Anatomy 2 exam 2

chapters 18,19,20

blood

• fluid connective tissue

• 5 L

• has plasma and formed elements

blood plasma

• 55% of whole blood

• least dense

• straw colored, viscous

• is 90% water and 10% solutes

what are the three categories of plasma proteins

1. albumins: smallest, most abundant, infleunce bp, flow, fluid balance

2. globulins (antibodies): provide immune system functions

3. fibrinogen: precursor of fobrin threads to help form blood clots

what is serum?

the same as plasma but doesnt have fibrinogen

formed elements

• come from bone marrow

• dont divide

• only survive for a few days

• erythrocytes

• leukocytes

• platelets

complete blood count (CBC)

• hematocrit

• hemoglobin concentration

• total count of RBS, reticulocytes, WBCs

• differential WBC

• RBC size

erythrocytes and hemoglobin

the concentration shows how much oxygen blood can carry

hematocrit: percentage of blood volume that is RBCs, 45%

hemoglobin concentration: 15 g/dL

RBC count: 5 million

hematopoiesis

• blood cells form in red bone marrow (in axial skeleton, proximal epiphysis)

• hemocytoblasts: stem cells, give rise to formed elements

erythrocytes

red blood cells

• bioconcave discs

• anucleate

• hemoglobin

• function to transport O2,

• hemoglobin binds reversibly with oxygen

transport of respiratory gases

oxygen: 98.5% in hemoglobin, 1.5% in plasma

carbon dioxide: 7% dissolved in plasma, 23% in hemoglobin, 70% as bicarbonate ions

erythropoiesis

red blood cell production

erythropoietin (EPO): direct stimulus

• released by the kidneys in response to hypoxia

causes of hypoxia

• hemorrhage or increased RBC destruction reduces RBC numbers

• insufficient hemoglobin

• reduced O2 availibility

erythrocyte destruction

life span :100-120 days

old RBCs become fragile, Hb degenerates

macrophages eat dying RBCs in spleen and liver

antigens

-molecules on the surface of cell membranes that activate an immune response

• genetically unique

• generates an immune response

agglutinogens

• antigens on the surface of RBC for blood typing

• A, B, Rh

antibodies

• proteins secreted by plasma cells

• bind to antigens and mark them for destruction

• forms antigen-antibody complexes

aggultinins

• antibodies in the plasma that bring about transfusion mismatch

• anti-a, anti-b

O blood

• has no antigens

• has anti a and anti b antibodies

• universal donor

a blood

a antigen

anti b antibody

can receive A and O blood

B blood

has B antigen

has anti a antibodies

can receive B and O blood

AB blood

has A and B antigens

has no antibodies

can receive A, B, AB, O

universal recipient

blood typing

clumping occurs if matchig anti body finds antigen

if it clumps, you have it

transfusion reaction

• mismatch of RBS donation

• agglutination: each antibody can attach to several foreign antigens

• can block blood vessels,

• Hb blocks kidney tubules and cause renal failure

Rh group

• came from rhesus monkey

• + or -

• anti-D agglutinins not normally present

• hemolytic disease of the newborn

• prevention: rhoGAM given to pregnant rh- women

blood transfusions

• whole blood transfusions used when blood loss is substantial

• packed red cells are used to restore oxygen carrying capacity

• plasma in electrolyte solution for restoring blood volume

• transfusion of wrong blood can be fatal

leukocytes

• least abundant formed element

• protects against pathogens

• nucleus

• has organelles for protein synthesis

• spends few hours in bloodstream before migrating to connective tissue

• leaves via diapedesis

2 types of leukocytes

1. granulocytes

2. agranulocytes

types of granulocytes

1. neutrophils

2. eosinophils

3. basophils

types of agranulocytes

1. lymphocytes

2. monocytes

neutrophils

• granulocyte

• 60-70%

• 3-5 lobed nucleus

• antibacterial

• “bacteria slayers”

eosinophils

• granulocytes

• destroys parasites

• rosy pink

• 
  

basophils

• granulocyte

• secretes histamine

• chicken pox, sinusitis, diabetes

• can barely see nucleus

lymphocytes

• infections and immune responses

• agranulocytes

• b cells and t cells

• very large nucleus

• comes from lymphoid stem cell

monocytes

• agranulocyte

• viral infections and inflammation

• leaves blood stream and becomes macrophages

• kidney shaped nucleus

platelets

• thrombocytes

• required fro blood clotting

• contains: serotonin, ca+, enzymes, adp, PDGF

• formation is regulated by thrombopoietin

hemostasis

• the cessation of bleeding

• 3 mechanisms:

