Cardiovascular System: Blood

o Lactate:
TOPIC 1. Introduction to Blood  Produced by skeletal muscles during anaerobic
 Blood is often referred to as the "essence of respiration, transported to the liver to be
life" because its uncontrolled loss can lead to converted into glucose.
death. 3. Transport of Regulatory Molecules:
 It’s a remarkable fluid connective tissue,  Blood carries vital regulatory substances like
meaning it connects various parts of the body hormones and enzymes from their production
by transporting substances and maintaining sites to target tissues to regulate body
balance. processes.
 It’s composed of plasma (the liquid extracellular 4. Regulation of pH and Osmosis:
matrix) and formed elements (the cells and cell  Blood plays a critical role in maintaining the
fragments within it). Studying blood body's internal balance.
scientifically reveals its complex and essential o pH Regulation:
characteristics, and diagnostic tests evaluating  Contains buffers that help maintain blood pH
blood composition are crucial for understanding within its narrow normal limits of 7.35–7.45.
a patient's health. Deviations outside this range can be dangerous.
 The heart continuously pumps blood through a o Osmotic Regulation:
vast network of blood vessels throughout the  The osmotic composition of blood is crucial for
body. maintaining normal fluid and ion balance
between the blood and surrounding tissues.
TOPIC 2. Functions of Blood This water balance is largely influenced by
 Blood performs numerous functions essential solutes like ions (Na+, Cl-) and plasma proteins,
for maintaining homeostasis within the body. especially albumin.
Let’s break down the seven primary functions: 5. Maintenance of Body Temperature:
1. Transport of Gases, Nutrients, and Waste Products:  As blood flows through metabolically active
 Blood acts as the body's major transport areas, it absorbs heat. This warm blood is then
medium. transported to the body's surface, where heat is
o Oxygen (O2): released, helping to regulate overall body
 Enters the blood in the lungs and is carried to temperature.
every cell in the body. 6. Protection Against Foreign Substances:
o Carbon Dioxide (CO2):  Blood contains specialized cells and chemicals
 Produced by cells as a waste product and is that are part of the immune system. These
carried in the blood to the lungs for expulsion. components protect the body against
o Nutrients, Ions, and Water: pathogens (like microorganisms) and toxins.
 Transported from the digestive tract to cells 7. Clot Formation:
throughout the body.  When blood vessels are damaged, the blood's
o Cellular Waste Products: ability to clot is a crucial protective mechanism.
 Carried from cells to the kidneys for elimination o It prevents excessive blood loss.
from the body. o It's the vital first step in tissue repair and restoring
2. Transport of Processed Molecules: normal function after injury.
 Some substances are produced in one organ
and then transported by blood to another TOPIC 3. Composition of Blood
location to be further modified.  Blood is a type of connective tissue made of a
o Vitamin D Precursor: liquid matrix called plasma and formed
 Produced in the skin, transported to the liver, elements (cells and cell fragments).
then to the kidneys for activation, and finally to 1. Plasma:
the small intestine to promote calcium uptake.
  This pale yellow fluid makes up slightly more  These account for slightly less than half
than half (approximately 55%) of the total blood (approximately 45%) of the total blood volume.
volume. They include three main types:
o Red Blood Cells (RBCs) / Erythrocytes:
o Components:  The most abundant (nearly 95% of all formed
 Water (91%): elements).
 Serves as a solvent and suspending medium for o White Blood Cells (WBCs) / Leukocytes:
blood components.  Account for part of the remaining 5% of formed
 Proteins (7%): elements.
 Unlike fibrous connective tissues, plasma o Platelets / Thrombocytes:
proteins are dissolved. Key plasma proteins  Cell fragments also making up part of the
include: remaining 5% of formed elements.
 Albumin (58% of plasma proteins): o Abundance:
 Contributes significantly to blood's osmotic  RBCs are about 700 times more numerous than
pressure, helping maintain water balance WBCs and 17 times more numerous than
between blood and tissues, and functions as a platelets.
transport molecule.
