Physiology Essay Questions – Flashcards

Intrinsic Pathway: 1. The Hageman factor( is also factor XII)- found in the blood activated when it comes in contact with collage; can also become activated with other things 2. Active Hageman factor activates factor XI 3. Factor XI activates factor IX 4. Factor IX activates the enzyme factor X (The Stuart-Prower factor of the common pathway)- the first clotting factor in common pathway 5. Active factor X converts prothrombin(Factor II) to thrombin in the presence of calcium and factor V 6. Thrombin converts fibrinogen(factor I) to fibrin 7. Thrombin also activates factor XIII, fibrin stabilizing factor which causes cross-linked fibrin Extrinsic Pathway: ( comes from damaged tissue) 1. Tissue factor (factor III) - activates clotting factor VII 2. Tissue factor acts as a cofactor and activates VII complex 3. The VII complex activates factor X-which is the start of common pathway Note: calcium (factor IV) is used as a cofactor in coagulation along with other phospholipid molecules. *Fibrinolysis-breaking down of fibrin As the damaged vessel wall begins to repair itself, the clot disintegrates because of the enzyme plasmin -The inactive plasminogen is going to become part of the clot -The activation of plasminogen occurs through several pathways. A molecule called prekallikrein- that will be activated into kallikrein (which is activated by factor XII) and convert plasminogen into plasmin -Tissue plasminogen activator, produced by many tissues, activates plasminogen into plasmin; thrombin is also needed for his process

Leukopoiesis • CSFs are so named because of their ability to grow WBCs in culture. • CSFs are made by endothelial cells, WBCs, and marrow fibroblasts to regulate leukopoiesis (production of WBC) • CSFs induce progenitor cells to commit to a specific pathway • G-CSF - helps to trigger the pathway that leads to neutrophil; which are really important in day to day infections GM-CSF -main trigger for monocyte production and macrophage production • It is interesting that existing WBCs-can communicate to each other as more WBC are produced • Differential WBC counts are used by clinicians • Bacterial infections- Neutrophils tend to increase • Patients with viral infections-lymphocyte variation; T and B cells are good at making antibodies • Parasitic worm infections-Eosinophils have the capability of fighting of the parasites; they increase in number Thrombopoietin Regulates Platelet Production • TPO is a glycoprotein produced primarily by the liver and helps with the production and maturation of megakaryocytes • The gene for TPO was cloned in 1994- Erythropoietin: Regulates RBC Production • Erythropoiesis, RBC production, is controlled by the glycoprotein erythropoietin (EPO)- made by the kidney; produces when you have low oxygen • The stimulus for synthesis and secretion is • Hypoxia triggers the production of a transcriptional factor called hypoxia-inducible factor 1 (HIF-1) • Increased EPO, increases red blood cells

1. Atrial and Ventricular diastole (the heart at rest): it is starting to fill with blood because the pressure in the heart is low. The pressure in the heart is essentially low 2. Atrial Systole (Completion of ventricular filling): Most blood enters the ventricles when the atria are relaxed * When atrial systole occurs it pushes the remaining percentage of blood into ventricles to fill * This event follows the p-wave 3. Isovolumetric Ventricular Contraction (and the first heart sound): the depolarization wave of the conduction cells flows down the AV bundle and reaches the Purkinje fibers * Ventricular systole slowly begins and causes the AV valves to close * Closure of the AV valves represent the first heart sound (S1) = lub * This event follows the QRS complex * Ventricular pressure is rising, but is still less than the pressure in pulmonary trunk & the aorta * The volume in the ventricles is the EDV 4. Ventricular Ejection (the heart pumps): as pressure rises * The semilunar valves have to open so blood can leave the heart * High pressure blood forces low pressure blood farther through the circulatory system * The AV valves remain closed (tricuspid & bicuspid) * The volume of blood pumped: Stroke volume (EDV-ESV=SV) 5. Isovolumetric Ventricular Relaxation (and the second heart sound): Repolarization * The T wave is what you see on ECG (resting state) * Ventricular pressure begins to drop below the pressure in the Arteries * 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 heart is relaxing; Isovolumic ventricular relaxation

1. Iron is ingested from the diet 2. Iron is absorbed in the small intestine 3. Iron is transported by Transferrin through the blood 4. Bone marrow takes up iron and uses it to make heme that will eventually turn into hemoglobin 5. RBCs live about 120 days in the blood 6. Macrophages in the spleen, liver, and bone marrow will help to remove RBCs and are left with pieces: heme with turns into bilirubin 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. The liver metabolises bilirubin and it is excreted in bile 8. Bilirubin and metabolites are excreted in uine and feces 9. Iron that has been ingested in greater amounts than needed is stored in the liver as Ferritin , or it will never be absorbed • Clinical: Hemochromatosis (iron overload) is due to excess iron in the body and is toxic. Initial symptoms include : bloating, GI pain, cramping; more severe internal bleeding, blood in stool, vomiting blood, it can get to liver failure, kidney failure, arthritis, hear problems Clinical: Jaundice, yellowing of the skin, occurs when bilirubin in the skin becomes elevated.

