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Lecture 1
Albumin
Attracts water which prevents edema
Gamma Globulin
Used to treat viral hepatitis. Abs secreted from lymphocytes.
Cellular Respiration
ATP Production from mitochondria
RBC Life Span
120 days
Eryhtropoietin
Stimulates bone marrow to secrete red blood cells. Stimulated by kidney (90%) & Liver (10%). After 120 days, it results in dead RBCs that would be reaccumulated by the spleen & liver.
B lymphocytes
Release Abs which detect Ags, creating the antibody-antigen complex.
Antigen-Antibody Complex
Signal other WBCs to arrive to targeted cell for degredation.
Antigen Effect on T Cells
Their Cell membranes change as endocytosis to consume antigens.
During embryonic life at four weeks
The embryo is connected to yolk
Yolk Wall’s two functions
Produces Stem Cells of blood & Germ Cells
Germ Cells
XX for female; XY for male
Yolk Sac Nutrition
Caused by no complete connection of placenta/embryo in first few weeks of pregnancy. Yolk sac only form of nutrition for embryo.
Embryo
First 8 Weeks of Development
Fetus
Week 9 to Birth
Once fetus develops liver
The liver controls RBC production
After fetus is birthed
Bone marrow controls RBC production
Mother Cells
Become blood stem cells (Myeloid & Lymphoid)
Myeloid produce
Eryhrocytes, Platelets, Nonlymphatic Leukocytes (Eosinophils, Basophils, Neutrophils, Monocytes)
Lymphoids produce
B & T Lymphocytes
Myeloid Pathway for Erythrocytes:
Myeloid Stem Cell → Proerythroblast → Early Erythroblast → Late Erythroblast → Normoblast → Reticulocyte
Required for Reticulocyte to Erythrocyte Conversion
Vitamin B12, Folic Acid, Iron
Anemia
Deficiency of Vitamin B12, Iron, Folic Acid
Anemia’s secondary cause:
Cancer patient receiving chemotherapy. Damages bone marrow → less RBCs produced.
Polycythemia (Polyvera)
Excess Erythrocytes
Primary Polyvera/Polycythemia
Irritation of bone marrow → Excess RBC production
(WBC/Platelets also increase)
Secondary Polyvera/Polycythemia:
Overproduction of Erythropoietin
Effect of RBC Overproduction
Blood is Concentrated → Hypertension, Headaches, Nose bleeding, Vertigo
Effect of Immature WBCs Overproduction
Weak Immune System
Overproduction of Platelets
Blood Clots → Myocardial Infarctions, Atherosclerosis, Stroke
Sickle Cell Anemia
Abnormal Hemoglobin; RBCs can’t carry oxygen
Effects of Sickle Cell Anemia
Increased infection, Femur/Bone Pain, Bilirubin increase → Jaundice, Fever
Sickle Cell Anemia Treatment
Folic Acid Supplements, antibiotics for bacterial infections, Vaccines for Viral
Normocytic Anemia
Abrupt blood loss (Stab, Car Accident, Heavy Hemorrhage)
Macrocytic Anemia
Vitamin B12 or Folate Deficiency
Microcytic Anemia
Iron Deficiency
Leukemia (Blood Cancer)
Overproduction of Immature / Mature WBCs
Lymphocytic Leukemia
Large Number of Mature WBCs
Myelocytic Leukemia
Large Number of Mature/Immature WBCs (ML)
Leukemia Treatment Steps
Chemotherapy
Interferon Alpha
Radiation Therapy
Stem Cell Transplant
Effect of INFa Therapy
Controls Immature WBC Production
Effect of Radiation Therapy
kills Tumor Cells
Effect of Stem Cell Transplant
Take Mother’s Cells from Healthy Bone Marrow & Transplant it
Aorta BP
Highest Blood Pressure
100 MmHg
Vena Cava BP
4 mmHg
Structures in Vein from low BP
Valves (Surrounded by Skeletal Muscle)
Capillaries
Effect of Valves
Skeletal Muscle Contraction → Blood flow increases in vein system
Effect of Capillaries
Main place of Gas Exchange, Fluid/Nutrients Absorption, Waste Excretion
Lecture 2
Endocardium
Papillary Muscles Tricuspid and Bicuspid
Deoxygenated Blood Flow
Vena Cava → Right Atrium → Tricuspid → Right Ventricle → Pulmonary Semilunar → Pulmonary A. → Lungs (Gas Exchange)
Oxygenated Blood Flow
4 Pulmonary v.s → Left Atrium → Bicuspid (Mitral) Valve → Left Ventricle → Aortic Semilunar → Aorta
Walls of Arteries and Veins
Smooth Muscle - Autonomic Nervous system
Capillary Walls
Pores, no smooth muscle, for gas exchange, absorption, secretion
Aorta BP
100 mmHg
Arteries BP
50 mmHg
Arterioles & Capillaries BP
20 mmHg
Blood Pressure Calculation
BP = CO x TPR
Pressure in aorta
higher than venous pressure
Reason for Arterioles & Capillaries BP
Smaller Diameter, More interstitial space
Total Peripheral Resistance
Increases pressure in arteries, aorta
Reason for thick aorta & artery walls
More elastic fibers
Arterial System Pressure
Stressed Volume
Velocity (cm/sec)
Speed of blood flow
Velocity-Determining factors
Interstitial Area, Diameter
Blood Flow Determining Factors
TPR, Cardiac Output
Blood Velocity Highest
Aorta, Arteries
Blood Resistance Highest
Capillary, Arterioles (Smaller Diameter, More Interstitial Area)
Resistance Dependent Factors
Vessel Radius, Vessel Length, Blood Viscosity/Concentration
Capacitance/Compliance Highest
Vein (Thinner Wall, Carries More Blood)
Systolic Pressure
The Pressure in Ventricles During Contractions
Diastolic Pressure
The Pressure in Ventricles During Relaxation
Pulse Pressure
Difference between Systolic & Diastolic Pressure
Hierarchy of Pressure
Arteries > Veins > Atrium
Reason for Hierarchy of Pressure
Atrium shows no resistance to venous system & receives large amounts of venous blood from 2 Vena Cava & 4 Pulmonary v.