 Globulins (38% of plasma proteins):
 Include antibodies and complement (part of the TOPIC 4. Red Blood Cells (RBCs)
immune system), transport molecules (binding 1. Structure:
to hormones), and some are clotting factors.  RBCs are distinctively biconcave disks. Their
 Fibrinogen (4% of plasma proteins): edges are thicker than their center, giving them
 A crucial clotting factor that is converted into a unique shape.
fibrin (a threadlike protein) to form blood clots.  Crucially, mature RBCs lose their nuclei and
 Other Components (2%): most organelles during development, making
 Ions, nutrients, gases, waste products, and them unable to divide.
regulatory substances. These include:  Their biconcave shape increases surface area
 Ions (e.g., Na+, Cl-, K+, bicarbonate): for efficient gas exchange (O2 and CO2) and
 Important for osmotic pressure, membrane allows them to bend and fold to pass through
potentials, and acid-base balance. narrow blood vessels like capillaries.
 Nutrients (e.g., glucose, amino acids, triglycerides): 2. Function:
 Serve as energy sources and building blocks for  The primary function is to transport O2 from
complex molecules. the lungs to the body's tissues and to assist in
 Gases (e.g., oxygen, carbon dioxide): transporting CO2 from tissues to the lungs.
 Involved in aerobic respiration.  This function is carried out by the protein
 Waste Products (e.g., urea, ammonia salts, hemoglobin.
bilirubin): 3. Hemoglobin:
 Breakdown products of metabolism,  Hemoglobin is a pigmented protein that
transported for elimination. constitutes about one-third of an RBC's volume
 Regulatory Substances (e.g., enzymes, hormones): and is responsible for the cell's red color.
 Catalyze reactions and regulate body functions. o Structure:
o Clinical Relevance:  Each hemoglobin molecule consists of four
 Plasma volume and composition are kept protein chains called globins, and each globin is
relatively constant through tightly regulated bound to a heme group. Each heme group
processes involving water intake/loss and the contains one iron atom, which is vital for
liver, kidneys, intestines, and endocrine glands. hemoglobin's normal function.
2. Formed Elements: o Oxygen Transport:
 Oxygen reversibly binds to the iron atom within
the heme molecule. A single RBC carries many
 hemoglobin molecules, ensuring sufficient O2 o Lifespan:
transport. About 98.5% of O2 transported in  RBCs live for approximately 120 days in males
blood is bound to hemoglobin. and 110 days in females.
o Color Change: o Nutritional Requirements for RBC Production:
 Hemoglobin bound to O2 is bright red, while  Folate and Vitamin B12:
hemoglobin without bound O2 is a darker red.  Essential for DNA synthesis, which is needed for
o Iron Importance: cell division during RBC production.
 Two-thirds of the body's iron is found in  Iron:
hemoglobin.  Required for hemoglobin production.
Dietary iron is needed to replace small losses, but  Clinical Connection:
existing iron is mostly recycled. Females require more  Deficiencies in any of these can interfere with
dietary iron due to menstruation. normal RBC production, leading to different
o Carbon Monoxide (CO) Risk: types of anemia.
 CO binds to the iron in hemoglobin about 210 o Regulation of RBC Production:
times more readily than O2 and tends not to  Production is stimulated by low blood O2 levels
unbind. This means hemoglobin bound to CO (hypoxia). Causes include low RBC count,
cannot transport O2, leading to severe defective hemoglobin, lung diseases,
consequences like nausea, headache, cardiovascular issues, high altitude, or increased
unconsciousness, and death from prolonged tissue demand for O2 (e.g., exercise).
exposure. This is a critical safety consideration  When O2 levels decrease, the kidneys release
in nursing. the hormone erythropoietin (EPO).
