Bio Exam 3 Terms

hematocrit

the percentage of blood volume that is RED blood cells (RBC)

• normal value = 45% (42-47%) → men tend to have a higher value due to testosterone stimulating RBC production

higher hematocrit = more oxygen-carrying RBCs

centrifugation

blood separates into:

1. plasma (55%) → mostly water, proteins, electrolytes\

2. buffy coat (<1%) → white blood cells and platelets

3. RBC layer (45%) → hematocrit value

plasma

The liquid portion of blood

contains:

• 91.5% water

• electrolytes (Na+, Cl-)

• proteins

• nutrients

• hormones

• waste products

proteins made by the liver

albumin

most abundant plasma proteins

functions:

• transport lipids and hormones

• maintain blood osmotic pressure

• keeps water inside blood vessels

fibrinogen

functions:

• blood clotting

• prevents excessive blood loss

globulins

functions:

• antibodies (immunoglobulins)

• immune defense against infection

serum

a clotting factor

• basically, plasma without fibrinogen and clotting protein

hematopoiesis

production of blood cells

where are blood cells made? - before birth

blood cell production occurs in the

• yolk sac

• liver

• spleen

• bone marrow

(liver and spleen most prominent → until moving to more heavy bone marrow in maturation - adult)

where are blood cells made? - adult

main sites:

• vertebrae (spine)

• pelvis

• sternum

• ribs

• femur

• tibia

(adults DO NOT primarily make blood cells in the femur or tibia → more in the vertebrae and pelvis)

hematopoietic stem cells

they can:

1. divide by mitosis

2. renew themselves

3. become all blood cell types

they produce:

• RBCs

• platelets

• all white blood cells

(one SC source → all blood cell linages)

red blood cells (RBCs)

strcuture:

• biconcave discs → more surface area for oxygen echange + flexible enough to squeeze through capillaries

• no nucleus

• no endoplasmic reticulum (ER) when mature

life cycle:

• development → 5-7 days

• lifetime → about 120 (couple months)

reticulocyte

immature RBCs

characteristic:

• no nucleus

• still contains endoplasmic reticulum (ER)

• matures into a normal RBC in circulation

requirements of RBC production

vitamin B12, folic acid, iron

erythropoietin (EPO)

hormone that stimulates RBC production

produced by:

• kidney = 80%

• liver = 20%

triggers of EPO release

low oxygen levels (hypoxia)

ex:

• blood loss

• anemia

• high altitudes

• exercise training

clincical connetion = kidney diseases → less EPO → less RBC production → refractory anemia

EPO feedback loop

low O2 → kidney senses low O2 → EPO released → bone marrow makes RBCs → O2 levels rises → EPO decreases

hemoglobin (HB)

carries oxygen in RBCs

structure:

• 4 protein subunits

• 2 alpha chains → 2 alpha each chain

• 2 beta chains → 1 beta each chain

• iron-containing heme group

(oxygen binding = 1 hemoglobin molecule binds → 4 oxygen molecules)

hemolysis

RBCs break down → normal life span about 120 days

extravascular hemolysis

90% → to store old/extra iron + retire RBCs

occurs in:

• liver

• spleen

Macrophages remove old RBCS

intravascular hemolysis

10% → less ideal due to the breakdown leading to toxins in the blood OR can be too valuable to be lost in the bloodstream

occurs in:

• within blood vessels (bloodstream)

iron recylcing

iron from destroyed RBCs is:

• recovered

• stored in liver

• reused to make new RBCs

polycythemia

too many RBCs

secondary polycythemia (good)

the body responds appropriately by making more RBCs:

• high altitude

• endurance training

• low oxygen levels

hematocrit usually → up to 50%

polycythemia vera (primary polycythemia)

the production of to many RBCs leading to thickening of the blood

cause:

• genetic mutation

• RBC production does NOT stop

characteristics:

• 7-8 million RBCs

• hematocrit 60-70%

problems:

• blood becomes thick

• increased clot risk

• increased strain on the heart

anemia

to few RBCs or insufficient hemoglobin

result:

• reduced oxygen delivery to tissue

symptoms:

• fatigue

• weakness

• dizziness

• pale skin

• shortness of breath

• rapid heart rate

aplastic anemia

a rare but serious blood disorder where the bone marrow fails to produce enough blood cell (destruction of bone marrow stem cells)

cause:

• radiation

• chemotherapy

• severe infections

results → bone marrow cannot make:

• RBCs

• WBCs

• platelets

treatment:

• bone marrow transplant

megaloblastic anemia

vitamin B12 deficiency occurs when the body does not get enough vitamin B12 or folate (diet)

• B12 + folate are needed for DNA synthesis

without them:

• DNA produced impaired

• RBC maturation impaired

• cells become abnormally large (megaloblasts)

causes of B12 deficiency:

