BIOS255: Exam 1 Review

Professor Haneen Salhieh, M.S.

Wks I t 2 Blood Heart

5
39 MCQ 2 Essay Short Answer pts
100 pts
Functions of the Circulatory System

• Cardiovascular system: heart and blood vessels

• Circulatory system: heart, blood vessels, and blood

• Functions of the circulatory system:

• Transportation:
• O2, CO2, nutrients, wastes, hormones, and stem cells from bone
marrow
• Protection:
• Immune system WBCS
• Clotting Blood volume Blood
minimize blood
• Regulation: Pressure
• Fluid balance, pH, and temperature control
Components and General Properties of Blood

• Adults have 4 to 6 L of blood

• Composed of plasma and formed elements
• Slightly warmer than the body’s core temp (100.4°F).
• Color is dark red when oxygen is absent, bright red when bound to RBCs
• Normal pH range of 7.35-7.45
• Denser (heavier) than water
Components and General Properties of Blood
liquid CT TMI
Liquid (Plasma) Solid (Formed Elements)
Matrix cell
Water White blood cells (WBCs) or
leukocytes

Proteins Red blood cells (RBCs) or

erythrocytes

Nutrients and electrolytes Platelets

Wastes Tnot cells cell
fragments
from megakaryocyte
Components and General Properties of Blood
Centrifugation: heaviest
components settle to bottom of
tube
• Plasma: clear, yellow fluid stays
on top of tube
• Buffy coat: narrow band of white
blood cells and platelets
• Erythrocytes/RBCs: heaviest,
settle to bottom
• Hematocrit (Hct): packed cell
value, percentage of whole blood
occupied by RBCs
Blood Plasma thickness of particles
551 viscosity concentration

p
Plasma: liquid portion of blood
osmolarity
• Proteins:
• Albumin: transport substances; influences blood
601 viscosity & osmolarity
osmosis wherever solutes are
351• Globulins (antibodies): secreted to combat
pathogens in specialized immune responses
51• Fibrinogen: component of blood clots ws
• Wastes: nitrogenous wastes (urea)
• Nutrients: sugars, fats, amino acids, vitamins, and
minerals
• Gases: dissolved O2, CO2, and nitrogen
• Electrolytes: K+, Cl-, Mg+, Ca2+Na+

Serum: remaining fluid when blood is allowed to coagulate

(clot) and solids are removed
• Identical to plasma except for the absence of
fibrinogen (clotting proteins)
Hematopoiesis

• Production of blood (plasma and formed elements)

• Billions of platelets, RBCs, and WBCs must be made each day

• Hematopoietic tissues:
RED
• All other formed elements produced in bone marrow Sternum ribs
vertebrae pelvis skull
• Hematopoietic stem cells (HSCs): bones
• Multipotent stem cells in bone marrow ends of long
• Give rise to all formed elements
• Must continue creating new cells throughout lifetime
Erythrocytes (Red Blood Cells)

Principal functions: transport

gas
• Carry oxygen from lungs to tissues
• Carry CO2 from tissues to lungs

Cells designed to maximize gas

exchange and transport
• Lose nearly all organelles during
development
• No mitochondria (don’t use O2 for energy)
• No nucleus
• Consists mostly of hemoglobin to carry
gases
Hemoglobin

Each hemoglobin (Hb) protein consists

of: iron

• Four protein subunits (globins)

• Four heme groups
• Heme is respiratory pigment, turns red
when binds O2
00
• Iron atom (Fe) at core binds O2
• Four O2 binding sites per Hb

4 Hemes 4 irons
402
Oz binds to Iron of heme groups
of
Erythropoiesis
Erythropoiesis: RBC production from hematopoietic stem
cells (HSCs) in bone marrow
• 1 million RBCs are produced per second
• Average life span of about 120 days
• Stimulated by erythropoietin (EPO) produced mainly
by kidneys
851 kidneys

