ESSAY Questions Unit 3 – Flashcards

Intrinsic Pathway: Chemical signals within plasma. 1.The Hageman factor is activated by collagen in the blood. 2. Active Hageman factor activates factor XI. 3. Factor XI activates factor IX (xmas factor). 4. Factor IX activates the enzyme factor X. 5. Active factor X converts prothrombin (factor II) to thrombin. Requires Calcium. 6. Thrombin converts fibrinogen (factor I) to fibrin. 7. Thrombin also activates fibrin stabilizing factor or factor XIII (cross links proteins). Extrinsic Pathway: Chemical signals outside plasma. 1. Tissue factor (factor III) comes from damaged tissue. 2. Tissue factor acts as a cofactor and activates factor XII. 3. The VII complex activates factor X. Fibrinolysis: -A damaged vessel wall will start to repair itself, making the clot disintegrate. The enzyme plasmin will help break this down. -The inactive plasminogen will become plasmin. -The molecule prekallikrein helps this activation which must be activated into kallikrein using the Hageman factor. -tPA (tissue plasminogen activator) converts plasminogen into plasmin.

Erythropoiesis: RBC production that is controlled by the glycoprotein erythropoietin (EPO) made by kidneys. Hypoxia (low oxygen in body) is the stimulus used for synthesis and secretion of RBCs. Hypoxia triggers production of a transcriptional factor HIF-1 (hypoxia inducible factor 1). Increased EPO=Increased RBC production. Leukopoiesis: regulated by colony stimulating factors. CSF's are made by endothelial cells, can grow on WBCs, and induce the production of WBCs. G-CSF makes neutrophils and GM-CSFs make monocytes and give rise to macrophages. WBCs make their own chemical signals to communicate affecting production. Differential WBC counts help diagnose diseases: bacterial infections increase WBC count, viral infections increase lymphocyte count, and parasitic worm infections increase eosinophil count. Thrombopoiesis: regulates platelet production and is triggered by the hormone TPO. TPO is a glycoprotein produced by the liver, triggers production of platelets, and comes from the megakaryocyte.

1. Atrial and ventricular diastole (heart at rest): not contracting, pressure in heart is essentially zero and will fill with blood. 2. Atrial systole: most blood enters the ventricles during diastole. When atrial systole occurs it pushes about 20-30% of blood into ventricles. This event follows the P wave on the ECG. 3. Isovolumetric Ventricular Contraction: the depolarization wave of the conduction cells flows down the AV bundle until it reaches the Purkinje fibers resulting in ventricular systole. •Ventricular systole slowly begins and causes the AV valves to close as the pressure increases in the system •Closure of the AV valves represent the first heart sound (S1: lub) •This event follows the QRS on ECG •Ventricular pressure is rising, but is still less than the pressure in the pulmonary trunk and aorta, valves are still closed. •The volume in the ventricles is the EDV, not changing until eject blood. 4. Ventricular Ejection (the heart pumps): pressure in the ventricles is above the aorta/pulmonary truck •The semilunar valves blow open and blood enters arteries •High pressure blood forces low pressure blood through system •The AV valves remain closed so blood doesn't go into atria. •The volume of blood pumped is the stoke volume. 5. Isovolumetric Ventricular Relaxation (2nd heart sound): valves close. •The T wave on ECG repolarization, ventricles relax. •Ventricular pressure begins to drop below the pressure in the arteries. Prevents backflow. •The backflow is prevented by the closure of the semilunar valves and creates the second heart sound (S2) = dup. •Once the semilunar valves are closed the ventricle is a sealed chamber again, isovolumetric relaxation, valves closed.

Hemoglobin synthesis requires adequate iron from diet. 1. Iron is ingested from the diet (animal products, vitamins, spinach, etc.) 2. Iron is absorbed in the small intestine. 3. Iron is transported through transferrin, how iron moves in our bloodstream. 4. Bone marrow takes up iron and uses it to make heme of hemoglobin. 5. RBCs live about 100-120 days in the blood, fragile over time, no organelles or machinery to maintain themselves. 6. Macrophages in the spleen, liver, and bone marrow eat RBCs and recycle them. 7. Amino acids from the globin are recycled for protein synthesis, iron can be recycled to the liver and returned to the bone marrow, and the heme group is converted to bilirubin. 8. Bilirubin and metabolites are excreted in urine (kidneys) or bile, as well as fecal matter (intestines). 9. Iron that has been ingested in greater amounts than needed can be stored in liver and used later (excess iron). Clinical: Hemochromatosis (iron overload) is due to excess iron in the body and is toxic. Initial symptoms include cramping, irritation of GI tract, bloating, internal bleeding, overall corrosion of digestive system. Clinical: Jaundice, yellowing of the skin, occurs when bilirubin in the skin becomes elevated. Too much breakdown of RBCs, can't get rid of fast enough in the bile. Bilirubin is not being eliminated in fecal matter or urine.