1. vascular spasm

2. platelet plug formation

3. blood clotting

platelet functions

• secreete vasoconstrictors

• stick together to form platelet plugs

• secrete procoagulants to promote clotting

• formation of clot-dissolving enzyme

• chemically attract neutrophils and monocytes to inflammation

• destroy bacteria

• secreete growth factors

vascular spasm

• constriction of a broken vessel

• caused by pain receptors, smooth muscle injury, plateletes release serotonin

• effects: constriction, time for other clotting pathways

platelet plug formation

• platelet psuedopods stick to damage vessel and collagen

• contract to form a plug

• positive feedback cycle is active until break in small vessel is sealed

coagulation

• fibrinogen → fibrin to form clot

• clotting factors profuces by liver in plasma

• 
  

the phases

phase 1: prothrombin activator

phase 2: parathrombin → thrombin

phase 3: fibrinogen → fibrin in soluble → cross-linked fribrin mesh

cascade of clotting

• factor XII

• factor XI

• factor IX

• Factor VIII

• factor X

• prothrombin activator

• thrombin

• fibrin

fate of blood clots

• clot retraction occurs in 30 minutes

• PDGF secreted by platelets and endothelial cells

• fibrinolysis terminates clot and plasminogen changes to plasmin, the enzyme to break it up

prevention of inappropriate clotting

platelet repulsion: dont adhere to prostacyclin endothelium

thombin dilution: rapidly flowing heart

natural anticoagulants: heparin, antithrombin

low doses aspirin

anemia

• blood has low O2 carrying capacity

• sign rather than disease itself

• fatigue, paleness, SOB

• cant support normal metabolism

• causes: inadequate erythropoiesis, hemorrhagic anemias from bleeding, hemolytic anemias from RBC destruction

consequences of anemia

1. tissue hypoxia and necrosis

2. blood osmolarity is reduced, tissue edema

3. blood viscosity is low, bp drops, cardiac failure

sickle cell disease

• hereditary defects

• caused by recessive allele that modifies structure of Hb

• doesnt bind to O2 well

• can lead to kidney or heart failure

• heterozygotes are resistant to malaria

polycythemia

• excess RBCs

• primary polycythemia: cancer of erythropoietic cell line in red bone marrow, as high as 11million

• secondary polycythemia: from dehydration, emphysema, high altitude, up to 8 million

• dangers: increased viscosity, volume, pressure

leukopenia

• low wbc count

• below 5,000

• causes: radiation, poisons, infectious disease

• effects: elevated risk of infection

leukocytosis

• high wbc count

• above 10,000

• causes: infection, allergy, disease

• differential wbc count: identifies what percentage is eacg type

leukemia

• cancer of hemopoietic tissue, producing high umber of leukocyte

• myeloid, lympoid, acute, chronic

• effects: impaired cltting, disrupted cell percentages

embolus

a thrombus freely floating in the blood stream

thrombus

clot that develops and persists in an unbroken blood vessel

thromboembolytic conditions

• undesirable clot cormation

• infarction may occur if clot blocks blood supply

• 650,000 american die annually

hemophilia

• family of hereditary diseases

• sex linked recessive (x), a missing factor VIII(83%)

• hemophilia b missing factor IX (15%)

• hemophilia c missing factor XI (autosomal)

• physical exertion causes bleeding and excruciating pain

• treatment: transfusion of plasma or purified clotting factors

thrombocytopenia

• deficient number of circulating platelets

• petechiae appear due to spontaneous hemorhage

• due to suppression or destruction of bone marrow

• platelet count <50,000

• treated with transfusion of concentrated platelets

right side vs left side of heart

right side: pumps for the pulmonary circuit

left side: pumps for the systemic circuit

location of heart

in the mediastinum, anteriorly behind sternum

layers of the pericardium

1. fibrous layer

2. serous layer

2a: parietal pericardium- pericardial cavity, filled with pericardial fluid

2b: visceral pericardium (same as epicardium)

layers of the heart wall

1. epicardium (visceral pericardium)

2. myocardium

3. endocardium

the epicardium

aka visceral pericardium

• adipose in thick layer in some places

• coronary blood vessels travel through this layer

endocardium

• smooth inner lining of heart and blood vessels

• covers the valve surfaces and is continuous with endothelium of vessels

myocardium

• layer of cardiac muscle proportional to work load

• muscle spirals around heart which makes wringing motion

heart valves

function: make unidirectional blood flow

AV valves

SL valves

major vessels of the heart entering

entering right atrium:

• superior and inferior vena cava

• coronary sinus

entering left atrium:

• right and left pulmonary veins

major vessels of the heart leaving

leaving right ventricle: pulmonary trunk

leaving left ventricle: aorta

major coronary arteries

• right coronary artery

• left coronary artery

• circumflex artery

coronary sinus

• large transverse vein in coronary sulcus on posterior side of the heart

• collects blood and empties into the right atrium

coronary circulation

• 5% of blood is pumped by heart to the heart

• 250 mL per minute

• needs lots of O2

• flows through arteries os greatest when the heart relaxes

myocardial infarction (MI)