Myocardial Autorhythmic Cells: These cells generate action potentials without input from the nervous system because of an unstable RMP. 1. The unstable RMP starts at -60mV constantly moving towards threshold (around -40) 2. The pacemaker cells have If channels or HCN (hyperpolarizing cyclic nucleotide) channels let Na & K flow through (more sodium goes through) 3. After a hyperpolarizing event the HCN channels open and we get a pacemaker potential 4. The greater influx of Na (along with Ca entry through a different channel) bringsit to threshold 5. The opening of Ca VGCs at threshold gives you the depolarization spike 6. The Ca VGC close and K VGC open and repolarization occurs which leads to A hyperpolarization 7. The ANS (autonomic nervous system) will change the HR (heart rate): parasympathetic & sympathetic events

Endothelial cells release anticoagulants to prevent coagulation. •Heparin activates antithrombin Which can block factor IX- herapin disrupts clotting factors •Protein C: blocks clotting factors like V and VIII, which prevent ability to clot •Fibrinolytic drugs are used to prevent clots. •Streptokinase: bacterial enzyme; which activates plasminogen; •Recombinant tissue plasminogen activator: (made in laboratory) using it as a clot buster; activates plasminogen and activates clots •Antiplatelet agents are used to prevent clots. •Antagonists to platelet and sticking to collagens Ex: Aspirin inhibits COX enzymes •Acetylsalicylic acid (aspirin): inhibits cyclooxygenase enzyme •Coumarin anticoagulants block vitamin K activity. •Warfarin (Coumadin): blocks vitamin K, which is a cofactor for making clotting factors in the liver Calcium chelators remove calcium from blood samples. Sodium citrate: calcium chelator; meaning it binds on to it and prevents clotting EDTA: calcium chelator; binds to calcium to prevent clotting Inherited disorders effect coagulation. Hemophilia A: recessive sex linked disorder with factor 8 deficiency Hemophilia B (Christmas disease): recessive sex linked disorder with factor 9 deficiency There is also vWF disease and Hemophilia C (deficient factor 11)

1. An action potential enters a cardiac muscle cell T-tubule 2. Voltage gated Ca channels open and Ca2+ enters the cell 3. Ryanodine receptor Ca release channels in the SR(sarcoplasmic reticulum) open by the influx of calcium 4. Stored Ca in the SR is released and generates a Ca spark. Sparks summate to give you a Ca2+ signal 5. The Ca signal diffuses to the sarcomere 6. Ca binds troponin to move a protein tropomyosin 7. Relaxation occurs when Ca2+ unbinds from troponin by ATP 8. Ca is pumped back into the SR using a Ca2+ pump for storage 9. Ca is also removed from the cell by antiporter 10. The Na/K pump allows the antiporter to be functional

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-if there is a clot Increased arterial blood pressure-having hypertension Right sided heart failure that leads to congestion in the venous system-leads to peripheral edema 3. A decrease in plasma protein concentration. ↓πcap Decreases osmosis of water into the venular ends of capillaries. May be cause by liver disease Kidney disease, and protein malnutrition 4. An increase in interstitial proteins. ↑ πIF Leakage of plasma proteins during inflammation-ex rolling your ankle Hypothyroidism Hyperthyroidism-bulging eyes

1. Orthostatic hypotension(changing body positions) which means low blood pressure that leads to baroreceptor response 2. When you are lying flat gravitational forces are distributed more equally; gravity affects more in an evenly distribution 3. When you stand there is a decrease in venous return to the heart 4. The decrease in venous return leads to decreased in end-diastolic volume which means there is a drop in stoke volume and decrease cardiac output which leads to decreased blood pressure 5. When less blood is pumped into circulation there is a lower overall blood pressure 6. The baroreceptors respond by sending a low action potential frequency to the medulla oblongata 7. The CVCC (cardio vascular control center) which increases sympathetic and decreases parasympathetic which means more Epinephrine will be released 8. More NE on the Beta 1 receptors of the heart increases heart rate 9. More NE on the Beta 1 receptors of the heart increases strength of contraction 10. More NE on the Alpha 1 receptors of arteriole smooth muscle are going to constrict and will have an increase in blood pressure 11. The changes in CO and R will increase blood pressure

