Human Physiology Study Guide 1

Disclaimer: Do not limit yourself to this guide—it is just a guide. References are to Textbook of Medical Physiology by Guyton and Hall, 11th Ed.

Answers to this study guide will not be posted. If a few questions stump you, I would be happy to discuss them during my office hours.

Review the following from chapter 1, 2, and 3 and the gene expression special topics lecture

  1. General cell structure (membrane, cytoplasm, Extracellular fluid, ICF, etc.) and the role of each of the intracellular organelles
  2. gene expression- what are the steps of gene expression? Where do these steps occur.
  3. Primary-quaternary structure of proteins.
  4. Be able to describe the “anatomy” of an amino acid and describe the role the “R” group can play with respect to a protein’s function in the cell.
  5. What can cause a protein to denature?
  6. If a gene experiences a mutation does this mean a protein will NOT be synthesized? If a protein is made, will it be useless? In other words, do all mutations lead failed gene expression?
  7. What is the difference between the genome versus a gene? How many genes are in the human genome. Is the rest of the DNA useless? Give an example of how RNAi and RNAa ‘s can be used for medicine.
  8. Understand the basic process of transcription and translation.
  9. What is DNA damage? What is a mutation. Define pluripotent, multipotent and unipotent.

Lecture One--Homeostasis, temperature regulation - Chapter 1 and 73

  1. Define homeostasis. What is the ultimate goal in homeostasis?If we didn’t have homeostasis, what would happen to cells and proteins?
  2. Does every system in the body help maintain homeostasis? Does every system have the same stringency with set points and allowed deviations? What is the specific role of the neural and endocrine systems in homeostasis? In what ways are these two systems different from each other? How are they similar?
  3. What is set point? Deviation? Correction?
  4. Identify the two mechanisms used to achieve homeostasis, and differentiate between them. Which one is used the most by body systems to maintain homeostasis? Which one is associated with health?
  5. Are we ever at (or locked at) our set point? When correction is made does it end AT the set point? Do the corrective measures remain fully engaged as the variable approaches set point or do they taper down as the variable approaches set point.
  6. Does homeostasis mean we are at equilibrium or are we at a steady state? What is the difference between those terms? What is the price of homeostasis?
  7. Body temperature helps maintain homeostasis—be able to describe the reflex arc involved with thermoregulation.
  8. How is heat generated within our bodies? How do we lose heat? In what way do we loose most of our heat.
  9. Where are the detectors for body temperature?
  10. What are the mechanisms to increase body temperature?
  11. What are the mechanisms to decrease body temperature?
  12. What is the most common environmental cause of hyperthermia? What about the most common environmental cause of hypothermia—specifically, how do those people lose heat? (how did the people on the Titanic die?).
  13. Continuing with above, why is Bear Gryls smart to remove his clothing before jumping into icy water and what is his reasoning to ‘dry off’ with snow before putting on his clothing? How does clothing reduce the amount of heat you lose? How does a wet-suite keep you warm?
  14. Why does your body temperature rise at the beginning of your work out, but then stays at a steady-state, elevated value, while you continue to exercise?
  15. How does a fever re-set the set point? Review the importance of cytokines like interleukin one.
  16. What is the time course of a fever? What is cyclooxygenase? How can this enzyme’s activity lead to a fever? How can we stop this enzyme’s activity? What are NSAIDS? Is acetaminophen a permanent or temporary COX inhibitor.
  17. How does exercise induced hyperthermia differ from fever induced hyperthermia? Be ready to analyze, using a graph, their time course (see the end of that powerpoint).

Body Fluid Compartments chapter 25 (pages 292-295; 296-301) and osmolality review from special topics.

