Blood Physiology: Blood Types, Immune Reactions, and Disorders

Blood Physiology

Cauterization of a Nosebleed with Silver Nitrate

Cauterization is a chemical method used to stop persistent anterior nosebleeds (epistaxis) when other measures such as pressure, ice, or nasal packing fail. Silver nitrate is applied to visible bleeding vessels on the anterior nasal septum, causing a chemical burn that leads to coagulative necrosis of mucosal tissue.

• Chemical Reaction: Silver nitrate reacts with tissue proteins to form an Ag-protein complex and nitric acid.

• Equation: $\mathrm{AgNO_3 + \text{Tissue Proteins} \rightarrow Ag\text{-protein complex} + HNO_3}$

• Silver ions (Ag+) precipitate tissue proteins, forming a barrier and are reduced to metallic silver (Ag0).

• Nitric acid (HNO3) contributes to local tissue destruction, aiding coagulation.

Blood Types and Transfusion Compatibility

ABO and Rh Blood Group Systems

Blood types are determined by the presence or absence of specific antigens on the surface of red blood cells (RBCs). The two main systems are the ABO system and the Rh factor.

• ABO System: Types A, B, AB, and O refer to different surface antigens.

• Rh System: Presence (Rh+) or absence (Rh−) of the D antigen.

• Example: A+ blood has A antigens and the Rh antigen; B− has B antigens but no Rh antigen.

Antigens and Antibodies

Antigens are found on the surface of RBCs and act as cell ID tags, determining blood type. Antibodies are found in blood plasma and target foreign antigens.

• Innate ABO Antibodies: Individuals are born with antibodies against A or B antigens they do not possess.

• Type A: Has A antigens, anti-B antibodies.

• Type B: Has B antigens, anti-A antibodies.

• Type O: No antigens, both anti-A and anti-B antibodies.

• Type AB: Both antigens, no ABO antibodies.

Transfusion Reactions

If mismatched blood is transfused, an immediate immune response (hemolytic reaction) occurs, destroying the donor RBCs. Symptoms can include fever, chills, back pain, hemoglobinuria, shortness of breath, hypotension, chest pain, nausea, vomiting, and jaundice.

Symptom	Cause
Fever and chills	Immune response to foreign blood cells
Back or flank pain	Kidney stress due to filtering damaged red cells
Dark/red urine	Free hemoglobin from destroyed RBCs excreted by kidneys
Shortness of breath	Reduced oxygen-carrying capacity
Low blood pressure	Immune activation and systemic inflammation
Chest pain	Reduced oxygenation and stress on the heart
Nausea and vomiting	Systemic inflammatory response
Jaundice (delayed)	Breakdown of RBCs releasing bilirubin

Complications of Untreated Hemolytic Reactions

• Acute kidney injury from hemoglobin buildup

• Shock from widespread immune response

• Disseminated intravascular coagulation (DIC): widespread clotting followed by bleeding

• Death in severe, untreated cases

Diagnosis and Prevention

• Immediate cessation of transfusion

• Blood tests (e.g., direct antiglobulin) to confirm immune hemolysis

• Urine test for free hemoglobin

• Prevention: Careful blood type matching is essential.

Rh System: Acquired Antibodies and Rh Incompatibility

Unlike the ABO system, individuals are not born with anti-Rh antibodies. Rh-negative individuals can develop anti-Rh antibodies after exposure to Rh-positive blood (e.g., pregnancy, transfusion). Once sensitized, the immune system can attack Rh-positive blood in the future.

• Rh reactions may develop over time after sensitization, especially dangerous in pregnancy or repeat transfusions.

Rh Incompatibility in Pregnancy

Rh incompatibility occurs when an Rh-negative mother carries an Rh-positive fetus. The mother's immune system may produce antibodies against fetal RBCs, which can cross the placenta and attack the baby's RBCs, leading to hemolytic disease of the newborn (HDN) or erythroblastosis fetalis.

• Usually not a problem in the first pregnancy, but risk increases with subsequent Rh-positive pregnancies if sensitization has occurred.

• Mild cases: Anemia, jaundice

• Severe cases: Heart failure, brain damage, stillbirth

Prevention with RhoGAM

• RhoGAM is an injection given to Rh-negative mothers around 28 weeks of pregnancy and within 72 hours after delivery if the baby is Rh-positive, or after any bleeding, miscarriage, or invasive procedures.

• It prevents the mother's immune system from producing anti-Rh antibodies.

• Blood type tests early in pregnancy identify risk; if both parents are Rh-negative, there is no risk.