The equation is BF (Q) = ΔP π r4 8 L η Where P is pressure gradient, r is radius of the vessel, L is the length of the tube, and η is the viscosity 1. As the viscosity increases BF decreases (indirect) 2. As the length of tube increases BF decreases (indirect) 3. As the radius increases BF increases (direct) 4. As the pressure gradient increases BF increases (direct) Since length and viscosity are relatively constant, that leaves vessel radius to affect resistance the most in circulation. Since the radius is to the fourth power it has a dramatic effect on flow with small changes in radius.

Percent saturation of hemoglobin is the amount of oxygen bound to Hb at any given partial pressure of oxygen. Oxyhemoglobin saturation (dissociation) curves are a way to express the physical relationship between oxygen and hemoglobin The shape of the curve reflects the properties of the Hb molecule and its affinity for oxygen. The curve is sigmoidal rather than linear so we are able to sustain high saturation values for oxygen and hemoglobin Hb demonstrates cooperative binding properties: physical change in the structure of hemoglobin that makes it easier for oxygen to bind During unloading and loading the next one is easier to take off and the the next one is harder If you look at the normal dissociation curve, at normal partial pressure of oxygen (100 mm Hg), 98% of Hb is saturated. The curve is relatively flat, even as pressure is dropped specially when changing altitude As long as the PO2 stays above 60 mmHg there is a 90% saturation and above Hb saturation declines more rapidly when we get into the steep portion of the curve, at 40mmHg, the biggest drop is between 20-40 mmHg The physiological significance is that even in the venous system with a partial pressure of 40 mm Hg, you still have at least 75% oxygen Several Factors Affect Oxygen-Hb Binding Any factor that alters the conformation of the hemoglobin protein may affect its ability to bind oxygen. Ex. pH, temperature, CO2 levels Changes in pH, temperature, PCO2, and 2-3 DPG alter the binding of Hb and thus change the oxyhemoglobin dissociation curves. Increased temperature, increased PCO2, increased 2-3 DPG, and decreased pH (increase in H+)= shift it to the right When there is a shift to the right you unload more oxygen ex. When exercising, hypoventilation, anemia Decreased temperature, decreased PCO2, decreased 2-3 DPG, and increased pH (decrease in H+)= shift to the left When there is a shift to the left you hold on to oxygen more readily ex. Hyperventilation, hypothermia, dehydration

1. Scuba divers breathe a mixture of gases during their descent, the mixture is nitrogen and oxygen 2. As the diver descends farther, the partial pressure of nitrogen increases according to Dalton's Law of Partial Pressure; for every ten meters there is another 760mmHg 3. The amount of gas dissolving in the blood is proportional to the partial pressure according to Henry's Law; if partial pressure increases the amount of gas in the blood also increases 4. As the diver ascends, inert gases should be off gassed 5. The ascent rate to prevent DCS is 10 meters/minute 6. If the ascent is too quick, improper decompression will occur, which will lead to bubbles in the circulatory system 7. This DCS most frequently causes joint pain, but can lead to neurological symptoms: dizziness, altered mental status, seizures, paralysis and death 8. Treatment is hyperbaric oxygen therapy in a recompression chambers 9. DCS can also be caused by leaving a high pressure environment or ascent to high altitude.

Inspiration Occurs When Alveolar Pressure Decreases: For air to enter the alveoli, the pressure in the lungs must be less than atmospheric pressure Boyle's Law states that if the volume increases pressure decreases Contraction of the diaphragm helps increase thoracic cavity volume The external intercostals and scalenes muscles that help make the thoracic cavity bigger Notice during inspiration that the alveolar pressure drops below atmospheric pressure intrapleural pressure is less than atmospheric pressure; should always stay below intrapulmonary Expiration Occurs When Alveolar Pressure Increases: Elastic recoil of the lungs and thoracic cage returns the diaphragm and rib cage to their original positions this makes volume smaller and pressure should increase This process is passive, and thus normal expiration is called passive expiration: you don't need muscle contraction to exhale instead muscle relaxation As volume decreases, pressure in the lungs increases and air should go out of the lungs Notice during expiration that the alveolar pressure goes above atmospheric and intrapleural pressure rises but does not go above atmospheric pressure intrapleural pressure will always stay below intrapulmonary Forced exhalations or active expiration uses the internal intercostals and abdominal muscles