Blood Pressure Definition
Pressure from blood vessel walls
Hypertension
Factors leading to vasoconstriction, vaso-obstruction, vaso-destruction
Clinical Case: 35 year old female has severe headache, hypertension, sometimes nose bleeding, vertigo. Had a cardiac infarction but the doctor checked the blood pressure and told her that she may have a stroke because the blood test shows high levels of platelets, RBCs, neutrophils, and ultrasound shows enlargement of spleen.
Polycythemia (?)
Clinical Case 2: Pregnant female has delivery of the baby but has heavy bleeding during delivery that dropped blood volume and pressure resulting in a coma.
preeclampsia (?)
Lecture 3!
Blood Pressure
The pressure which comes to the wall of blood vessels by blood flow via ventricular contraction/relaxation
Total Peripheral Resistance (TPR) Site
Arterioles
Reason for Total Peripheral Resistance (TPR)
Arterioles have small diameters & more interstitial area, leading to more blood flow resistance
Primary Hypertension
Environmental Factors (diet, lifestyle, stress) leading to hypertension
Cortisol’s Role on Primary Hypertension
Cortisol increases during stress → Increase in TPR → Increase in Systolic/Diastolic BP
Cause of Primary Hypertension
Unknown; There are only known external factors
Sodium’s Effect on Primary Hypertension
NaCl important for depolarization.
Residual Sodium Enters → Depolarization → Calcium Channels Open → Calcium Enters → Muscle Contraction (Vasoconstriction)
Obesity’s Impact on Primary Hypertension
Obesity associated with endocrine hormone disorder, Type 2 Diabetes
Sympathetic Overstimulation (Primary Hypertension)
Alpha 1 involved in BP. Overstimulation of A-1 → Vasoconstriction
Aldosterone Hormone
Increases BP & Sodium Blood Concentration
Hypernaturinia
High Blood Sodium
RAAS System (Primary Hypertension)
Secretes aldosterone that causes vasoconstriction via hypernatremia.
Prostaglandin & Bradykinin Vessel Effect
Vasodilators / Vasorelaxers
Prostaglandin & Bradykinin Deficiency (Primary Hypertension)
No relaxation → Hypertension
Cause of 90% of Secondary Hypertension
Hormones (Hormonal Disorder, Endocrine Disorder)
Hormones that cause Secondary Hypertension
Aldosterone, Cortisol, Norepinephrine, Epinephrine, PTH, T3/T4, Calcitonin Deficiency, Prostaglandins
Adrenal Cortex Hormone Secretion
Aldosterone, Cortisol, Androgen
Adrenal Medulla Hormone Secretion (Secondary Hypertension)
Adrenaline, Noradrenaline
Hormones involved in blood pressure
↑ Aldosterone, ↑ Cortisol
RAAS System
Low BP / Hyponatremia → Enzyme Conversion (Angiotensinogen → Angiotensin 1) → ACE Conversion (Angiotensin 1 → Angiotensin 2) → Angiotensin 2 causes Aldosterone secretion → Blood carries Aldosterone to kidney → Aldosterone Binds on Tubule Receptor → Sodium Reabsorption
Angiotensin 2 Effects
Vasoconstriction, Increase of Aldosterone of Cortex
Aldosterone Allows ___ Reabsorption and ___ Excretion
Sodium, H₂O, and Bicarbonate from urine → Blood
H+ , K+ → urea