = less Hb

pernicious anemia

inadequate vitamin B12

• poor nutrition

• lack of intrinsic factor (facilitates B12 absorption)

• common in elderly due to not enough intrinsic factor

  • intrinsic factor is what helps us absorb B12

hypoplastic anemia

decline in RBC production

• kidney failure - insufficient erythropoietin hormone production

• destruction of myeloid tissue

  • radiation, viral infection, poisoning, autoimmune disease

aplastic anemia

complete cessation of RBC production

• cause is unknown

hemorrhagic anemia

loss of blood

hemolytic anemia

RBC destruction

• mother-fetus mismatch, mushroom toxins, snake or spider venom, drug reactions, malaria

consequences of anemia

• tissues are deprived of O2 (hypoxemia/hypoxia)

  • shortness of breath

  • lethargy (lack of energy)

  • tissue necrosis (tissue destruction)

• reduced blood osmolarity (less cells = more fluid)

  • edema - fluid leaves bloodstream and enters tissues

• reduced blood viscosity - less blood flow resistance

  • heart beats faster

  • BP drops

• heart failure

sickle cell disease

hereditary Hb defects caused by recessive allele that modifies the structure of the hemoglobin molecule

• differs only on the 6th amino acid of the beta chain

• HbS does not bind oxygen well

• RBCs become rigid, sticky, pointed

• clump together and block small blood vessels → pain

• can lead to kidney/heart failure, stroke, rheumatism, paralysis

• HbS is indigestible to malaria parasites

leukopenia

low WBC count (<5000/microliter)

• causes include radiation, poisons, infectious disease

• effects include elevated risk of infection

leukocytosis

high WBC count (>10,000/microliter)

• causes include infection, allergy, and disease

• differential count distinguishes % of each cell type

leukemia

cancer of hemopoietic tissue

• myeloid and lymphoid - uncontrolled WBC production

• acute or chronic - death in either months or years

• effects: noraml cell % disrupted, patient subject to opportunistic infection, anemia & impaired clotting

platelet formation

small fragments of megakaryocytes

• thrombopoiesis is productionof platelets

  • contain granules and organelles

  • amoeboid movement and phagocytosis

• normal count - 130,000 to 400,000 platelets/microliter

• 2 to 4 micrometer diameter

platelet function

• secretion

  • clotting factors

  • growth factors for endothelial repair

  • vasoconstrictors in broken vessels

• form temporary platelet plugs

• dissolve old blood clots

• phagocytize bacteria

• attract WBCs to sites of inflammation

3 hemostatic mechanisms

1. vascular spasm

2. platelet plug formation

3. blood clotting

vascular spasm

prompt constriction of a broken vessel

• most immediate protection against blood loss

causes = pain receptors, smooth muscle injury, platelets release serotonin

effects = constriction of a broken vessel

• pain receptors - minutes

• smooth muscle injury - longer time

platelet plug formation

platelet pseudopods stick to damaged vessel and other platelets, pseudopods contract and draw walls of vessel together forming a platelet plug

• platelets degranulate releasing contents

  • serotonin (vasoconstrictor)

  • ADP attracts and degranulates more platelets

  • thromboxane A2 which promotes platelet aggregation, degranulation, and vasoconstriction

positive feedback cycle → until break in vessel is sealed

coagulation

clotting - last and most effective defense against bleeding

• conversion of plasma protein fibrinogen into insoluble fibrin threads to form framework of clot

• extrinsic pathway = initiated by release of tissue thromboplastin (factor III) from damaged tissue

  • cascade to factor VII, V, and X

• intrinsic pathway - initiated by platelets

  • cascade to factor XI, IX, VIII, V

calcium required for both

fibrinolysis

dissolution of a clot

• plasminogen converted into plasmin (dissolves clots)

prevention of inappropriate coagulation

• platelet repulsion

  • platelets do not adhere to prostacyclin-coating

• thrombin dilution

  • normally diluted by rapidly flowing blood

• natural anticagulants

  • antothrombin produced by the liver deactivates thrombin before it can act on fibrinogen

  • heparin secreted by basophils and mast cells interferes with formation of prothrombin activator

consequences of inefficient clotting

• thrombocytopenia - platelet count below 100,000/microliter

• hemophilia - genetic lack of clotting factor

  • sex-linked recessive in males (inherit from mom)

  • physical exertion causes bleeding and pain

thrombosis

abnormal clotting in unbroken vessel

• thrombus - clot

• most likely to occur in leg veins of inactive people

embolus

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

• ex. pulmonary emoblism where clot breaks free and moves from veins to lungs

infarction

tissue death, may occur if clot blocks blood supply to an organ

disseminated intravascular coagulation

widespread clotting in unbroken vessels

• caused by septicemia and cardiac arrest

clinical management of blood clotting

• vitamin K required for formation of clotting factors

  • Vitamin K antagonists like coumarin, warfarin help thin the blood

  • aspirin suppressed thromboxane A2

Dissolving clots that already formed:

• streptokinase dissolved clots in coronary vessels, digest any protein

• tissue plasminogen activator (TPA)

• hementin (produced by Amazon leech)

What makes up the cardiovascular system?

heart, blood vessels

pulmonary vs systemic circuits

• pulmonary = delivers blood from heart to lungs; right side of heart

• systemic = delivers blood from heart to all organs of body; left side of heart

size, shape position of heart

• located in thoracic cavity (mediastinum)