o Carbon Dioxide (CO2) Transport:  EPO stimulates the red bone marrow to
 CO2 is transported from tissues to the lungs in produce more RBCs, increasing the blood's O2
three ways: transport capacity, thereby maintaining
 70% as bicarbonate ions (HCO3-): homeostasis via a negative-feedback
 The enzyme carbonic anhydrase, found mechanism.
primarily in RBCs, catalyzes the conversion of  Conversely, if blood O2 levels rise, less EPO is
CO2 and water into hydrogen ions and released, and RBC production decreases.
bicarbonate ions. 5. Destruction and Recycling:
 23% bound to hemoglobin: o Old, abnormal, or damaged RBCs are removed from
 CO2 binds reversibly to the globin part (not the the blood by macrophages in the spleen and liver.
heme/iron part) of the hemoglobin molecule. o Hemoglobin Breakdown:
 7% dissolved in plasma.  Globin chains:
4. Life History and Production (Hematopoiesis):  Broken down into amino acids, which are
o Production: reused to produce other proteins.
 The continuous process of producing formed  Heme groups:
elements is called hematopoiesis. After birth, it  Iron is released and then transported in the
primarily occurs in the red bone marrow. blood back to the red bone marrow for reuse in
o Stem Cells: new hemoglobin (iron recycling).
 All formed elements originate from  The heme molecules (without iron) are converted to
hematopoietic stem cells (hemocytoblasts). bilirubin, a yellow pigment.
These differentiate into myeloid stem cells o Bilirubin Excretion:
(producing most formed elements) and  Bilirubin is normally removed from the blood by the
lymphoid stem cells (producing lymphocytes). liver and released into the small intestine as part of
o RBC Maturation: bile.
 Myeloid stem cells give rise to proerythroblasts,  In the intestine, bacteria convert bilirubin into other
which undergo cell divisions and manufacture pigments, some of which give feces their
large amounts of hemoglobin. Finally, they lose characteristic brown color.
their nuclei to become mature RBCs.
 Other pigments absorbed from the intestine are  Eosinophils (2–4% of WBCs): Often have a bilobed
modified by the kidneys and excreted in the urine, nucleus and cytoplasmic granules that stain bright
contributing to its yellow color. red or orange-red.
o Clinical Connection:  Function: Involved in inflammatory responses
 Jaundice: associated with allergies and asthma, and their
 If the liver isn't functioning normally or bile flow chemicals help destroy certain worm parasites.
is hindered, bilirubin builds up in the blood and
can be deposited in tissues, causing jaundice (a
yellowish discoloration of the skin). This is an
important observation for nursing students. o Agranulocytes (have very small, inconspicuous
granules):
 Lymphocytes (20–25% of WBCs): The smallest
TOPIC 5. White Blood Cells (WBCs) WBCs, with a large, round nucleus and cytoplasm
1. General Characteristics: forming a thin ring around it.
 WBCs are spherical cells that lack hemoglobin.  Function: Crucial for the immune response.
 They are larger than RBCs and each possesses a They produce antibodies and other chemicals
nucleus. that destroy microorganisms, contribute to
 In a centrifuged blood sample, WBCs (along allergic reactions, graft rejection, tumor control,
with platelets) form the buffy coat, a thin, white and regulate the immune system.
layer between the plasma and RBCs.  Monocytes (3–8% of WBCs): The largest WBCs, with
 While transported by blood, their primary a round, kidneyshaped, or horseshoe-shaped
function occurs in other body tissues, where nucleus.
they leave the bloodstream via ameboid  Function: After leaving the blood and entering
movement. tissues, monocytes enlarge and become
2. Functions: macrophages. Macrophages are powerful
 Their main roles are to protect the body against phagocytic cells that engulf bacteria, dead cells,
invading microorganisms and other pathogens. cell fragments, and other debris. They can also
 They also remove dead cells and debris from present processed foreign substances to
tissues through phagocytosis (cell eating). lymphocytes, activating them as part of the
3. Types of WBCs: immune response.
 There are five main types, classified based on
the presence or absence of visible cytoplasmic
granules in stained preparations. TOPIC 6. Platelets (Thrombocytes)
o Granulocytes (contain large cytoplasmic granules): 1. Structure and Origin:
 Neutrophils (60–70% of WBCs): The most common  Platelets are not complete cells but minute
type. They have a multi-lobed nucleus (2-4 lobes) fragments of cells, each surrounded by a cell
and granules that stain light pink or reddish-purple. membrane and containing granules.