Management if Sensitization Occurs

Step	Goal
Monitor antibody levels	Assess risk to fetus
Ultrasound & Doppler	Detect fetal anemia
Intrauterine transfusion	Treat anemia in womb
Early delivery	Prevent worsening damage
NICU care	Support after birth

White Blood Cells (WBCs) and Immune Function

Types of White Blood Cells

White blood cells are part of the immune system, produced in bone marrow and found in blood and lymphatic tissue. They are classified as granulocytes or agranulocytes based on the presence of cytoplasmic granules.

Group	Cell Types	Key Feature
Granulocytes	Neutrophils, Eosinophils, Basophils	Visible granules in cytoplasm
Agranulocytes	Lymphocytes, Monocytes	Lack visible granules

Cell Type	Function	Nucleus	Granules?	Size (µm)
Neutrophils	Phagocytose bacteria	Multi-lobed	Yes (fine)	12–15
Eosinophils	Fight parasites, allergies	Bi-lobed	Yes (red)	12–17
Basophils	Release histamine	Obscured	Yes (dark)	12–15
Lymphocytes	Antibody & T-cell immunity	Large, round	No	7–10 (small), 10–15 (large)
Monocytes	Phagocytosis, become macrophages	Kidney-shaped	No	15–20

Disorders of the Blood and Immune System

Mononucleosis

• Viral infection, most commonly caused by Epstein-Barr virus (EBV)

• Spread mainly through saliva

• Common in teens and young adults

• CBC may show elevated lymphocytes and atypical lymphocytes

Sickle Cell Disease

• Hereditary blood disorder caused by a mutation in the HBB gene affecting hemoglobin (HbS)

• RBCs become sickle-shaped, rigid, and sticky, leading to anemia and vessel blockage

• Inheritance: Two copies of the gene cause disease; one copy = carrier (trait)

Eosinophilia

• Elevated eosinophil count (>500 cells/µL)

• Causes include parasitic/fungal infections, allergies, drug reactions, hematologic malignancies, autoimmune diseases, and adrenal insufficiency

• Eosinophilia is a sign, not a disease; identifying the cause is critical

Anemia

Anemia is a condition where the blood lacks enough healthy RBCs or hemoglobin, leading to reduced oxygen delivery to tissues. It is a sign of underlying disease, not a disease itself.

• Normal hemoglobin levels: Men 13.5–17.5 g/dL, Women 12.0–15.5 g/dL

Type	Cause	RBC Appearance
Iron-deficiency	Poor diet, blood loss	Small (microcytic), pale
Vitamin B12/Folate	Malabsorption, poor intake	Large (macrocytic)
Hemolytic	RBC destruction (e.g., autoimmune, sickle cell)	Normal or varied
Aplastic	Bone marrow failure	Low count of all cells

Blood Clotting and Cardiovascular Risk

Blood Clots (Thrombi)

A blood clot is a clump of blood that has changed from liquid to a gel-like state, part of the body's natural response to stop bleeding (hemostasis). Beneficial clotting involves vascular spasm, platelet plug formation, and coagulation.

• Platelets, clotting factors, and fibrin are essential for clot formation.

LDL Cholesterol and Clot Risk

LDL (low-density lipoprotein) is known as "bad cholesterol" because high levels can lead to plaque formation in arteries (atherosclerosis). Plaques can rupture, triggering clot formation inside arteries, which may result in myocardial infarction (heart attack) or stroke.

Feature	Fibrous Plaque	Complicated Plaque
Structure	Stable core of lipids, thick fibrous cap	Ruptured/eroded cap, exposed core
Stability	More stable, less likely to rupture	Unstable, high risk of rupture
LDL Role	Accumulated but contained	Core filled with oxidized LDL, inflammatory cells
Inflammation	Low to moderate	High
Thrombosis Risk	Low	High
Clinical Impact	Gradual narrowing of arteries	Sudden blockage → heart attack or stroke

Harmful Clotting (Thrombosis)

• Clots can form inside blood vessels, leading to heart attack (coronary thrombosis), stroke (cerebral thrombosis), or deep vein thrombosis (DVT) which can cause pulmonary embolism.

Summary Table: White Blood Cell Types and Functions

Cell Type	Size (µm)	% of WBCs	Function	Nucleus	Granules
Neutrophils	12–15	60–70%	Phagocytose bacteria	Multi-lobed	Pale, fine
Eosinophils	12–17	1–4%	Combat parasites, allergies	Bi-lobed	Red
Basophils	12–15	<1%	Release histamine	Obscured	Dark
Lymphocytes	7–10 (small), 10–15 (large)	20–25%	Produce antibodies, kill infected cells	Large, round	None
Monocytes	15–20	3–8%	Phagocytosis, become macrophages	Kidney-shaped	None