• Hematocrit, WBCs and Platelets
• Hematocrit are the RBCs and the rest is the so-called buffy coat.

A) 92% water

B) 7% proteins- help keep osmotic pressure, can act as buffers; mostly made in liver.  Are 4 major plasma proteins...

C) 1% other:

    1 - inorganic ions maintain pressure, pH and aid metabolism

    2 - gases - O2/CO2 from cellular respiration

    3 - nitrogenous waste - urea, ammonia, uric acid

    4 - regulatory substances - i.e. hormones, enzymes, etc.

    5 - Organic nutrients

1 - PROTHROMBIN

2 - FIBRINOGEN

3 - ALBUMINS - also transport large molecules esp bilirubin

4 - GLOBULINS -

     ALPHA & BETA - bind metal ions and fat soluble vitabins, also binds lipids forming LIPOPROTEINS which transport CHOLESTEROL; GAMMA - antibodies made by WBCs

BOOK:

by liver and spleen by macrophages.  Hemoglobin  is released, broken into AAs and recycled throughout the body.  Iron is returned to marrow for reuse.  Heme part is degraded and excreted as bile pigments (bilirubin) by liver into bile

WIKI:

The heme constituents of hemoglobin are broken down into iron (FE3+) and biliverdin which is reduced to bilirubin, released into the plasma and recirculated to the liver bound to albumin. Bilirubin is then excreted in bile and urine. The iron is released into the plasma to be recirculated by a carrier protein called transferrin.

1 - VASCULAR SPASM - vessel constricts, platelets release serotonin to prolong this

2 - PLATELET PLUG FORMATION - exposure of CT, platelets stick and release substances, e.g. one increases platelet aggregation

3 - COAGULATION = clotting.  Requires VIT K to form prothrombin (from green veggies and intestinal bacteria).  Also requires many clotting factors, in blood im inactive state, mostly made in liver.

1. PROTHROMBIN ACTIVATOR (PTA) is produced simultaneously in two ways (intrinsically by factors in blood, and extrinsically by release of TISSUE THROMBOPLASTIN from damaged tissue)
2. PTA converts prothrombin (already in blood) to THROMBIN
3. Thrombin breaks up fibrinogen (already in blood) and reforms it's peices into FIBRIN
4. Fibrin threads wind around platelet plug formed during hemostasis and traps RBCs
5. Clot retraction - serum is squeezed from clot, shrinking it and PLASMIN destroys the fibrin network.

1. HEMOLYTIC - RBCs are destroyed; e.g. hemolytic disease of the newborn and SICKLE CELL where hemoglobin is abnormally shaped and fragile.
2. DIETARY - Iron (most common) and pernicious (B12) from inadequate gut absorption
3. APPLASTIC - red marrow damaged from toxins
4. HEMMORHAGIC - may require transfusion

a pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases. DIC leads to the formation of small blood clots inside the blood vessels throughout the body. As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin (e.g. from sites where blood samples were taken), the gastrointestinal tract, the respiratory tract and surgical wounds. The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result.

DIC can occur acutely but also on a slower, chronic basis, depending on the underlying problem. It is common in the critically ill, and may participate in the development of multiple organ failure, which may lead to death.

Can occur with snake bite, and seretonin syndrome.  Many other pathologies can cause also.

Regarding labor and delivery:

Disseminated intravascular coagulation is a condition in which small blood clots develop throughout the bloodstream, blocking small blood vessels and depleting. The increased clotting depletes the platelets and clotting factors needed to control bleeding, causing excessive bleeding

• There are a number of possible causes, including infection and surgery.
• Excessive clotting is followed by excessive bleeding.

Disseminated intravascular coagulation (DIC) begins with excessive clotting. The excessive clotting is usually stimulated by a substance that enters the blood as part of a disease (such as an infection or certain cancers) or as a complication of childbirth, retention of a dead fetus, or surgery. People who have a severe head injury or who have been bitten by a poisonous snake are also at risk. As the clotting factors and platelets are depleted, excessive bleeding occurs.

1. ENDOCARDIUM - 1 layer simple squamous, continues into vessels; smooth
2. MYOCARDIUM - thickest, muscular
3. EPICARDIUM = VISCERAL SEROUS PERICARDIUM which folds over forming the PARIETAL SEROUS PERICARDIUM which is fused to outermost FIBROUS PERICARDIUM (thick and anchors to large vessels, diaphragm and mediastinal walls).  The parietal and visceral serous pericardium secrete pericardial fluid.

