LECTURE NOTES EXAM 3 PHYSIO

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276 Terms

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Lecture 1
Albumin

Attracts water which prevents edema

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Gamma Globulin

Used to treat viral hepatitis. Abs secreted from lymphocytes.

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Cellular Respiration

ATP Production from mitochondria 

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RBC Life Span

120 days

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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. 

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B lymphocytes

Release Abs which detect Ags, creating the antibody-antigen complex. 

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Antigen-Antibody Complex

Signal other WBCs to arrive to targeted cell for degredation.

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Antigen Effect on T Cells

Their Cell membranes change as endocytosis to consume antigens.

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During embryonic life at four weeks

The embryo is connected to yolk

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Yolk Wall’s two functions

Produces Stem Cells of blood & Germ Cells

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Germ Cells

XX for female; XY for male

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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.

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Embryo

First 8 Weeks of Development

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Fetus

Week 9 to Birth

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Once fetus develops liver

The liver controls RBC production

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After fetus is birthed

Bone marrow controls RBC production 

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Mother Cells

Become blood stem cells (Myeloid & Lymphoid)

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Myeloid produce

Eryhrocytes, Platelets, Nonlymphatic Leukocytes (Eosinophils, Basophils, Neutrophils, Monocytes)

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Lymphoids produce

B & T Lymphocytes

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Myeloid Pathway for Erythrocytes:

Myeloid Stem Cell → Proerythroblast → Early Erythroblast → Late Erythroblast → Normoblast → Reticulocyte

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Required for Reticulocyte to Erythrocyte Conversion

Vitamin B12, Folic Acid, Iron

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Anemia

Deficiency of Vitamin B12, Iron, Folic Acid

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Anemia’s secondary cause:

Cancer patient receiving chemotherapy. Damages bone marrow → less RBCs produced.

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Polycythemia (Polyvera)

Excess Erythrocytes

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Primary Polyvera/Polycythemia

Irritation of bone marrow → Excess RBC production
(WBC/Platelets also increase)

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Secondary Polyvera/Polycythemia:

Overproduction of Erythropoietin

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Effect of RBC Overproduction

Blood is Concentrated → Hypertension, Headaches, Nose bleeding, Vertigo

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Effect of Immature WBCs Overproduction

Weak Immune System

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Overproduction of Platelets

Blood Clots → Myocardial Infarctions, Atherosclerosis, Stroke

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Sickle Cell Anemia

Abnormal Hemoglobin; RBCs can’t carry oxygen

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Effects of Sickle Cell Anemia

Increased infection, Femur/Bone Pain, Bilirubin increase → Jaundice, Fever

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Sickle Cell Anemia Treatment

Folic Acid Supplements, antibiotics for bacterial infections, Vaccines for Viral

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Normocytic Anemia

Abrupt blood loss (Stab, Car Accident, Heavy Hemorrhage)

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Macrocytic Anemia

Vitamin B12 or Folate Deficiency

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Microcytic Anemia

Iron Deficiency

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Leukemia (Blood Cancer)

Overproduction of Immature / Mature WBCs

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Lymphocytic Leukemia

Large Number of Mature WBCs

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Myelocytic Leukemia 

Large Number of Mature/Immature WBCs (ML)

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Leukemia Treatment Steps

  1. Chemotherapy 

  2. Interferon Alpha

  3. Radiation Therapy

  4. Stem Cell Transplant

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Effect of INFa Therapy

Controls Immature WBC Production

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Effect of Radiation Therapy

kills Tumor Cells

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Effect of Stem Cell Transplant

Take Mother’s Cells from Healthy Bone Marrow & Transplant it

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Aorta BP

Highest Blood Pressure
100 MmHg

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Vena Cava BP

4 mmHg

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Structures in Vein from low BP

Valves (Surrounded by Skeletal Muscle)
Capillaries 

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Effect of Valves

Skeletal Muscle Contraction → Blood flow increases in vein system

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Effect of Capillaries

Main place of Gas Exchange, Fluid/Nutrients Absorption, Waste Excretion

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Lecture 2
Endocardium

Papillary Muscles Tricuspid and Bicuspid 

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Deoxygenated Blood Flow

Vena Cava → Right Atrium → Tricuspid → Right Ventricle → Pulmonary Semilunar → Pulmonary A. → Lungs (Gas Exchange)