• sudden death of patch of myocardium from long-term obstruction of coronary circulation

• atheroma obstructs arteries

• cardiac muscle downstream dies

• 27% of all deaths in the US

coronary artery disease

• contriction of coronary arteries

• result of atherosclerosis

angina pectoris

• chest pain from partial obstruction of coronary blood flow

• caused by ischemia of cardiac muscle

• partially blocks blood flow

• myocardium shifts to anaerobic fermentation, lactate stimulates pain

Cardiac muscle

• striations

• intercalated discs - join cardiomyocytes with junctions

• uninucleated

• branching

metabolism of cardiac muscle

• aerobic respiration

• huge mitochondria (25% of cell)

• adaptable to different organic fuels

• fatigue resistant because doesnt use anerobic mechanisms

intrinsic conduction system

• depolarization of the heart is rhythmic and spontaneous

• 1% of cardiac cells have automaticity

• gap junctions ensure heart contracts as a unit

the flow of intrinsic conduction system

1. SA node fires

2. excitation spreads through atrial myocardium

3. AV node fires

4. excitation spreads down AV bundle

5. subendocardial conducting network distributes excitation through ventricular myocardium

Sinoatrial (SA) node

• modified cardimyocytes

• “pacemaker”

• initiates each heartbeat

• spontaneous is around 100 bpm

• rate decreases with age

atrioventricular (AV) node

• near right AV valve

• electrical gateway to the ventricles

• fibrous skeleton- insulator prevents currents from getting to ventricles any other way

• spontaneous rate of 5- bpm with no SA node

atrioventricular (AV) bundle (bundle of his)

• forks right and left bundle branches

• pass through interventricular septum

• delays impulse by 0.1 second

subendothelial conducting networks (purkinje fibers)

• nerve-like processes spread throughout ventricular myocardium

• cardiomyocytes then pass signal from cell to cell through gap junctions

maximum heart rate

220 - age in years

• genetically determined, cannot be modified by exercise training or other factors

extrinsic innervation of the heart

• cardiac center in medulla oblongata

• activity modified by the ANS

• 
  

ANS regulation - sympathetic system

• activated by emotional or physical stressors

• norepinephrine causes pacemaker to fire more rapidly

• increases HR

• increases force of contraction

ANS regulation - parasympathetic

• activated during rest

• acetylcholine hyperpolarizes pacemaker cells by opening K+ channels

• little or no vagal stimulation of the myocardium

• decreases HR

• limited effect on force of contraction

electrocardiogram

• ECG

• p wave- depolarization of SA node

• QRS complex: ventricular depolarization

• T wave: ventricular repolarization

p wave

• SA node fires, atria depolarize and contract

• atrial systole begins 100 ms after SA signal

QRS complex

• ventricular depolarization

• complex shape of spike due to different thickness of the two ventricles

ST segment

• ventricular systole

• corresponds to plateau in myocardial action potential

T wave

• ventricular repolarization

• relaxation

what can deviations of ECG indicate

• myocardial infarction

• abormalities in conduction pathways

• heart enlargement

• electrolyte and hormone imbalanves

ventricular fibrillation

• arrhythmia caused by electrical signals traveling randomly

• hall mark of heart attack (MI)

• kills quickly if it isnt stopped

• defibrillation- electrical shock to depolarize entire myocardium to reset it

sinus rhythm

a normal heart beat by SA node

• at rest 70-80 bpm (vagal tone)

• normal is 60-100

ectopic focus

• a region of spontaneous firing orther than the SA node

• may govern heart rhythm if the SA node is damaged

• nodal rhythm: if SA is damaged, set by AV node (40-50)

the heart sounds

1st sound: av valves closing

2nd sound: SL valves closing

valvular insufficiency

• any failure of a vlave to prevent reflux, backward flow of blood

valvular stenosis

• cusps are stiffened and opening is constricted by scar tissue

• a result of rheumatic fever, autoimmune attack on mitral and aortic valves

• heart voerworks and may become enlarged

• heart murmur- abnormal sound from regurgitation

mitral valve prolapse

• insufficiency where one or both mitral valve cusps bulge into atria during ventricular contraction

• 1/40 people

• may cause chest pain and SOV

congestive heart failure

• results from the failure of either ventricle to eject blood effectively

• due to a weakened heart

left ventricular failure

• blood backs up into the lungs causing pulmonary edema

right ventricular failure

• blood backs up in the vena cava causing systemic or generalized edema

• eventually leads to total heart failure