1. superior vena cava - collects from head and upper extremities
2. inferiour vena cava - lower body
3. coronary sinus - heart

LUB - AV valves closing when ventricles contract

DUP - SL valves closing from relaxation

=Bundle of His

down ventricular septem, then branches into many PURKINJE fibers

events of 1 heart beat, are 3 phases:

1. Atrial Systole, about .15 sec, both atria contract, ventricles are relaxed, forces blood through opened AV valves.  Ends when increasing ventricular pressure slams AV valves shut = LUB
2. Ventricular Systole, about .3 sec, ventricles contract forcing orpen SL valves, ends when SL valves shut = DUP
3. Atiral and Ventricular Diastole, about .4 sec, both relaxes, r atrium fills, pressure is down, both AV valves are open and SL valves closed.

= volume of blood pumped from a ventrible in 1 minute, about 5.25 liters

= heart rate X stroke volume

• CARDIOREGULATORY CENTER in the medulla oblongata receives information from cardiovascular receptors, e.g. baroreceptors in aorta and carotids.  Includes blood pressure reflexes.  Is under influence of cerebrum and hypothalamus, sympathetic inervation (psychological).
• Adrenal medullary NE and epi increase heart rate
• Relaxation stimulates vagus parasympathetic
• Electrolyte concentrations

• strength of contraction, by ANS, electrolytes, venous return, etc
• venous return by BP difference in veins, skeletal/respiratory pumps and total blood volume
• Difference in BP, heart vs aorta.

1. TUNICA INTERNA - endothelium
2. TUNICA MEDIA - thick middle, smooth muscle and elastic fibers
3. TUNICA EXTERNA - outer CT elastic/collagen fibers

• Arterial end - blood is oxygen rich and BP is higher than bloods osmotic pressure, forcing out (filtration) small molecules like nutrients and water.
• Midsection - simple diffusion; oxygen moves into tissue fluid and CO2 moves into plasma
• Venule end - BP is greatly reduced, osmotic pressure is greater, pulling in water from tissues, along with it wastes

result of vessel diameter and length of vessel.  For every lb of fat about 200 miles of vessel!

Neurally and hormonally regulated

• Epi/NE increases HR, constrincts arterioles of skin, abdominal ciscera and kidneys
• RENIN - by kidneys when sodium/blood volume is low.  Stimulates adrenal cortex to excrete ALDOSTERONE (mediator is ANGIOTENSIS), excretes arterioles.
• ADH(VASOPRESSIN) increases blood volume and pressure by water retention, also affects cardiac output, vasoconstriction.
• ANP

1. Ascending - R/L Coronoary arteries
2. Arch - Braciocephalic (becomes R Carotid and R Subclavian), L Common Carotid, L Subclavian
3. Descending - Thoracic and Abdominal; ends when branches into R/L Common Iliacs

sustemic circuit doesn't pump enough blood (decreased CO) backing up into pulmonery circuit, causing pulmonary edema; SOB, fatigue, sweating, enlarged and distressed heart, constant cough with pink sputum; can be caused from hypertension (increases peripheral resistance) and decreased contractile force.

heart damage --> decreased ventricular contraction --> ventricular dilation, heart enlargment (myocardial hypertrophy), increased heart pressure, weaker and stiffer --> decreased cardiac output --> decreased renal profusion --> sodium retention --> increased osmotic pressure of blood, water retention --> TISSUE EDEMA, especially of lower extremities leading to further heart damage.

A type of arteriosclerosis leaving fatty deposits in arteries.  3 stages of progression

1. Injury to arterial wall from smoking, HT, high lipids, high homocysteine from protein metabolism, low level infections, gum disease, H. Pylori, etc.
2. Then an immune reaction - macrophages stick to site and inject LDL cholesterol creating a "fatty streak"
3. Smooth muscle covers and bibroblasts scar.  Calcium inos invade and caise hardening/plaque, making a rough surface for platelets to stick to , forming thrombi.  This may weaken wall leading to aneurysm.

• Myocardial infarction (MI) is the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque in the wall of an artery. The resulting ischemia and oxygen shortage can cause damage or death of heart myocardium.
• Classical symptoms of acute myocardial infarction include sudden chest pain (typically radiating to the left arm or left side of the neck), shortness of breath, nausea, vomiting, palpitations, sweating, and anxiety. Women may experience fewer typical symptoms than men, most commonly shortness of breath, weakness, a feeling of indigestion, and fatigue.^[2] Approximately one quarter of all myocardial infarctions are "silent", without chest pain or other symptoms and can cause sudden death.