 Function: Primarily phagocytize microorganisms  They are produced in the red bone marrow
and other foreign substances. They are short- from very large cells called megakaryocytes,
lived in the blood (10-12 hours) before moving from which small fragments break off to
into tissues. Accumulations of dead neutrophils, become platelets.
cell debris, and fluid form pus at infection sites. 2. Function:
 Basophils (0.5–1% of WBCs): The least common  They play an absolutely critical role in
type. They have indistinctly lobed nuclei and large preventing blood loss.
cytoplasmic granules that stain blue or purple.  Preventing Blood Loss (Hemostasis) When a
 Function: Release histamine (which promotes blood vessel is damaged, the body employs
inflammation) and heparin (which prevents clot three main processes to minimize blood loss:
formation). 1. Vascular Spasm:
 This is an immediate but temporary constriction of  Three Stages of Clot Formation:
the damaged blood vessel. ▪ Stage 1: Prothrombinase Production:
 The smooth muscle within the vessel wall contracts, This can be initiated in two ways:
which can completely close small vessels and stop  (a) inactive clotting factors contact exposed
blood flow. connective tissue, or
 It's stimulated by chemicals released by damaged  (b) chemicals like thromboplastin are released
vessel walls and platelets, such as thromboxanes from injured tissues. A cascade of reactions
and endothelin. leads to the formation of prothrombinase.

2. Platelet Plug Formation: ▪ Stage 2: Thrombin Production:

 A platelet plug is an accumulation of platelets that  Prothrombinase converts the inactive clotting
can seal up small breaks in blood vessels, especially factor prothrombin into its active form,
in capillaries and smaller vessels where minor tears thrombin.
occur daily. ▪ Stage 3: Fibrin Production:
 The process involves a series of steps:  Thrombin then converts the plasma protein
▪ Platelet Adhesion: fibrinogen into the insoluble, threadlike protein
 Platelets stick to the collagen exposed by the fibrin, which forms the meshwork of the clot.
damaged blood vessel. This is largely mediated o Key Requirements:
by von Willebrand factor, a protein that bridges  Most clotting factors are produced in the liver
collagen and platelet surface receptors. and many require Vitamin K for their synthesis.
▪ Platelet Release Reaction: Calcium ions (Ca2+) and chemicals released
 Once adhered and activated, platelets release from platelets are also essential.
chemicals like ADP and thromboxane, which ▪ Nursing Alert:
bind to receptors on other platelets, activating  Low Vitamin K, low Ca2+, low platelet count, or
them in a positive feedback loop. liver dysfunction can impair clotting. Newborns
 Activated platelets also express fibrinogen routinely receive Vitamin K injections because
receptors. they lack intestinal bacteria that produce it.
▪ Platelet Aggregation: o Control of Clot Formation:
 Fibrinogen (a plasma protein) forms bridges  The body has natural anticoagulants (e.g.,
between the fibrinogen receptors of numerous antithrombin, heparin) that prevent widespread
platelets, resulting in the formation of a platelet clotting under normal conditions by inactivating
plug. thrombin. At an injury site, the rapid activation
o Clinical Relevance: of clotting factors overwhelms these
 Drugs like aspirin inhibit thromboxane anticoagulants, allowing a localized clot to form.
synthesis, thereby reducing platelet activation o Abnormal Clots:
and plug formation. This is why aspirin is used ▪ Thrombus:
to prevent and treat clotting events like heart  An attached clot that forms in damaged or
attacks, but it also increases the risk of bleeding. diseased blood vessels or heart walls.
