PNB 2275 1st EditionExam # 1 Study Guide Lectures: 1 – 71/20- It is a connective tissue consisting of plasma (46-63%), cells such as RBC(most abundant cells & WBC and platelets (37-54%)*major difference between plasma & interstitial fluid (liquid between cells) is the presence of plasma proteins*testosterone stimulates RBC production- Blood is mostly water that maintains a pH level roughly 7.4- RBC have no nucleus, Bi-concave shape, 120 days of life, can fold and flex- Platelets are regulated by thrombopoietin (essential for clotting) Plasma Proteins: mostly water, all mostly made in the liverAlbumin (60%-majority): osmotic pressure(prevents edema), transport lipids, hormones and steroidsGlobulins: antibodies- made by WBCFibrinogen: ESSENTIAL for clottingRegulatory Proteins: enzymes, proenzymes, and hormones,- Functions- Transportation (gases, nutrients, & waste)- Regulation(pH, osmolarity, temperature[38°]-done through the venous system)- Protection(key component of the immune system)- Hemoglobin- can bind 4 molecules of oxygen (3 types)- Oxyhemoglobin= contains bound O2, oxygenated Hb- Deoxyhemoglobin= deoxygenated Hb - Carbaminohemoglobin= carries carbon dioxide*Bohr effect: Hb binds CO2 and H+ facilitating the release of O2 at the tissue*Haldane Effect: Hb’s ability to carry CO2- Anemia- low hematocrit or non-working Hb *checked by Hematocrit (centrifuge separates everything by weight)- Insufficient number of RBC’s :Hemorrhage- caused by blood lossPernicious- deficiency of B12- Macrocytic anemia, canbe caused by gastric bypass surgeryAplastic- a disorder of the red bone marrow- Low Hb- iron deficientAbnormal HbThalassemias-underproduction of Hb, fewer RBC thannormalSickle-cell anemia- mutation (in Hb-beta chain) in the shape of the RBC 1/22Clicker Questions & Review:*Newborn infant homozygous for HbS WILL NOT exhibit symptoms of sickle-cell anemia-they will not exhibit symptoms until they begin to develop adult Hb-treatment for sickle cell anemia involves stimulating HbF production -fetal Hb has a higher affinity for O2 than adult Hb-Liver is important in removing bilirubin from the blood- Carbon dioxide is transported by both plasma and erythrocytes (RBC’s) - RBC Formation-live to about 120 days- Erythropoeisis : needs Iron, B12, Folic AcidEPO- leads to productions and maturing of RBC; decrease in blood oxygen in Kidney leads to its release that goes to red bone marrow and causes production.*RBC are formed in Red bone marrow in adults- Blood doping- increases number of RBC’s in blood, athletes doing this can pass tests by - RBC Catabolism- Macrophages from liver & spleen perform phagocytosis on RBCs and Hb- Recycles Fe+2 and amino acids via transferrin- Heme is converted to biliverdin which then becomes bilirubin and released into blood where it then binds albumin and is excreted by the liver in bile*jaundice- excessive bilirubin in blood which causes skin and sclera (eyes) to turn yellow- Blood Group- to differentiate each blood group has an antigen with an affinity for the type of the blood and an antibody against the opposing blood type- For example: Blood type A has antigens for A and antibodies for B.- AB blood type has AB antigens and neither A or B antibodies- O blood type has neither antigen but antibodies for A&B- Rh- can only receive blood from Rh- (*Rh antibodies can only be present after exposure to Rh antigen, one parent has to have it, mother can pass it to the second kid after birth of the first child with Rh+ blood*)- WBC-nonspecific immune systemProperties:1. WBC leave blood by margination (bind to capillary wall) and pass through endothelial cells by emigration2. move by amoeboid movement3. positive chemotaxis- capable of recognizing chemical signals4. capabale of phagocytosis (neutrophils-first responders to kill bacteria & form pus at wound, monocytes or “macrophages”-aggressive phagocytic cells , and eosinophils-attacklarger pathogens)Inflammation ResponseSteps:1. release histamines and increase blood flow to injured area2. histamines release phagocytes and clotting factors into the wound3. Phagocytes engulf bacteria, dead cells, and debris4. Platelets move out of capillary to seal the injuryM-CSF: increases production monoblast (myeloblast level)G-CSF: formation of granulocytes (myeloblast level) GM-CSF: progenitor cell level, monoblast or myeloblast MULTI-CSF: myeloid stem level-Hemostasis (stop bleeding1. Vascular Spasm- blood vessel constricts 2. Platelet Phase- plug formation3. Coagulation Phase- convert fibrinogen to fibrin 1/29: Heart I-Heart and Lung expel equal volume, working as two pumps together. -the heart is double layered 1. Fibrous pericardium 2. Serous pericardium; serve to minimize friction between pumps and prevent infection *excess fluid can cause major problems with heart- Atrium= input & ventricle= output- Murmur= blood swirling back through dysfunctional valves, can be diagnosed by valves- Insufficiency= AV valve doesn’t close properly which leads to regurgitation back into the atria*Blood Flow: 1. Vena Cava 2. Right Atrium 3. Right Ventricle 4. Pulmonary Trunk 5. Pulmonary Veins6. Left Atrium 7. Left Ventricle 8. Aorta*AV bundle propagates signal to ventricle-Different from muscles: branching fibers, intercalated discs, and source of Ca2+, long refractory period & auto rhythmic 2/3: Heart II-the heart is auto rhythmic, controlled by the SA node, it is the pacemaker (AV can take over is SA node isnot working properly, just works a bit slower 40-60 bpm)-caffeine leads to Ca2+ increase, ryanodine receptors activating and activation of an inward current-ischemia leads to the inhibition of NA+/K+ pump*Ach lowers membrane potential & Iso raises it*Iso decreases diastolic voltage range and Ach increases itThreshold= activate voltage dependent Ca2+ channels *occurs near intercalated disk because stimulus is spreading near herePeak= opens K+ channels and inactivated T-type Ca2+ channelsRepolarization=outward K+ current*If SA & AV nodes are damaged then Purkinje fibers can keep the heart going at 20-40 bpm*the absolute refractory period is determined by the voltage dependent properties of NA+ channels2/3- Heart III&IV-preload is the degree of ventricle filling-increasing preload stretches the heart out-when the heart stretches out it can create a stronger contraction, a drop in SV increases ESV which increases EDV and increases contractility*decreases in CO activated the sympathetic system thus increasing heart rate