5) lifespan of RBC in females= 110 days; males= 120 days
Breakdown of Hemoglobin from lysed RBC
1) remenants get trapped in two organs ( liver and spleen/rbc graveyard)
a) macrophages enzymatically seperate Heme from globin
- globin is broken down into amino acids ( then amino acids are used for protein synthesis)
- heme ( Fe portion is transported to bone marro and used to make more Hb)
( pigment is converted to bilirubin and becomes part of bile secreted by the liver)
Hemostasis
3 steps
- vascular spasm
- platelet plug formation (has its own three steps)
- Coagulation
Fibronolysis occurs after 3 steps
Vascular Spasm in Hemostasis
1) Immediate but temporary closure of damage blood vessel
- due to reflexive retraction of smooth muscle within vessel wall
2) Triggered by two different things
- endothelin from damages blood vessel endothelial cells
- nervous system due to stimulation of local pain receptors(nociceptors)
Platelet Plug Formation of Hemostasis
1) an accumulation of platelets at injury cite
2) occurs in a series of steps
a) Platelet adhesion
b) Platelet release reaction
c) Platelet aggragation
Platelet adhesion in PPF
1) injured endothelial cells produce a protein called Von WillenBrand Factor
- allows platelets to bind to collagen that has been exposed due to injury
Platelet release reaction of PPF
1) Platelets bound to collagen and become activated , which causes platelets to release chemicals from their cytoplasmic granules
a) ADP
-Thromboxane A2 are released from granules ( recruits more platelets to injury cites)
Platelet aggragation of PPF
Plasma protein fibrinogen facilitates binding of platelets together PGI1 released from damaged endothelial cells (limits the aggragation to only damaged area)
Coagulation of Hemostasis
- Prothrombin turns into Thrombin (by prothrombin activator from damaged endothelial cells) (prothrombin is made by liver and is not active)
- Fibrinogen turns into Fibrin ( by Thrombin) (Fibrinogen is mage by the liver and Fibrin is what holds the clot together)
Fibronolysis (clot resolution) of Hemostasis
-cells around clot release a protein called Tissue Plasminogen Activator (TPA)
plasminogen -----> Plasmin (activated by TPA) (plasminogen is made by liver and Plasmin causes hydrolysis of fibrin holding clot together)
Damaged Endothelial Cells Release 5 Things
- Edothelin
- Von WillenBrand Factor
- PGI2
- Prothrombin activator
- Tissue Plasminogen Activator
Pericardial Sack
double layered closed sack surrounding the heart
a) fibrous pericardium
- tough fibrous CT
- prevents fro moverdistension of heart, anchors w/ in the mediastium
b) Serous pericardium ( simple squamous epithelium)
T-wave- ventricles repolarize .225 sec later ventricles relax
EKG PIC
Heart Sounds
use a Stethoscope to listen
1st is "Lubb"- AV valves closing (beginning of ventricular systole)
2nd is "Dubb"- SL valves closinf and begining of ventricular diastole
Abnormalities of Heart
1)Tachycardia
2) Bradycardia
3) Arythmias
Tachycardia
abnormal high rate- 100bpm
Bradycardia
abnormal low rate- less than 60bpm
Arythmias
are abnormal series of excitement
1) SA nodal Block (missing P-wave and HR decreases)
2) AV nodal Block - ventricles dont recieve all implulses from atria
3types: 1st(interval between P and QRS > .2 sec)
2nd (some P waves trigger QRS and some dont)
3rd ( complete heart block / atrial bpm 100 and ventricle bpm lower than 40)
V-fib- ventricles never fully fill or empty( drecrease blood supply to tissues)
Cardiac Output (CO)
1) amount of blood pumped through heart per minute
- HR times SV
- SV is amount of blood the heart beats per beat
Regulation of Heart
1)Intrinsic- the more the ventricle muscle is stretched the more
forceful the next contraction would be
- occurs when venous return increase (amount of blood entering the right atrium from superior vena cava)
-if you increase venous return you increase SV and therfore CO
Blood Vessel Walls have 3 Layers
Tunica Intima
Tunica Media
Tunica Adventitia
Tunica Intima of BV
contacts blood
endothelial cells and basement membrane cells
Tunica Media of BV
smooth muslce and is innervated from sypmathetic nervous system which causes vasoconstriction and lack mean vasodialation
Tunica Adventitia of BV
outermost layer
has collagen fibers tha anchor BV to the surrounding structure
Capillaries
Continuous Capillaries
Fenestrated Capillareis
Sinusoidal Capillaries
Contiuous Capillaries
skin, muscle, and blood brain barrier
most common
least permeable
intercellular clefts- unjoined membrane
Fenestrated Capillaries
large pores (fenestrations)
SI, Kidneys, Endocrine organs
Sinusoidal Capillaries
leaky capillaries
most permeable
liver, bone marrow. adrenal medulla, spleen
Hepatic macrophages ( kuppfer cells)
Veins
have much thinner tunica media and have larger lumens
cna hold up to 65% of blood volume at one time
are blood reservoirs
venus valves- prevents blood from pooling to ensure one way flow to heart
Regulation of BP
Neural regulation
Chemical regulation
Neural regulation of BP
receptors involved
Baroreceptors- sense pressure in Arch of Aorta and bifurcation of carotids
monitors minute to minute fluctuations
affaerent signals are sent from aorta to the vagus (X) adn from the carotids to the glosspharyngeal (IX)
efferent signals are then sent to cardioregulatory systems and medulla oblongata
Neural regulation of BP
Centers involved
1) vasomotor center
2) Vagal Center
3) Processes invovled
Vasomotor Center
is sympathetic and recieve afferent signals from baroreceptors
if BP decreases it will efferently stimulate nerves in the thoracic region( T1-T2)
the release of norepinepherine or epinephrine one the Beta recpetors on the heart( increase CO and BP) and the alpha receptors on the blood vessels ( vasoconstriction to increase TPR)
Vagal Center
in under parasympathetic control and it recieves afferent signals from the baroreceptors
-stimulated by an increase in BP
-sends effernent signals via the vagus which causes the release of Ach on the M2 receptors on the heart
-Decreases HR and CO
- lack of stimulation from barorecptors causes vasodialation and decrease in TPR
-this yeilds a decrese in BP
Process of Regulation of BP
-an increase in BP will excite the Vagal center and inhibit the vasomotor center( cause decrese in BP)
- a decrese in BP will excite the Vasomotor center and inhibit the Vagal center ( cause increase in BP)
Chemical Regulation (hormones) of BP
1) ADH( anti-diuretic hormone)
2) Renin
ADH
vasopressin
1) made by hypothalamus
2) stored in Posterior pituitary
3) release of ADH is triggered by a decrese in BP
4) ADH targets the kidney tubule system ( cause more water reabsorbtion)
5) increse BC, venous return, SV, CO, and therefor BP
Renin
1) made by kidneys
2) triggered by decrese in BP
3) once in the blood it cuases and enzyme to catalyze production of Angiotensin 2
- A2 targets adrenal gland and cause the adrenal cortex to release Aldosterone
- aldosterone cause incres in NaCl reabsorbtion in circulatory system ( water follow osmatically)