3. Blood Clotting (Coagulation): ▪ Embolus:
 For larger tears or cuts, vascular spasm and platelet  A thrombus that breaks loose and floats
plugs are insufficient. Here, coagulation forms a through the circulation.
stable clot, which is a network of threadlike protein ▪ Danger:
fibers called fibrin that traps blood cells, platelets,  Both thrombi and emboli can be fatal if they
and fluid. block vessels supplying vital organs like the
 Clotting Factors: This complex process relies on heart (heart attack), brain (stroke), or lungs.
numerous inactive clotting factors (proteins) found ▪ Treatment:
in plasma. These factors become activated in a  Anticoagulants like heparin (fast-acting) and
specific sequence following injury. warfarin (slower-acting, inhibits Vitamin K-
 dependent clotting factors) are used to prevent can damage kidney tissue and potentially cause
abnormal coagulation. death.
o Clot Retraction and Fibrinolysis (Clot Removal): 2. ABO Blood Group System:
▪ Clot Retraction:  This system categorizes blood based on the
 After formation, the clot condenses into a presence or absence of two specific antigens on
compact structure. Platelets contain contractile RBCs: Type A antigen and Type B antigen.
proteins (actin and myosin) that pull on the o Blood Types and Antigens:
fibrin, squeezing serum (plasma without clotting  Type A blood:
factors) out of the clot. This pulls the edges of  Has Type A antigens on RBCs.
the damaged vessel together, aiding healing.  Type B blood:
▪ Fibrinolysis:  Has Type B antigens on RBCs.
 As damaged tissue is repaired, clots are  Type AB blood:
dissolved. An inactive plasma protein,  Has both Type A and Type B antigens on RBCs.
plasminogen, is converted to its active form,  Type O blood:
plasmin, by thrombin, other clotting factors,  Has neither A nor B antigens on RBCs (the "O"
and tissue plasminogen activator (t-PA). Plasmin signifies absence).
slowly breaks down the fibrin. o Blood Types and Antibodies in Plasma:
▪ Therapeutic Use:  A person produces antibodies against antigens
 Plasmin activators like streptokinase and t-PA they do not possess.
are injected to quickly dissolve dangerous clots  Type A blood plasma:
(e.g., in heart attacks) to restore blood flow and  Contains anti-B antibodies.
reduce tissue damage.  Type B blood plasma:
 Contains anti-A antibodies.
 Type AB blood plasma:
TOPIC 7. Blood Grouping  Contains neither anti-A nor anti-B antibodies.
 Understanding blood groups is crucial for safe  Type O blood plasma:
blood transfusions (transfer of blood from one  Contains both anti-A and anti-B antibodies.
individual to another). Early transfusion o Antibody Development:
attempts were often unsuccessful due to  Unlike other antibodies, anti-A and anti-B
transfusion reactions, involving clumping antibodies are typically present in blood even
(agglutination) or rupture (hemolysis) of RBCs without prior exposure to foreign RBC antigens.
and clotting in vessels. These reactions are This is thought to be due to exposure to similar
caused by interactions between antigens on A or B antigens on bacteria or food in the
RBC surfaces and antibodies in the plasma. digestive tract. These antibodies usually appear
1. Antigens and Antibodies: around 2 months after birth.
o Antigens: o Transfusion Reactions:
 Molecules on the surface of red blood cells.  If a recipient receives blood with antigens that
o Antibodies: their plasma antibodies react against, a
 Proteins in the plasma that bind specifically to transfusion reaction occurs.