• poor diet

• fish tapeworm infestation

• malabsorption disorders

pernicious anemia

specific type of vitamin B12 deficiency, resulting in a reduced production of healthy red blood cells (stomach damage prevents B12 absorption)

problem:

• ulcers/chronic gastritis damage parietal cells → no intrinsic factor → NO B12 absorption → leads to anemia

(no intrinsic factor = no B12 absorption)

hypochromic anemia

iron deficiency → due to the lack of iron through diet

effects:

• less hemoglobin

• pale RBCs

• smaller RBCs (microcytic)

causes:

• poor diet

• menstruation (women)

• hookworm infection

• GI bleeding (ulcers)

(small pale RBC = due to low iron)

thalassemias

inherited disorder affecting hemoglobin production\

• alpha/beta thalassemia

alpha-thalassemia

normal → 4 a-genes (in each chain):

• 1 deleted = carrier → mutation may cause the protein not to work

• 2 deleted = minor → mild/chronic anemia

• 3 deleted = HbH disease → severe form of anemia

• 4 deleted = hydrops fetalis (fatal) → in fetus leading to miscarriage

beta-thalassemia

normal → 2 b-genes

defect causes → minor & major:

• mild to severe anemia

• enlarged spleen

• increased RBC production

treatment → often requires:

• blood transfusion

• bone marrow transplant in severe cases

sickle cell anemia

point mutation in beta-globin gene

• glutamic acid → valine at position 6

how?:

• at low oxygen → hemoglobin molecules stick together → form fibers → RBC becomes sickle-shaped

problem:

• RBC destruction (hemolysis)

• anemia

• capillary blockage

• pain crises

• organ damage

sickle cell anemia positive feedback loop

more sickling → less oxygen delivery → more sickling

• this is why sickle cell crises can rapidly worsen

leukemia

uncontrolled production of abnormal white blood cells

types:

• lymphogenous → starts in lymph tissue

• myelogenous → starts in the bone marrow stem cells

effects → WBC not functioning properly:

• frequent infections

• bleeding (platelet shortage)

• severe anemia

• high metabolic demand

(lots of WBC but they don’t work)

ABO blood types

type O, A, B, AB + antigens

type O

antigens = none

antibodies = anti-A, anti-B

type A

antigens = A

antibodies = anti-B

type B

antigens = B

antibodies = anti-A

type AB

antigens = A & B

antibodies = none

universal donor

type O

universal recipient

type AB

antigens

molecular markers that help the immune system identify whether something in the body is harmful

• recognize “self” or “non-self”

antibodies

protective proteins produced by the immune system in response to foreign substances called antigens (“NON-SELF”)

Rh immune response factors

Rh-positive = has D antigen

Rh-negative = No D antigen

erythroblastosis fetalis

Rh-negative mother + Rh-positive baby

• → during the first pregnancy, the mother becomes sensitized

• → later pregnancies, mothers produce anti-Rh antibodies = antibodies attack the fetus’ RBC

treatment:

• RhoGAM injection prevents antibody formation (scrub the antibody form the blood)

cardiac muscle

makes up most of the heart → specialized to contract continuously throughout life

characteristics:

• striated (like skeletal muscle)

• contains actin and myosin filaments

• very rich in mitochondria and myoglobin → heart needs constant ATP production

• highly fatigue resistant

intercalated discs

connect cardiac muscle cells together → contain gap junctions + demosomes

• require both because the heart needs both electrical communication and mechanical strength (gap junction = electricity desmosomes = strength)

gap junctions

allows electrical signals to move from cell to cell (electricity passes neighbor to neighbor)

desmosomes

hold cells tightly together → prevent cells from pulling apart during strong contractions

pacemaker

starts the heart to give it a rhythm

cells:

• generate electrical impulses automatically

• do not need nervous stimulation to begin beating

• allow the heart to continue beating even if removed from the body temporarily

atria

are booster pumps (NOT main pump)

• 75% of ventricular filling occurs passively

• only adds a small extra push at the end of filling

right ventricles

the MAIN pumping chambers

• pumps blood to the lungs

• low-pressure system

• lungs are delicate and can be damaged by high pressure

• de-oxygenated blood

left ventricles

the MAIN pumping chambers

• pumps blood to entire body → aorta

• must generate much higher pressure

• MUST have a much thicker muscle wall

• oxygenated blood

arteries

always carry blood AWAY from the heart (oxygen rich)

• UNLESS a pulmonary artery

veins

always carry blood TO the heart (oxygen poor)