Myocardial Autorhythmic Cells: generate AP without input from the nervous system because of their unstable RMP. 1. The unstable RMP starts at -60mV and will slowly move to threshold. 2. The pacemaker cells have If channels of HCN channels that open Na+ and K+ to flow through them because of cyclic AMP or hyperpolarization. Na+ in, K+ out. 3. After a hyperpolarizing event the HCN channels will let Na+ enter and depolarize the cell (pacemaker potentials). 4. The greater influx of Na+ (along with Ca+ entry through a different channel) creates threshold and opens Ca+ voltage gated channels. 5. The opening of Ca+ VGCs at threshold result in a depolarization spike. 6. The Ca+ VGC close and K+ VGC open which will repolarize the cell and repeats. 7. The ANS will change the heart rate. Sympathetic increases heart rate and parasympathetic decreases heart rate. -parasympathetic control involves the release of ACh. -ACh binds to muscarinic receptors in the SA node activating the G protein. -Potassium permeability increases opening channels, K+ flows out of the cell causing a hyperpolarizing effect. -Ca+ permeability decreases which causes slower depolarization. - Sympathetic control involves the release of norepinephrine. -NE/E activate Beta 1 adrenergic receptors of the SA node working through G proteins and activates adenylate cyclase. Beta 1 receptor effects heart. Beta 2 receptor effects lungs/respiratory. -Adenylate cyclase generates cAMP which increases the flow of Na+ through HCN channels. -Increased Na+ and Ca+ entry into the cell increases the rate of depolarization, which increases the heart rate.

Anticoagulants Prevent Coagulation 1.Endothelial cells release anticoagulants to prevent coagulation. ~Heparin activates anti-thrombin, inhibits thrombin ~Protein C: inhibits factor V and VIII 2. Fibrinolytic drugs are used to prevent clots, clot buster ~Streptokinase: made by bacteria, turns on plasminogen, eats your fiber ~Recombinant tissue plasminogen activator: converts plasminogen to plasmin 3. Antiplatelet agents are used to prevent clots. ~Antagonists to platelet proteins called integrin-protein used by platelet to interact with collagen, ~Acetylsalicylic acid (aspirin): inhibits cyclooxygenase enzymes=used to make prostaglandins, COX-1 and 2 which inhibit prostaglandin production and inhibit clotting 4. Coumarin anticoagulants block vitamin K activity. ~Warfarin (Coumadin): inhibits Vit K vit K is necessary for clotting factors II, VII, IX, and Xinhibiting clotting factors or anticoagulants 5. Calcium chelators remove calcium from blood samples. ~Sodium citrate: bind up calcium so not involved, blood can't clot ~EDTA: bind calcium, can't start the pathway, will not clot 6. Inherited disorders effect coagulation. ~Hemophilia A: recessive sex linked disorder with factor 8 deficiency.Found on sex X chromosome, 80% of all hemophilia, cannot coagulate effectively, need injections of factor XIII to treat ~Hemophilia B (Christmas disease): recessive sex linked disorder with factor 9 deficiency. Factor IX, named after patient/ case study, treated by injection of factor 9, can also suffer from hemophilia A ~There is also vWF disease and Hemophilia C (deficient factor 11).

1. An action potential enters the T Tubule contractile cells (AP starts from pacemaker cells). 2. Ca+ VGC open and an influx of Ca+ triggers receptor on smooth ER. 3. Ryanodine receptor Ca release channels in the SR and are induced by influx of Ca+. 4. Stored Ca+ in the SR is released and generates a Ca spark (signal). Ca+ sparks add together to get bigger signal. 5. The Ca signal diffuses through cytoplasm and activates contractile part of cell. 6. Ca binds to troponin and initiates contraction. 7. Relaxation occurs when Ca+ unbinds troponin. 8. Ca is pumped back into the SR using Ca+ pumps (ATP). 9. Ca is also removed from the cell using a Ca+/Na+ antiporter. 10. The Na/K pumps are always working/running. Na+ IN, Ca+ OUT.

Several causes of edema are as follows 1. Obstruction of the lymphatic system. Parasites, cancer, or fibrous tissue growth can block lymph flow. Elephantiasis is a chronic condition caused by a filarial worm. Treatment includes diethylcarbamazine or ivermectin for worm infestations and ultimately prevention of infection. 2. An increase in capillary hydrostatic pressure. ↑ Pcap -Venous obstruction: push the blood back thru capillaries to the arteries (blood clot). -Increased arterial blood pressure: heart pumping too much blood into the system, high blood pressure -Right sided heart failure that leads to congestion in the venous system leads to peripheral edema. 3. A decrease in plasma protein concentration. Causes in ↓πcap -Liver failure -Kidney failure, allowing proteins to escape bloodstream -Malnutrition: not being able to make proteins 4. An increase in interstitial proteins. Causes of ↑ πIF -Leakage of plasma proteins: during inflammation, allergies, -Hypothyroidism: leaking mucin proteins. -Hyperthyroidism: bulging eyes, fluid accumulation Clinical: Kwashiorkor, protein malnutrition that leads to abdominal edema (ascites).