certain antigens. o "Universal Donor" (Type O):
o Agglutination:  Historically, Type O individuals were considered
 When antibodies bind to red blood cell "universal donors" because their RBCs lack both
antigens, they form molecular bridges, causing A and B antigens, so they won't react with a
the red blood cells to clump together. recipient's anti-A or anti-B antibodies. However,
o Hemolysis: this term is misleading. Donor blood still
 The antigen-antibody interaction can also contains antibodies (anti-A and anti-B for Type
trigger reactions that rupture RBCs, releasing O) which, though diluted in the recipient's
hemoglobin. The debris and free hemoglobin blood, can cause reactions. More importantly,
 other blood groups must also be matched to  Consequences of HDN:
prevent reactions.  Can be fatal to the fetus. Monitoring antibody
o "Universal Recipient" (Type AB): levels and potentially performing transfusions
 Historically, Type AB individuals were called (via umbilical cord) or early delivery may be
"universal recipients" because their plasma necessary.
lacks both anti-A and anti-B antibodies,  Prevention:
meaning they won't react to A or B antigens in  HDN can often be prevented by injecting the
donated blood (within the ABO system) [67, Rh-negative mother with Rho(D) immune
Apply It 3]. This term is also misleading for globulin (RhoGAM). This preparation contains
similar reasons as the universal donor antibodies against Rh antigens that bind to any
designation; other blood groups must be fetal Rh-positive RBCs that enter the mother's
matched [67, Apply It 3]. blood, inactivating them and preventing the
3. Rh Blood Group System: mother's sensitization.
 Named after its discovery in rhesus monkeys.
o Rh-positive:
 Individuals have certain Rh antigens on their TOPIC 8. Diagnostic Blood Tests
RBC surfaces (about 85% of white individuals,  As nurses, you will frequently encounter and
95% of black individuals). interpret results from various blood tests.
o Rh-negative: Here's an overview:
 Individuals do not have these Rh antigens. 1. Type and Crossmatch:
o Antibody Development: o Blood Typing:
 Unlike ABO antibodies, antibodies against Rh  Determines the ABO and Rh blood groups of a
antigens do not develop unless an Rh-negative blood sample by testing for antigens on the RBC
person is exposed to Rhpositive red blood cells. surface using known antibodies. Agglutination
This can happen via transfusion or during indicates the presence of the specific antigen.
pregnancy. The plasma is also tested for antibodies.
o Rh Incompatibility and Hemolytic Disease of the o Crossmatch:
Newborn (HDN):  Before a transfusion, this procedure mixes the
 This is a critical concern in pregnancies. donor's RBCs with the recipient's serum and the
 Scenario: donor's serum with the recipient's RBCs. A
 Occurs when an Rh-negative mother is pregnant transfusion is considered safe only if no
with an agglutination occurs in either match, ensuring
 Rh-positive fetus. compatibility beyond just ABO/Rh.
 First Pregnancy: 2. Complete Blood Count (CBC):
 Fetal blood (Rh-positive) can leak into the  A comprehensive analysis providing much
mother's circulation, usually late in pregnancy useful information about blood composition. It
or during delivery. The mother becomes includes:
sensitized and produces anti-Rh antibodies. o Red Blood Cell Count (RBC):
Typically, there isn't enough time or sufficient  Measures the number of RBCs per microliter
antibody production during the first pregnancy (μL) of blood. Normal ranges: Males 4.6–6.2
to harm the fetus. million/μL; Females 4.2–5.4 million/μL.
 Later Pregnancies:  Erythrocytosis:
 If subsequent fetuses are Rh-positive, the  An overabundance of RBCs, which can increase
mother's immune system, now sensitized, blood viscosity, reduce flow rates, and
rapidly produces large amounts of antiRh potentially plug capillaries.
antibodies. These antibodies can cross the  This can be due to dehydration, certain
placenta and destroy the fetal Rh-positive RBCs, diseases, or decreased O2 supply (e.g., high
leading to HDN (also called erythroblastosis altitudes, chronic lung disease) stimulating EPO.
fetalis).