• Must have sufficient iron (Fe) from diet, Vitamin B 12, 151 liver
folic acid, Vitamin C, and copper are required
• Controlled by negative feedback loop
Erythrocyte Disorders: Excess & Deficiency
• Polycythemia: an excess of RBCs
• Primary: due to cancer in erythropoietic cell line in bone marrow
• Secondary: dehydration, smoking, air pollution, excessive aerobic
exercise
stomach
• Anemia: deficiency of RBCs or hemoglobin intrinsic
• Hemorrhagic anemias: excessive bleeding factor
• Hemolytic anemias: excessive RBC destruction
• Inadequate erythropoiesis
• Pernicious anemia: inadequate Vitamin B12 absorption because of helps
reduced production of intrinsic factor by stomach Absorb
• Iron deficiency
vitamin
• Aplastic Anemia
• Sickle-Cell anemia B12
used to make
Blood Types

• Blood types are based on interactions between

antigens and antibodies
• Antigen (Ag): on cells
•
tags
Genetically unique molecules that occur on the surface of ALL
cells
• Enable our body to distinguish its own cells (self) from foreign
materials (non-self).

• Antibody (Anti-):
• Proteins that are secreted as part of a specific immune response
whenever a foreign antigen is detected
• Bind to the antigens and mark them for destruction.
ABO Blood Groups whatever have
Antigen you
Determined by the presence or absence of
antigens on RBCs
that is your blood type
• RBCs can have:
• A antigen
• B antigen
• both A and B
• Neither

Type A blood: presence of A antigen

Type B blood: presence of B antigen
Type AB blood: presence of A & B antigens
Type O blood: no antigens present

Blood plasma contains antibodies

opposite of the Antigens to like antibodies will attack
g
antibodies like antigens
www.ogetns A antigen A antibody
ABO Blood Typing

Hemagglutination assay: I 2 3 4
• Clumping (agglutination) of red
blood cells is a positive reaction
• Blood to be tested is added
A
separately to serum containing
anti-A and anti-B antibodies y
B
• Type A blood will react with
anti-A serum
C X
• Type B blood will react with
anti-B serum
D y
• Type O blood will not react
with either
antibody

Intifada
 Anti Hf Cantibody

0 B
0

0 At
3

4 0 AB
 no A B Antigens
Transfusion Reaction
Of
have antigen
• Type O- commonly known as the “universal donor”
• Why? No antigen A or antigen B on RBCs  no antigens for the antibodies from donor
blood to attack!
• Type AB+ commonly known as the “universal recipient”
• Why? No anti-A or anti-B antibodies in plasma  no antibodies that can attack
any antigens

a tyf Antigen D Rh Antigen

at antibodies D
no one is born
Leukocytes: White Blood Cells (WBCs)
identify them
Travel in blood to tissues to combat function
pathogens and foreign substances
and play a role in responding to
tissue damage.
BEN is a G
• Granulocytes:
• Neutrophils
• Eosinophils
• Basophils

• Agranulocytes:
• Lymphocytes
• Monocytes
Leukocytes: Granulocytes red pink bunch of
cytoplasm granules

is

Neutrophils Eosinophils Basophils

Most abundant (60-70%) 2-4% of total WBCs Least abundant (<1%)

3-5 lobed nucleus, Red/orange granules in Many dark violet granules

granules in cytoplasm cytoplasm in cytoplasm
2 lobes
Aggressively phagocytize Respond to parasitic Release: PYhffatumnat.io
bacteria infections; dispose of Histamine – vasodilator
allergens Heparin - anticoagulant
Leukocytes: Agranulocytes

Lymphocytes Monocytes
25-33% of total WBCs 3-8% of total WBCs

Horseshoe-shaped or kidney-shaped nucleus,

Large, dark nucleus, little cytoplasm
largest WBC
T cells: directly attack infected or abnormal
cells Become macrophages that phagocytize
B cells: become plasma cells that produce microbes and cellular debris
antibodies
clean up the cells
Platelets and Hemostasis—The Control of Bleeding

Hemostasis: the cessation of bleeding

• Stopping potentially fatal leaks

• Platelets (thrombocytes): small fragments of megakaryocyte cells

• Secrete clotting factors to promote blood clotting, stick together to help seal
breaks in injured blood vessels, can dissolve blood clots that are no longer
needed
Hemostasis Exposed
platelets
attach

tariff
1. Vascular spasm: 2. Platelet plug formation: 3. Coagulation: next slide
• Blood vessel walls rapidly • Platelets stick to injured • Fibrinogen protein in
constrict to reduce blood endothelial cells and each blood is converted to
loss other to loosely block sticky fibrin, which
injury forms clot of platelets
and blood cells
Coagulation
3. Coagulation (clotting)
stage faint
• Conversion of plasma protein fibrinogen into insoluble fibrin threads to form framework of clot

• There are two pathways to coagulation: intrinsic and extrinsic mechanisms.