• Fatigue
  
• decreased energy
  
• weakness
  
• shortness of breath
  
• lightheadedness
  
• palpitations (feeling of the heart racing or beating irregularly)
  
• looking pale

Symptoms of severe anemia may include:

• chest pain, angina, or heart attack
  
• dizziness
  
• fainting or passing out
  
• rapid heart rate

• Vitamin K is a fat-soluble vitamin. The "K" is derived from the German word "koagulation."
• itamin K is essential for the functioning of several proteins involved in blood clotting
• There are two naturally occurring forms of vitamin K. Plants synthesize phylloquinone, which is also known as vitamin K₁. Bacteria synthesize a range of vitamin K forms using repeating 5-carbon units in the side chain of the molecule. These forms of vitamin K are designated menaquinone-n (MK-n), where n stands for the number of 5-carbon units. MK-n are collectively referred to as vitamin K₂ (2).
• he only known biological role of vitamin K is as a cofactor for an enzyme that catalyzes the carboxylation of the amino acid, glutamic acid, resulting in its conversion to gamma-carboxyglutamic acid (Gla) (5), critical to the calcium-binding function of those proteins (6, 7).
• The ability to bind calcium ions (Ca²⁺) is required for the activation of the seven vitamin K-dependent clotting factors, or proteins, in the coagulation cascade.
• Vitamin K-dependent gamma-carboxylation of specific glutamic acid residues in those proteins makes it possible for them to bind calcium.
• Vitamin K-dependent coagulation factors are synthesized in the liver. Consequently, severe liver disease results in lower blood levels of vitamin K-dependent clotting factors and an increased risk of uncontrolled bleeding (hemorrhage) (8).
• Although vitamin K is a fat-soluble vitamin, the body stores very little of it, and its stores are rapidly depleted without regular dietary intake. Perhaps, because of its limited ability to store vitamin K, the body recycles it through a process called the vitamin K cycle.

• Is the most abundance plasma protein.
• Essentioal for maintaining osmotic pressure
• Acts as a carrier of steroid hormones, fatty acids, thyroid hormones.
• Is produced in the liver
• Too much can be bad

• Some globulins are produced in the liver, while others are made by the immune system.
• The term globulin encompasses a heterogeneous group of proteins, are many globulins, categorized into the following four categories

1. Alpha 1 globulins, examples are α₁-antitrypsin, Alpha 1-antichymotrypsin, Orosomucoid (acid glycoprotein), Serum amyloid A, Alpha 1-lipoprotein

2. Alpha 2 globulins, examples are Haptoglobin, Alpha-2u globulin, α₂-macroglobulin, Ceruloplasmin, Thyroxine-binding globulin, Angiotensinogen

3. Beta globulins.  Examples of beta globulins include plasminogen, angiostatins, properdin, sex hormone binding globulin, transferrin

4. Gamma globulins - The most significant gamma globulins are immunoglobulins, more commonly known as antibodies, although some Igs are not gamma globulins, and some gamma globulins are not Igs.
   

Hematapoiesis is the formation of blood cellular components. All cellular blood components are derived from haematopoietic stem cells.  Includes all WBCs, RBCs, platelets, etc.

RBC creation is ERYTHROPOESIS, which is a type of HEMATOPOESIS

• Sickle cells contain abnormal hemoglobin that causes the cells to have a sickle, or crescent, shape. These cells don't move easily through your blood vessels. They're stiff and sticky and tend to form clumps and get stuck in the blood vessels.
• In sickle cell anemia, the number of red blood cells is low because sickle cells don't last very long. Sickle cells usually die after only about 10 to 20 days. The bone marrow can't make new red blood cells fast enough to replace the dying ones.

• The most common symptom of anemia is fatigue (feeling tired or weak). Other signs and symptoms of anemia may include:

• Shortness of breath
• Dizziness
• Headaches
• Coldness in the hands and feet
• Paler than normal skin or mucous membranes (the tissue that lines your nose, mouth, and other organs and body cavities)

• Excess potassium reduced heart rate and strength of contraction.
• Excess calcium causes spastic contraction; decreased calcium causes reduced heart rate and strength (like excess potassium)
• Excess sodium depresses heart function by competing with calcium; Sodium deficiency can cause cardiac fibrillation where heart contracts extemely fast and irregularly causing blood to not be pumped to the body.  This can be lethal.