• UNLESS a pulmonary vein

atrioventricular (AV) valve

between aria and ventricles

• tricuspid = right

• mitral/bicuspid = left

semi-lunar valves

between ventricles and arteries

• pulmonary valve

• aortic valve

chordae tendineae

“heart strings” → attach AV valves to papillary muscle

→ ensure one‑way blood flow by keeping atrioventricular valves closed under high pressure

papillary muscle

contracts during ventricular contraction → prevent valves from flipping backwards (eversion)

• they DO NOT open valves - ONLY pressure opens valves

→ only keep the valves from opening in the wrong direction

stenosis (valve disorders)

valves become narrow

result:

• harder for blood to leave

• disrupted blood flow

• murmur

  • WON’T OPEN

insufficiency (regurgitation) - (valve disorder)

valve becomes leaky

result:

• blood flows backward

• disrupted blood flow

• murmur

  • WON’T CLOSE

conduction system

SA Node → Internodal Pathway → AV Node → Bundle of His → Right + Left Bundle branches → Purkinje Fibers

SA Node

pacemaker of the heart → boss because it fires faster than all the others

characteristics:

• fastest firing cells

• set normal heart rate

• 70 BPM

AV Node

allows ventricles time to fill before contracting → delay electrical signals

→ ventricles take time before squeezing

characteristic:

• 50 BPM

Bundle of His

conducts electrical impulses from the atrioventricular (AV) node to the ventricles → leading to the right and left branches

Bundle Branches

electrical impulse comes down the interventricular septum, ensuring coordinated and simultaneous contraction of the ventricles → leading to the Purkinje fibers

Purkinje Fibers

conduct electrical impulses through the ventricles, ensuring fast, synchronized ventricular contraction for efficient blood ejection

characteristics:

• distribute the signal rapidly through the ventricles

• ventricles contract from the apex upwards

• creates efficient pumping action

• 30 BPM

SA Node Failure (backup)

AV node take over → slower (50 BPM)

cons:

• lose artial pumping

• missing maximum filling = cardio output less than normal)

• fatigue, dizzy, fainting → strains heart

• NOT COMMON

AV Node Failure (backup)

purkinje fibers take over partially → WAYYY slower (30 BPM)

cons:

• atrium going to fast → ventricles going to slow (due to 30 BPM) = ventricles not filling properly

• COMMON

ectopic focus (backup)

abnormal region starts firing faster than SA node (places that have AP that should NOT have AP)

results:

• arrhythmia (irregular heartbeat - to fast, slow, or erratic)

• abnormal pacemaker activity

Ventricular Cells (AP)

requires 3 channels + 4 phases

1. voltage-gated Na+ channels

2. voltage-gated Ca2+ channels

3. voltage-gated K+ channels

phase 1 (AP)

rapid depolarization

• Na+ channels open

• Na+ RUSHES INN REALLY FAST (due to the heart always being active)

• membrane becomes positive

phase 2 (AP)

partial repolarization

• Na+ channels close

• Ca2+ channels begin to open

phase 3 (AP)

plateau

• Ca2+ channels stay open for a LONGGGG time (refractory period)

• maintain contraction force

→ prevents tetanus/ backflow + ensures only ONE contraction occurs at a time, and

phase 4 (AP)

repolarization

• Ca2+ channels close

• K+ channels open

• returns the cell to resting state (-90)

Nodal Action Potential (SA Node)

requires 4 major channels:

1. Na+ leak channels

2. fast Ca2+ channels (T)

3. slow Ca2+ channels (L)

4. K+ channels

Pacemaker cells fire automatically:

→ their membrane slowly drifts toward threshold due to…

1. K+ channels gradually closing

2. Na+ leaks inward

3. Ca2+ triggers AP

→ 1st Ca2+ (T) rapidly gets us to threshold → 2nd Ca2+ (L) does everything above threshold

cardiac cycle

sequence of events in one heartbeat, consisting of systole (contraction) and diastole (relaxation)

• 4 phases

cardiac cycle - phase 1

ventricular filling

• AV valves open

• semi-lunar valves closed

• ventricles fill with blood

• diastole (relaxation)

cardiac cycle - phase 2

isovolumetric contraction

• all valves closed

• ventricles contract

• pressure rises

• volume STAYS THE SAME

cardiac cycle - phase 3

ventricular ejection

• semi-lunar valves open

• blood leaves ventricles

• systolic pressure produced (contraction)

cardiac cycle - phase 4

isovolumetric relaxation

• all valves closed

• pressure falls

• volume unchanged

1st heart sound

ALWAYS WHEN A VALVE CLOSES → “Lub”

• occurs when AV valve closes = beginning of systole (contraction)

2nd Heart Sound

ALWAYS WHEN A VALVE CLOSES → “Dub”

• occurs when aortic + pulmonary valves close = beginning of diastole (relaxation)

A wave

artial contraction

C wave

ventricular contraction causes bulging of AV valve towards the atria

V wave

blood accumulates in the atria while the ventricles contract