 The intrinsic mechanism is the reaction pathway that uses clotting factors that are within the
blood itself.
 The extrinsic mechanism is initiated by clotting factors that are released by the damaged blood
vessel or nearby tissues.
• Both pathways will eventually arrive to activate Factor X.

In the presence of Ca2+, factor X combines with factor III and produces the enzyme prothrombin
activator. This converts a plasma protein called prothrombin to thrombin. Thrombin is an enzyme
that will convert fibrinogen to fibrin.
cast
Extrinsic or Intrinsic Pathway  Factor X  Prothrombin activator  Thrombin  Fibrinogen
into Fibrin
thrombin

find
•
Iron
The Fate of Blood Clots

Fibrinolysis: Dissolution of a clot

• Plasmin: converts inactive plasminogen into
stone
active plasmin
• Plasmin dissolves clot

Anticoagulants: help prevent inappropriate

coagulation
• Heparin interferes with formation of
prothrombin activator
• Antithrombin deactivates thrombin before it
can act on fibrinogen
The Pulmonary and Systemic Circuits

Pulmonary circuit: right side of heart

• Oxygen-poor blood arrives in right
side of heart from inferior and
superior venae cavae
• Blood sent to lungs via pulmonary
trunk for gas exchange and back to
heart
Systemic circuit: left side of heart
• Fully oxygenated blood arrives in left
side of heart from lungs via
pulmonary veins
• Oxygenated blood sent to all organs of
the body via aorta and returned to the
heart
The Pericardium

Pericardium: double-walled sac that

A
encloses the heart
• Allows heart to beat without
friction, provides room to expand,

man
yet resists excessive expansion

• Parietal layer: lines fibrous

pericardium
• Visceral layer: covers heart wall
• Pericardial cavity: space
between two layers, contains
pericardial fluid
The Heart Wall

1. Epicardium (aka visceral layer of

serous pericardium): serous
membrane covering heart,
contains some adipose tissue
2. Myocardium: layer of cardiac
muscle, thickness proportional to
workload HI
• left ventricle thickest
3. Endocardium: smooth inner
lining of heart and blood vessels
The Four Heart Chambers

Atria: superior chambers lunas

body
• Receive blood returning to heart, pump
blood to ventricles
• Right Atrium: receives DO2 from body
• Left Atrium: receives O2 from lungs
•
I AV

ᵈaf
Ventricles:
• Inferior chambers
• Pump blood into arteries
• Right Ventricle: pulmonary trunk
lungs
• Left Ventricle: aorta
body
 anyone pulmonary valve
The Valves
• Atrioventricular (AV) valves: control
Anterior
blood flow between atria and
ventricles
• Right AV/tricuspid valve has three
cusps
• Left AV/mitral/bicuspid valve has
two cusps
• Semilunar valves: control flow from
ventricles into great arteries
2

0
• Pulmonary semilunar valve:
opening between right ventricle
and pulmonary trunk
• Aortic semilunar valve: opening
between left ventricle and aorta

posterior Right AV
left AV
 Blood Flow Through the Chambers

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Myocardial Blood Supply

Don’t forget the heart itself needs oxygen and nutrients

• Delivering oxygen-rich blood: left & right coronary arteries branching off aorta
• Draining oxygen-poor blood from myocardium: coronary sinus
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1 the
Structure of Cardiac Muscle

• Found only in the heart wall

• Short, branched, thick cells striated
• Under involuntary control
• Contain intercalated discs:
• Cell junctions that join
cardiomyocytes to join
cells together and allow
ions to flow between cells
Cardiac Conduction System
1. Sinuatrial (SA) node: pacemaker, in
right atrium; initiates heartbeat
• ectopic focus: a region of spontaneous
firing other than the SA node if it is
damaged (usually AV node)
2. Signals spread throughout atria
1