• size of a fist

• weighs 10 oz

• 2/3 of heart to left of midsaggital plane due to liver

base of heart

broad, superior portion

apex of heart

inferior end, tilts to left and tapers to a point

pericardium

• double-walled membranous sac that protects heart from surroundings

• allows heart to beat w/o friction, gives it room to expand, and resists excessive expansion

pericarditis

inflammation of the pericardium

• painful friction between the 2 membranes when the heart beats

cardiac tamponade

abnormal accumulation of fluid in the pericardial cavity

• compresses the heart

• interferes with ventricular filling

3 layers of the heart wall

• epicardium

  • outermembrane covers heart

  • fat deposits for protection

  • coronary blood vessels travel through this layer

• myocardium

  • thick muscular layer

  • fibrous skeleton (collagenous and elastic fibers for support, attachment, and electrical excitation)

• endocardium

  • smooth inner lining of chambers and valves

  • continuous with endothelium of blood vessels

  • direct contact with blood

heart chambers

• right atria

• right ventricle

• left atria

• left ventricle

atrium receives blood returning to heart

ventricles pump blood into arteries and have thicker walls

atrioventricular (AV) or coronary sulcus

• encircles entire heart

• boundary separating atria from ventricles

anterior & posterior interventricular sulci

• extends from AV sulcus to the apex of heart

• separates right and left ventricles

trabeculae carnae

internal ridges in ventricles

pectinate muscles

internal ridges of myocardium in right atrium and both auricles

chordae tendinae

cords connect AV valves to papillary muscles on floor of ventricles

atrioventricular valves (AV)

• right AV valve (tricuspid) has 3 cusps

• left AV valve (bicuspid) has 2 cusps

semilunar valves

control flow into great arteries

• pulmonary from right ventricle into pulmonary trunk

• aortic from left ventricle into aorta

coronary circulation

heart uses 5% of the circulating blood

• when ventricles relax, blood flows back down the aorta to fill the cusps, some blood is diverted to the coronary arteries

• body gets blood when ventricles contract

• heart muscle gets blood when ventricles relax

left coronary artery

• anterior interventricular brance

  • supplies blood to interventricular septum and anterior walls of ventricles

• circumflex branch

  • passes around left side of heart in coronary sulcus, supplies left atrium and posterior wall of left ventricle

right coronary artery

• right marginal branch

  • supplies lateral R atrium and ventricle

• posterior interventricular branch

  • supplies posterior walls of ventricles

myocardial infarction

heart attack - sudden death of heart tissue

• cause = fat deposits or blood clots

• lack of O2 → ischemia

• if O2 not restored → necrosis (tissue death)

angina pectoris

heart pain due to temporary and reversible myocardial ischemia

• brief few seconds of cut off blood flow

• hypoxia → myocardium does anaerobic fermentation → lactic acid → pain receptors stimulated

athersclerosis

• fatty deposits form in a coronary artery

• due to abnormal uptake of plasma lipids (cholesterol) by cells of blood vessel

  • correct by by-pass surgery, balloon angioplasty, or laser angioplasty

cardiac muscle

• striated

• involuntary

• one nucleus

• intercalasted discs join myocytes end to end

  • interdigitating folds increase surface area

  • desmosomes tightly join myocytes

  • electrical gap junctions allow ions to flow from cytoplasm to cell

myoglobin purpose

holds oxygen

glycogen purpose

holds glucose

myogenic

heartbeat originates within the heart, not the brain

autorhythmic

depolarizes spontaneously regulary

SA node

pacemaker

• initiates heartbeat, sets HR

• signal located in roof of R atrium

• signal spreads across R and L atria

AV node

electrical gateway to ventricles

• located in side wall of right atria

• can take over as pacemaker if SA node fails

AV bundle

pathway for signals from AV node

right and left bundle branches

divisions of AV bundle that enter interventricular septum and descend to apex

purkinje fibers

upward from apex spread throughout ventricular myocardium

systole

contraction

diastole

relaxation

sinus rhythm

normal rhythm set by SA node

• adult at rest is 70 - 80 bpm

ectopic foci

outside normal region

• region other than SA node sets rhythm

  • nodal rhythm - set by AV node; 40 - 50 bpm

  • intrinsic ventricular rhythm - AV bundle; 20-40 bpm

arrhythmia

abnormal cardiac rhythm

• caused by bundle disease/degeneration

ventricular fibrillation

uncoordinated contraction

• ventricles spasm → heart can’t pump → cardiac arrest

ventricular defibrillation - strong electrical shock to depolarize

contraction of myocardium

• myocytes have resting potential of -90 mV

• Depolarization

  • stimulus opens voltage regulated Na+ gates

  • Na+ rushes in (membrane depolarizes rapidly)

  • action potential peak at +30 mV

  • Na+ gates close quickly

• Plateau

  • slow Ca2+ channels open

  • Ca2+ binds to fast Ca2+ channels on SR

  • SR releases Ca2+ into cytosol

  • contraction

• Repolarization

  • membrane returns to resting potential

  • Ca2+ channels close

  • K+ channels open

  • rapid K+ out

electrocardiogram (ECG/EKG)

• detects electrical currents in the heart

• P wave = SA node fires, signal spreads through atria, atria depolarization

• PQ segment = atrial systole

• QRS complex = firing of AV node and ventricular depolarization

• ST segment = ventricular systole

• T wave - ventricular repolarization

1st heart sound

S1 = lubb; louder and longer

• occurs with closure of AV valves

2nd heart sound

S2 - dubb; softer and sharper

• occurs with closure of semilunar valves

heart murmur

sound of blood flowing backward due to vascular insufficiency

• valvular stenosis - cusps are stiffened

• mitral valve prolapse - mitral valve cusps bulge into left atrium

causes - hereditary, may lead to chest pain and shortness of breath

phase 1 of cardiac cycle

ventrical filing

• during diastole, ventricles expand

• pressure drops below that of the atria

• AV valve opens and blood flows into ventricles

phase 1 = rapid ventricular filling

phase 2 = diastasis (slower fillinf, p wave occurs at end when SA node fires)

phase 3 = atrial systole (atria contract)