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Oxygenated Blood Flow

4 Pulmonary v.s → Left Atrium → Bicuspid (Mitral) Valve → Left Ventricle → Aortic Semilunar → Aorta

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Walls of Arteries and Veins

Smooth Muscle - Autonomic Nervous system

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Capillary Walls

Pores, no smooth muscle, for gas exchange, absorption, secretion

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Aorta BP

100 mmHg

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Arteries BP

50 mmHg

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Arterioles & Capillaries BP

20 mmHg

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Blood Pressure Calculation

BP = CO x TPR

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Pressure in aorta

higher than venous pressure

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Reason for Arterioles & Capillaries BP

Smaller Diameter, More interstitial space

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Total Peripheral Resistance

Increases pressure in arteries, aorta

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Reason for thick aorta & artery walls 

More elastic fibers 

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Arterial System Pressure

Stressed Volume

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Velocity (cm/sec)

Speed of blood flow

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Velocity-Determining factors

Interstitial Area, Diameter

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Blood Flow Determining Factors

TPR, Cardiac Output

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Blood Velocity Highest

Aorta, Arteries

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Blood Resistance Highest

Capillary, Arterioles (Smaller Diameter, More Interstitial Area)

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Resistance Dependent Factors

Vessel Radius, Vessel Length, Blood Viscosity/Concentration

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Capacitance/Compliance Highest

Vein (Thinner Wall, Carries More Blood)

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Systolic Pressure 

The Pressure in Ventricles During Contractions 

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Diastolic Pressure

The Pressure in Ventricles During Relaxation

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Pulse Pressure 

Difference between Systolic & Diastolic Pressure 

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Hierarchy of Pressure

Arteries > Veins > Atrium

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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.

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Blood Pressure Definition

Pressure from blood vessel walls

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Hypertension

Factors leading to vasoconstriction, vaso-obstruction, vaso-destruction 

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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 (?)

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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 (?)

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Lecture 3!
Blood Pressure 

The pressure which comes to the wall of blood vessels by blood flow via ventricular contraction/relaxation

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Total Peripheral Resistance (TPR) Site

Arterioles

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Reason for Total Peripheral Resistance (TPR)

Arterioles have small diameters & more interstitial area, leading to more blood flow resistance

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Primary Hypertension

Environmental Factors (diet, lifestyle, stress) leading to hypertension

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Cortisol’s Role on Primary Hypertension

Cortisol increases during stress → Increase in TPR → Increase in Systolic/Diastolic BP

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Cause of Primary Hypertension

Unknown; There are only known external factors

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Sodium’s Effect on Primary Hypertension

NaCl important for depolarization.
Residual Sodium Enters → Depolarization → Calcium Channels Open → Calcium Enters → Muscle Contraction (Vasoconstriction)

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Obesity’s Impact on Primary Hypertension

Obesity associated with endocrine hormone disorder, Type 2 Diabetes

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Sympathetic Overstimulation (Primary Hypertension)

Alpha 1 involved in BP. Overstimulation of A-1 → Vasoconstriction

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Aldosterone Hormone

Increases BP & Sodium Blood Concentration

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Hypernaturinia

High Blood Sodium

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RAAS System (Primary Hypertension)

Secretes aldosterone that causes vasoconstriction via hypernatremia. 

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Prostaglandin & Bradykinin Vessel Effect

Vasodilators / Vasorelaxers

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Prostaglandin & Bradykinin Deficiency (Primary Hypertension)

No relaxation → Hypertension

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Cause of 90% of Secondary Hypertension

Hormones (Hormonal Disorder, Endocrine Disorder)

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Hormones that cause Secondary Hypertension

Aldosterone, Cortisol, Norepinephrine, Epinephrine, PTH, T3/T4, Calcitonin Deficiency, Prostaglandins 

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Adrenal Cortex Hormone Secretion 

Aldosterone, Cortisol, Androgen 

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Adrenal Medulla Hormone Secretion (Secondary Hypertension)

Adrenaline, Noradrenaline

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Hormones involved in blood pressure

Aldosterone, Cortisol

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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 

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Angiotensin 2 Effects

Vasoconstriction, Increase of Aldosterone of Cortex

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Aldosterone Allows ___ Reabsorption and ___ Excretion

Sodium, H₂O, and Bicarbonate from urine → Blood
H+ , K+ → urea 

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