  1. Name/define the major fluid compartments and their sub-compartments.
  2. Determine what percentage of total body weight each compartment accounts for.
  3. Describe the concentrations/ compositions, and volumes of the body fluid compartments. Are they the same? Which of the three (osmolality/comp/or volume) should be the same in the compartments?
  4. Know intracellular and plasma concentration values for sodium and potassium.
  5. What is osmotic pressure? If two compartments, separated by a membrane permeable only to water, hold different concentrations of a solution what will happen with respect to osmotic pressure? What if these two compartments were separated by equally concentrated solutions—say 5% glucose and 5% NaCl…would water move? Why or why not? Why do you need to consider dissociation in this problem?
  6. Be able to describe the proper sequence of events when concentrations of two solutions in different body compartments stray from each other—as you learned in lecture (diabetes and dehydration example).
  7. There are a number of plasma proteins made by the liver. Which plasma protein is the most abundant. How was this protein important in Kwashiokor? Explain the edema (ascites) in the abdominal cavity.
  8. Be sure you understand the difference between expressing solution concentrations in terms of gm%, molality, osmolality, and molarity. Review the problems in your homework packet to make a specific gm%, molal, molar, or osmolal (this will be tested on your lab exam).
  9. What is diffusion? What is osmosis? What is a semi-permeable membrane?
  10. What is a solute? What is a solvent? Can solutes always move? Are we most like water?

The endocrine System (Chapters 74-77; Chapter 79; Pages 979-980; 985-992).

  1. Review the connections, similarities, and differences between the nervous and endocrine system (from the homeostasis lecture).
  2. What are the basic hormone actions? How do hormones ULTIMATELY change cell activity?
  3. Do all cells respond to a hormone? What determines if a cell responds at all? Do all cells respond to the same hormone in the same manner? What determines how a cell will respond?
  4. Describe the three classes of hormones (amino acid derived, peptide/protein vs. lipid). Which class of hormones is the most abundant?
  5. What hormones are synthesized by the amino acid, tyrosine?
  6. Norepinephrine is primarily used by the body as a neurotransmitter or a hormone? What about epinephrine?
  7. How do hormones travel in the blood if they are hydrophilic or hydrophobic? How do the different classes of hormones communicate with their target cells/organs—that is which ones can enter the cell and which ones can’t? IF a hormone can’t enter the cell, how does the cell respond to the hormone?
  8. What are second messengers? Do all hormones use them? What types of second messenger systems are used?
  9. What are the fates of hormones?
  10. What mechanisms exist to trigger a hormone to be released?
  11. Familiarize yourself with the chain of command (hierarchy or axial relationship) commonly seen for endocrine glands. In which of the three mechanisms for hormone release would you see an axial relationship?
  12. What is the relationship between the hypothalamus and hypophysis (the pituitary: both anterior and posterior)? That is, how are they anatomically linked and how does the hypothalamus physiologically communicate to the hypophysis?
  13. Know the following information for these hormones: TH, Cortisol, aldosterone, Growth Hormone and parathyroid hormone, TRH, TSH (there are a lot of actions for this one—KNOW THEM see page 938), TH, CRH, ACTH, insulin, and glucagon.
  14. Where it is made
  15. Where is its target organ (cell),
  16. what the target organ/cell would do (the effect),
  17. and what mechanism stimulates the hormone release? (hormonal, humoral, or neural).
  18. Know the regulation of, and feedback mechanisms of the hormone
  19. Which of these hormones does not have an “axis?” Why? In other words, how is its release controlled? Does aldosterone TRULY follow an axial relationship? What about cortisol?
  20. How are levels of thyroid hormone and growth hormone dependent? What can extreme levels of cortisol do to levels of growth hormone?
  21. What would happen if there was a defective hormone or a defective receptor for a hormone in the HPT axis. in terms of homeostasis? How would this affect circulating levels of all the other hormones in the axis?
  22. How might an excess of an exogenous hormone (someone "taking hormones") affect release of "endogenous" hormone? Think about your negative feedback mechanisms!
  23. Review the diseases and the problems with the axial relationships: Grave’s disease, Hashimoto’s hypothyroidism, Iodide deficiency, Cushing’s disease/syndrome, congenital adrenal hyperplasia, gigantism, and Addison’s disease. Lastly, review Hypo/Hypercalcemia and potential hormonal disruptions that can cause these states.