  Blood doping is an artificial way to induce  Normal ranges: Males 40–52%; Females 38–
erythrocytosis to enhance athletic performance 48%. A decreased hematocrit can indicate
by increasing O2 transport, but it's dangerous anemia.
due to the risks of increased blood viscosity.  It's affected by both the number and size of
o Hemoglobin Measurement: RBCs.
 Measures the amount of hemoglobin in grams o White Blood Count (WBC):
per 100 mL of blood. Normal ranges: Males 14–  Measures the total number of WBCs per
18 g/100mL; Females 12–16 g/100mL. microliter of blood. Normal range: 5000–
 Anemia: 9000/μL.
 An abnormally low hemoglobin measurement  Leukopenia:
indicates anemia, which is a deficiency of  Lower than normal WBC count, due to
normal hemoglobin, resulting from a reduced decreased production or destruction (e.g.,
number of RBCs, reduced hemoglobin in each radiation, drugs, viral infections, vitamin
RBC, or abnormal hemoglobin production. deficiencies).
 Leukocytosis:
 Symptoms:  Abnormally high WBC count, often due to
 Lack of energy, excessive tiredness, pallor, bacterial infections stimulating neutrophil
shortness of breath on exertion. increase.
Causes:  Leukemia:
Insufficient RBC Production:  Cancer of the red bone marrow, characterized
 Aplastic Anemia: by abnormal production of non-functional
 Bone marrow inability to produce blood cells, WBCs, leading to increased susceptibility to
chemical/radiation damage. often due to infections and interference with RBC/platelet
 Iron-deficiency Anemia: formation (causing anemia and bleeding).
 Insufficient iron intake/absorption or excessive 3. Differential White Blood Count:
iron loss, leading to less hemoglobin and  Determines the percentage of each of the five
smaller RBCs. types of WBCs. This provides valuable insight
 Folate/Vitamin B12 Deficiency Anemia (Pernicious into a patient's condition. For example:
Anemia): o Increased neutrophil count:
 Inadequate folate or vitamin B12 (important for  often indicates bacterial infection.
DNA synthesis), leading to decreased RBC o Elevated eosinophil and basophil counts:
production.  often associated with allergic reactions.
Loss or Destruction of RBCs: 4. Clotting Tests:
 Hemorrhagic Anemia:  Measure the blood's ability to clot.
 Blood loss due to trauma, ulcers, or heavy o Platelet Count:
menstruation.  Normal range: 250,000–400,000 platelets/μL.
 Hemolytic Anemia:  Thrombocytopenia:
 Excessive rupture or destruction of RBCs, due  Greatly reduced platelet count, leading to
to inherited defects, drugs, snake venom, or chronic bleeding through small vessels. Causes
HDN. include hereditary disorders, vitamin B12
Defective Hemoglobin Production: deficiency, drug therapy, or radiation.
 Thalassemia: o Prothrombin Time (PT):
 Hereditary, reduced hemoglobin production.  Measures how long it takes for blood to start
 Sickle-cell Anemia: clotting (normally 9–12 seconds). It assesses
 Hereditary, abnormal hemoglobin causes RBCs the function of multiple clotting factors.
to sickle, plug vessels, and be fragile.  It's affected by Vitamin K deficiency, liver
o Hematocrit Measurement: diseases, and certain drugs. The International
 The percentage of total blood volume Normalized Ratio (INR) standardizes PT results
composed of RBCs. across labs.
5. Blood Chemistry:
 Tests measure the composition of dissolved or
suspended materials in plasma to assess the
functioning of various body systems. Examples:
o High blood glucose:
 May indicate insufficient insulin production
(pancreatic dysfunction).
o High blood urea nitrogen (BUN):
 Sign of reduced kidney function.
o Increased bilirubin:
 Can indicate liver dysfunction.
o High cholesterol:
 Increased risk of cardiovascular disease.