Cardio #75 Fri, 01/24/03, 1pm Exam Review Jennifer Uxer for David Jenkins Page 1 of 5 Exam 4 Review I. Exams A. Written 10am – 11am 25 questions Anatomy – 9 Physiology – 9 Histology – 4 Embryology – 3 B. Practical—Dr. Sheedlo We’re divided into 4 groups. Check the lists on the boards outside of the lab. You can trade with someone if you’d like. 23 questions Histology – 3 There is histology in the dissector. Scroll down to the bottom to find it. Exam images are similar to the histology in the dissector. Know the structure and characteristics of: a vein – flat, adventitia with endothelium; a large vein is flat an artery – has smooth muscle; a large artery is packed Know the distinguishing layers: tunica intima, media, and adventitia Heart-pericardium – 11 Mediastinum – 9 7—2nd order questions An artery is tagged: What’s its origin? A vein is tagged: Where does it drain? Know the diaphragm Gross Anatomy breakdown Heart – 11 Arteries – 1 (+1—because there are arteries inside the heart; go over these) Nerves – 3 Questions can be 2nd order, identify the tagged structure Veins – 3 Remember that there are veins in the heart Structures – 1 Includes things like the thoracic duct (which comes from a vein). Cross Section – 1 You can find this at the end of the dissector. Study cross sections 30 & 31. Each has 2 different labelings, so there are 4 drawings to study. Know what’s labeled on the cross sections—there is an exam question directly from this. C. Heart Development—embryology Go to the heart section in the clinical human embryology and print it. Septal formation (interventricular and interarterial) Cardio #75 Fri, 01/24/03, 1pm Exam Review Jennifer Uxer for David Jenkins Page 2 of 5 II. Fetal circulation, especially with regards to the heart (umbilical vein and artery, ductus arterioss, ductus venoss, foramen ovale) Early development of heart (regions—follow movie) Congenital anomalies of cardiovascular system, septa defes, patent foramen ovale, ductus arteriosus Individual Professors for Written A. Dr. Cammarata—Histology About 96% of the class got the histo questions right last year Go through the notes; don’t worry much about it if he didn’t talk about it in class. The book provides more details than he covered. Highlights were covered in the lecture—study the scribe. Know the morphology, structures of a blood vessel, the walls, sizes of blood vessels Note that a descriptive written question can be asked or shown as a picture in the practical to tell what type of vessel it is. He looked at the 3 practical questions and feels that they are fair. B. Dr. Leppi Writes questions as clinically oriented as possible This was said twice: Know the heart sounds and where they’re best heard (auscultation) on the chest 2 sounds—Know how they’re associated with the 4 heart valves S1 – lub S2 – dub Pericarditis—When the heart fills with inflammatory fluid, it forms a cardiac tamponade and the ventricles have a hard time contracting. Know how to perform the pericardiocentesis without hurting something. Mediastinum Know the relationships of structures in the superior mediastinum and how they relate to each other: aorta, pulmonary trunk, trachea, esophagus Some structures then continue to the posterior mediastinum and know their relationships to each other. Trachea stops at T4 Esophagus and aorta cross each other on the way to the diaphragm. Diaphragm—know the 3 openings. Inferior vena cava – T8, esophagus – T10, aorta – T12 Know the thoracic duct (whose contents flow up the body), azygous vein Refer to a normal PA (Posterior anterior) radiograph of the chest: know what’s along the left margin and right margin, know the normal space occupied by the heart Focus on the study questions that apply to what is in this review. C. Dr. Smith Cardio #75 Fri, 01/24/03, 1pm Exam Review Jennifer Uxer for David Jenkins Page 3 of 5 2 questions (integrate with Dr. Downey’s lectures) Sent an e-mail with comments of what to study and practice questions. The answers have now been e-mailed. Work on the practice questions Wigger’s diagram will be covered next week, so we’re not responsible for specifics Likes to ask questions like “If this happens, what will happen next, what will increase or decrease?” Dr. Downey asks questions like this, too. Know concepts: Electrical event precedes mechanical event Ohm’s Law CO = HR * SV D. Dr. Downey Sent out revised practice questions and their answers. He said that none are exactly like the exam questions, but they are representative. If you can work them with confidence, you’re pretty comfortable with the material. 