OF
3. Atrioventricular (AV) node: near the
right AV valve at lower end of interatrial
septum, spreads signal to ventricles
4. Atrioventricular (AV) bundle (bundle
of His): carries signal away from AV
node, forks into right and left bundle
branches
5. Purkinje fibers: spread signal
throughout ventricles
 Nat Kt Cast 1 depolarization Nat enters
Stimulation of the Myocardium cast enters
2 plateau phase
3 repolarization Kt leaves
an

cart entering
a
Stimulation of the Myocardium

• Depolarization phase: very rapid depolarization

• Stimulus opens voltage-regulated Na+ gates (Na+ rushes in),
membrane depolarizes rapidly (peak at +30 mV)
• Na+ gates close quickly
• Plateau phase: 200 to 250 ms, sustains contraction for expulsion of
blood from heart
• Voltage-gated slow Ca2+ channels open, Ca2+ inflow triggers
release of Ca2+ from sarcoplasmic reticulum (SR), binds to
troponin triggering contraction
Repolarization phase: Ca2+ channels close, K+ channels open, rapid
outflow of K+ returns cell to resting potential (-90 mV)
The Electrocardiogram: ECG/EKG

• P wave: represents atrial depolarization

when signals from SA node spread through
atria MY
• QRS complex: represents ventricular
depolarization when signals from AV node
spread through ventricles
• T wave: represents ventricular
repolarization when ventricles relax
• PR Interval: time it takes impulses to travel 1
from atria to ventricles
• QT interval: time it takes ventricles to
contract and relax
Normal Electrocardiogram
• PR interval: signal conduction through AV node, before activating
ventricles
• QT interval: duration of ventricular depolarization; shorter during
exercise
• ST segment: ventricular systole; corresponds to plateau in
myocardial action potential
Phases of the Cardiac Cycle

Cardiac cycle: series of events that occur in the heart during one
complete heartbeat
Involves the contraction and relaxation of the heart chambers.
• Systole: contraction of heart chambers  blood ejected out
• Diastole: relaxation of heart chambers  filling with blood or at rest

Two primary heart sounds are generated during the cardiac cycle:

 The first sound (S1 or “lub”): louder and longer sound caused by
the closure of the atrioventricular valves Atria now into ventricles
 ​The second sound (S2 or “dub”): softer and sharper sound
produced by closure of the aortic and pulmonary semilunar valves
ventricles now in pulmonary trunk
or aorta
 diastole relaxation
Phases of the Cardiac Cycle
systole contraction
1. Ventricular Filling: ventricles are relaxed and blood pours from
atria into ventricles
• End-diastolic volume (EDV): max volume ventricles can hold
(130 mL)
2.Lame
Isovolumetric Contraction: ventricles contract to increase
pressure enough that they can force semilunar valves open. No
blood ejected out
3. Ventricular Ejection: ventricles contract and blood ejected out
through semilunar valves and into pulmonary trunk and aorta
• Stroke volume (SV): blood ejected out of ventricles (70 mL)
• End-systolic volume (ESV): blood left in ventricles (60 mL

T I
4. Isovolumetric Relaxation: all heart valves closed so no blood
enters or leaves chambers. Ventricles expand and relax to start the
cardiac cycle over

effusion su but ESV EDU SV

0 0
in
form
Cardiac Output
Cardiac output (CO): volume ejected by each ventricle in 1 minute
• CO = heart rate (HR) x stroke volume (SV)
• About 4 to 6 L/min at rest, increases to about 21 L/min during vigorous exercise for
a fit person

Example 1: Example 2:
HR = 75 beats/min SV I HR = 75 beats/min
EDV = 140 mL
I
SV = 70 mL/beatz
Systolic BP = 124 mmHg EDU ESV ESV = 80 mL
Diastolic BP = 76 mmHG Systolic BP = 120 mmHg
140 80mLDiastolic BP = 82 mmHg
60m
CO HR SV CO HR SV
75 bpm 70 mL 00 75 bpm x

5 50 ml min CO 75 bpm
00 0 mumin
4
S25IMI
4.54M
Autonomic Innervation of the Heart
Heart rhythm and contraction are controlled by the cardiac centers in the medulla
oblongata
• Cardioacceleratory center: sympathetic innervation via the cardiac nerves
• Increases heart rate and contractility

In
• Cardioinhibitory center: parasympathetic innervation via the vagus nerve
• decreases heart rate