Physiology Past Paper PDF

30 Liyan khashan Sama Shannak Ebaa Alzayadneh  Aplastic Anemia Aplastic anemia occurs when there’s failure in the bone marrow function, which in turn causes the production of blood cells and many other cells to cease (stop). The Bone Marrow failure can be caused b...

30 Liyan khashan Sama Shannak Ebaa Alzayadneh  Aplastic Anemia Aplastic anemia occurs when there’s failure in the bone marrow function, which in turn causes the production of blood cells and many other cells to cease (stop). The Bone Marrow failure can be caused by: 1. Destruction of stem cells by radiation. 2. Chemotherapy. 3. Chemical toxins. 4. Auto-immune. (the body attacking itself in internal defense, these cells usually fall as collateral damage.) 5. Idiopathic. (reason unknown) Treatment can be done by transplantation of the bone marrow, or can be simply supported by blood transfusion, obviously the donor and recipient should be a match in both cases. Megaloblastic anemia can be caused by either, a decrease in folic acid or a decrease in the Vitamin B12. These two molecules decrease because: 1. Pernicious Anemia 2. Dietary deficiency 3. Malabsorption Megaloblastic anemia causes deficiency in building blocks which leads to impairment in DNA replication. This causes maturation failure. The formation of large, fragile cells with unusual and bizarre shapes (which rupture easily) causes profound anemia. Hemolytic anemia is a hereditary condition causing fragility, it happens when RBCs break down, two types of this anemia are: Hereditary Spherocytosis and Sickle Cell Anemia It can be caused by Immune-mediated destruction, for example there’s a mismatch when blood is transfused (this rarely ever happens), the immunoglobulins and antibodies from the recipient refuses the unit, which causes hemolysis. Another cause is a disease called Erythroblastosis Fetalis, this happens when there’s a mismatch between a mom and her fetus. In this case Hemolysis happens when antibodies and cells that have antigens on them meet up, this leads to RBCs breaking down.  Circulatory effects of Anemia 1. Viscosity of blood decreases 2. Decreased O2 – Carrying Capacity In response to this change of events the body tries to make up for the loss by increasing the heart rate and the vasoconstriction of the blood vessels tries to push more blood and thus causing a higher rate of venous return. This increases the cardiac output and by extension, partially makes up for the low oxygen carrying capacity by increasing the volume. The cardiac output for anemic individuals is high, so if this person exercises, their heart overloads. (when healthy people exercise, their heart rate increases) these individuals have reached the maximum cardiac output and thus tire really fast, this can be associated with chest pain, experiencing fatigue, and panting continuously. Normally these people have a pale-yellowish complexion and dark eyebags. In addition to their accelerated heart rate, the low viscosity of their blood leaves no room for a worthwhile resistance. POLYCYTHEMIA Polycythemia is when there’s an increased levels of RBC count; there’re two types: primary polycythaemia – there's a problem in the cells produced by the bone marrow that become red blood cells; the most common type is known as polycythaemia vera (PV) secondary polycythaemia – too many red blood cells are produced as the result of an underlying condition. Secondary Polycythemia: its more of a physiological response, comes secondary to a condition associated with hypoxia. For example, a person travelled to a high altitude region for a long time, the body in this case demands more oxygen, and thus increasing the production of RBCs. Another example is having a disease that results in hypoxia, could be a restriction or inflammation of the lungs or a heart issue where its not pumping enough blood. Normally the increase in RBCs in secondary polycythemia is around 30%, which means there’s from 6 to 7 million/mm^3 of RBCs. Polycythemia Vera: when there’s abnormalities in the lineages of the bone marrow, where there’s a high level of proliferation, this increases the levels of all blood cells types and not only the RBCs. the following happens: The RBCs could reach up to 7-8 million/mm^3 and the hematocrit up to 60-70% The blood volume doubles in size. Hyper-viscosity, up to 3 fold the normal amount (ten times more water). Effects of polycythemia on circulation: Now the higher the viscosity, the higher the resistance, the higher the arterial pressure. However, this increased viscosity, decreases the rate of the venous return. The blood flow is sluggish and slow. This results in a decrease in the cardiac output. So, from what was explained above, we deduct that there’s two opposing factors, where one is reduction of venous return reduces the pressure, the other is resistance where the higher it is the higher the pressure is, these two factors cancel each other out. 2/3 of these patients suffering polycythemia are normotensive, the 1/3 left are hypertensive. Another characteristic to those patients, that because of this sluggish flow, their venous plexus (the one situated right under the skin) completely fill up, along with the slow movement we understand that the venous circulation is deoxygenated and unsaturated, which gives it its dark bluish complexion. This is an indication of unbalanced oxygen levels or a sign of polycythemia. Laboratory related studies Packed cell volume (PCV) is measured by centrifuging a blood sample, it measures the count of RBCs from the total columnal number, for males the normal is around 47% and for females its 42%. A higher number is an indication of polycythemia or dehydration, a lower is a sign of anemia. Erythrocyte sedimentation rate (ESR), is a none specific test, so its better to follow it up with further tests, its major indication is when the erythrocytes precipitate. It indirectly measures the presence of inflammation in the body. Its rate is the length of the column it will create in a given time, if the formation of the column (the RBCs building up over each other) is rather quick, then the ESR is high. The ESR is high when there’s an inflammation within the body or in case of pregnancy, old age, anemia, could be technical factors like high temperature or tilted ESR tube. Coagulation levels also affect the ESR. This test depends on two factors, the shape of the RBCs, where if their shape was normal (disc shape) it will build up neatly with no problems. However, if their shape was round, ball-like, or sickle-like, they’d not build up/line up nicely. The other factor is the number of the RBCs. ESR depends on the formation of Rouleaux Phenomena. Where the RBCs build up neatly on their own. So how does the inflammation affect the lining up of the RBCs? The RBCs are normally negatively charged, so as standard, there’s always repulsion between them. Inflammation effects the distribution of proteins on the RBCs, this results in a part of it being positive, so now there’s both + and -, which means there’s attraction between them, so they stick together more and faster, hence why the ESR is faster. Factors that decrease the ESR include: 1. Abnormally shaped RBCs (sickle cells and spherocytosis) 2. Polycythemia 3. Technical factors such as low room temp, delay in test performance (over 2h) and a clotted blood sample Normal ESR values for adult males