7 questions from Dr. Downey He will be around Monday morning to answer last minute questions. He will also try to answer questions e-mailed to him. Note that his questions and Dr. Smith’s require us to think and demonstrate an understanding of the material in addition to memorizing information Rectification Resistance to current flow changes as a function of voltage. A resistor conducts current directly in proportion to the voltage. A rectifier changes resistance depending on the applied voltage. For K+, there’s an increasing driving force for K+ efflux during the plateau stage (Phase 2). Know this is true because the driving force = Em – EK+ = -95mV. (Em is calculated using the Nernst equation) During the plateau, the driving force is 20mV, yet efflux does not increase. Therefore, channels show rectification because they do not let as much K+ escape as you’d expect for such a large driving force. This is important because it keeps the K+ from repolarizing the membrane. During the plateau, need Ca influx and K+ efflux to equal. At the end, the Ca2+ influx decreases while K+ efflux decreases causing a repolarization of the membrane. Book calls it inward rectification because the efflux is slow since the channels are not open much. If the driving force is reversed experimentally, the channels happily conduct K+ inward quickly. So, they are called inward rectifiers. Know that the rectifiers prevent efflux of K+ in the plateau preventing repolarization of the membrane—allow it to remain depolarized for a sustained time. Cardio #75 Fri, 01/24/03, 1pm Exam Review Jennifer Uxer for David Jenkins Page 4 of 5 Need to know and appreciate that the K+ conductance decreases below its resting value allowing sustained depolarization. It then rises to its basal level to allow repolarization. Won’t ask us to ID specific K+ currents, I1 etc. Know that there are voltage- and ligand gated K+ channels. Ligand gated channels are sensitive to ATP and Acetylcholine. Ischemia Na+/ K+ pump is essential for maintaining transmembrane gradients. Pumps Na+ out, and brings K+ in. If it is compromised by a lack of energy (ATP), K+ is lost and not replaced, while Na+ enters and is not extruded. Consider the Nernst equation for K+, plug in values lower than normal. It won’t be as negative as usual. As this happens, membrane gets closer to the threshold for the Na+ channels, causing premature contractions. Na channels remain inactive because the membrane is not negative enough to move the inactivation gates. Thus, the Na channels are out of the picture. If transmembrane is more negative than Ca2+ threshold and rises to its level, the Ca2+ channels open and create a slow rising ventricular contraction. Na+/ K+ pump maintains normal transmembrane gradients. Efflux of K+ and waning Ca2+ current cause repolarization. Timing in the Heart There are questions on this in the practice questions. Example: How many msec are required for an electrical excitation from the pacemaker to the Bundle of His? If there aren’t any on the exam, they’ll help next week for ECGs. Heart Block Action potential conduction stopped in the AV nod due to intense parasympathetic stimulation. Factors responsible for diastolic repolarization in the pacemaker Decreasing K+ outward current allows inward Na+ current through the “funny channels” and transient Ca2+ current. These inward currents depolarize the membrane. Parasympathetic stimulation: Increases the probability for the K channels to open. The do, so more charge leaves the cell and competes with the positive inflow of ions. Threshold of the Ca channels may not be reached or may be reached at a later time. This causes the heart to beat at a slower rate. Sympathetic stimulation: Increases the influx of Ca2+ and Na+ in diastole causing a faster rise to threshold and a rapid heart rate. Cardio #75 Fri, 01/24/03, 1pm Exam Review Jennifer Uxer for David Jenkins Page 5 of 5 Practice questions on X, Y, Z #6 & #7 #6. Net negativity inside the cell. Ion X has equal concentrations inside and outside, so there’s no concentration gradient. There is an electrical gradient because the inside of the cell is negative and this is a positive ion, so X will enter the cell passively. Y & Z are in high concentrations outside and are attracted by the electronegativity inside the cell, so they will also enter. #7. Read questions carefully!! Inside concentration of Y & Z is higher than the outside. There’s a concentration gradient favoring their efflux, yet there’s an electrical gradient favoring their influx. Calculate the equilibrium potentials for Y & Z. These will be negative because there’s more inside than outside. This equilibrium potential won’t be as negative as the membrane potential, so Y & Z enter the cell. K equilibrium potential is greater than the membrane potential, so it passively leaves the cell. If this answer was -89mV, the driving force would be less, but the direction of movement would be the same.