1. Orthostatic hypotension triggers baroreceptor reflex. 2. When you are lying flat gravitational forces are distributed equally. 3. When you stand there is a decrease in venous return of blood to the heart. 4. The decrease in venous return leads to decreased EDV, which decreases SV and CO. 5. When less blood is pumped into circulation, your blood pressure drops. 6. The baroreceptors respond by sending a decreased AP frequency to the brain stem. 7. The CVCC (cardiovascular control center) in medulla oblongata increases sympathetic response. 8. More NE on the Beta 1 receptors of the heart will increase heart rate. 9. More NE on the Beta 1 receptors of the heart will increase contractility (pumping of the heart). 10. More NE on the Alpha 1 receptors of arteriole smooth muscle increase vasoconstriction. 11. The changes in CO and R will increase your blood pressure.

BF = ΔP/R --> blood flow=change in pressure/resistance Poiseuille's Law: R = 8 L η/π r4 --> Resistance=8 length*viscosity/eta*radius 4 The full equation for blood flow or flow rate (Q) is BF (Q) = ΔP π r4/ 8 L η -Increase pressure gradient, increase the blood flow (directly proportional). -Decrease resistance, increase blood flow (inversely proportional). -Increase resistance, decrease blood flow (inversely proportional). 1. Viscosity increases, blood flow decreases (inversely proportional). 2. Length of tube increases, blood flow decreases (inversely proportional). 3. Radius increases, blood flow increases (directly proportional). 4. Pressure gradient increases, blood flow increases (directly proportional). -Length and viscosity are relatively constant, that leaves the vessel radius to affect resistance the most. Since the radius is to the 4th power it has a dramatic effect on flow with small changes.

Oxyhemoglobin dissociation curves are a way to express the physical relationship between hemoglobin and PCO2. -The shape of the curve reflects the properties of the Hb molecule and its affinity for oxygen. -The curve is sigmoidal instead of linear and it reflects the way oxygen binds to Hb and the way it loads and unloads. -Hb works together with binding properties: as 1 O2 binds to a Hb, a shape change in the molecule makes it easier for the next O2 to bind. -During unloading its easy to remove the first O2, but harder to remove the next ones. - The curve is relatively flat, even as partial pressure drops, you still maintain high saturation. -As long as the PO2 stays above 60 mm Hg, youll have 90% or more saturation. Factors affecting the curve shift: 1. Changes in Ph, temperature, PCO2, and 2-3 DPG can alter the binding of Hb and essentially change the curve. 2. Increased temperature, increased PCO2, increased 2-3 DPG, and decreased Ph will shift curve to the right. -when this happens, Hb unloads more O2; happens during hypoventilation, high elevations, and excercising. 3. Decreased temperature, decreased PCO2, decreased 2-3 DPG, and increased pH will shift curve to the left. -When this happens, Hb holds on to O2, happens during hyperthermia, hyperventilation, dehydrated, and vomiting.

-Nitrogen is an inert gas that is abundant in the atmosphere and enters and leaves our respiratory system. It can become soluble in our blood due to higher pressure and could be problematic. -Dalton's Law says that the partial pressure of nitrogen is high in the atmosphere and alveoli but has low solubility. -In SCUBA diving, there is increases solubility of nitrogen. It goes up 1 atmospheric pressure every 10 meters. - As you dive deeper, the pressure increases. -Increases in the partial pressure of nitrogen, increases its solubility and cause nitrogen to enter the body's bloodstream. -If a diver ascends to quickly to the surface, nitrogen bubbles will develop in the blood ad the diver will suffer decompression sickness ("The Bends"). 1. Scuba divers breathe a mixture of gases including nitrogen and oxygen when descending. 2. As the diver goes deeper, the partial pressure of nitrogen increases, as well as its solubility. 3. Amount of gas dissolving in blood is proportional to the partial pressure of the gas. 4. As the diver ascends, inert gases should be released from the bloodstream (off-gasing). Must do slowly. 5. The slow ascent rate is to prevent DCS which is about 10 meters per minute with scheduled stops. 6. If the diver rises to quickly, improper decompression occurs, leading to nitrogen bubbles in bloodstream. 7. The DCS will cause joint pain and can lead to neurological symptoms such as seizures, paralysis, and difficulty breathing. 8. Treatment includes hyperbaric oxygen therapy in a decompression chamber. 10. DCS can also be due to high pressure environments or high altitudes.

Inspiration occurs when alveolar pressure decreases. -In order for air to enter the alveoli, the pressure in lungs must be less than the atmospheric pressure. -Boyle's law states that if the volume increases, the pressure will decrease. -Contraction of the diaphragm increases thoracic cavity volume. - The external intercostal and scalene muscles help expand the thoracic cavity. -The alveolar pressure drops below atmospheric pressure and the intrapleural pressure must be less than alveolar pressure. This allows lungs to expand and not collapse. Expiration occurs when alveolar pressure increases. -Recoiling of the lungs and thoracic cavity returns the diaphragm and rib cage to their original positions, the thoracic cavity volume decreases, gets smaller. -This is a passive process so normal expiration is called passive expiration because it does not require muscle contraction. -As volume decreases, pressure in the lungs increases, moving air out. -Alveolar pressure is above atmospheric pressure but intrapleural pressure is below atmospheric pressure and still below alveolar pressure.