Red blood cells—synthesis, destruction, recycling, and problems with RBCs (chapter 32 and pages 861-864)

  1. What are the physical characteristics of blood? What are the functions of blood?
  2. Define the components of whole blood. What components do you find in the formed element portion of whole blood? What components do you find in the plasma? What are normal blood values of protein? Glucose? Electrolytes?
  3. Where does hematopoiesis occur throughout the stages of life? What is a multipotent vs pluripotent stem cell? Which type is a hemocytoblast? Understand the difference of determination vs. differentiation as the formed elements are synthesized in red marrow. What factors stimulate mitosis and differentiation of the stem cell? How do cells change as they make their way along these pathways?
  4. Understand the lineage of erythropoiesis. When do RBCs enter the blood stream? Are they mature as they enter? What percentage of RBC’s are normally reticulocytes? How do reticulocytes differ in appearance from mature RBC’s?
  5. What is the recipe for normal erythropoiesis? What are coenzymes? Which two are important for erythropoiesis? Discuss the role of folic acid and Vitamin B12 in erythropoiesis. Where does the body store these coenzymes? How and where is Vit B12 absorbed from the GI tract? What is a necessary requirement for normal B12 absorption? Where is this "factor" produced and released?
  6. What are the components of RBCs? That is, what are they made of? What is hemoglobin? What is a normal blood Hb concentration value? What is heme? What are globin chains? Are there different globin chains expressed throughout life? IF so, which ones and when?
  7. What is iron? What state of iron can bind oxygen?
  8. Describe the physical characteristics of RBCs: why are they shaped the way they are?
  9. Describe centrifuged blood (the pellet (PCV), buffy coat and supernatant (plasma).)
  10. What is the difference between serum and plasma? Is whole blood just extracellular fluid? If not, what part of whole blood would be extracellular fluid?
  11. What is oxygen carrying capacity? What determines oxygen carrying capacity?
  12. Define each of the following terms (not just the names of the initials!) and give normal values for each of the following: Hb concentration, hematocrit, MCHC, MCH, MCV, MCD. Do you know how MCH, MCHC and Hb concentration terms differ from each other?
  13. What is the meaning of the terms poikilocytosis and anisocytosis?
  14. How is the rate of erythropoiesis regulated? Provide the complete feedback loop that controls this variable (RBC count.) What is sensed by the kidney in order to regulate the RBC count?
  15. What is the lifespan of an RBC? What is the role of ATP in keeping a RBC viable, i.e., do they have aerobic respiration?
  16. How and when are RBC’s removed from circulation? What is the role of the macrophage and liver and spleen in the destruction of the RBC and the handling of breakdown products of hemoglobin (Hb)? What happens to Fe, heme, and globin?
  17. Describe the handling of iron by the body for delivery and removal of iron. Know the functions of transferrin, ferritin. What happens to iron absorption when a person already has adequate stores of this element?
  18. What is jaundice? What would happen to the breakdown products of hemoglobin (heme) if there is liver failure? If there is a bile duct blockage?
  19. What disorders arise when there is excessive RBC production? How do we treat primary/secondary Polycythemia?
  20. Are all anemias the result of iron deficiency? Understand all anemias presented in class and their characteristics (e.g., are the RBCs ainsocytotic? Poikilocytotic? How are MCH, MCHC or MCV changed, etc.)
  21. Explain how a single point mutation on a gene can affect the structure of a globin chain (sickle cell anemia or thalassemia major.) What is the exact change in the globin chain in these disorders? Under what oxygen conditions does this affect RBC shape (if at all)? How does it change the cell's shape? Are there other globin chains made to compensate (e.g., HbF or HbE?)
  22. Are people with malaria at an advantage in life? Do people with sickle cell disease have an advantage? What if someone has sickle cell trait AND malaria?

Blood Typing and HDN (Chapter 35)

  1. What are antigens? Why must we be concerned with antigens during blood typing?
  2. What types of antigens are on RBCs that we must pay particular attention to? Are there more than these? If so, why aren’t we so worried about them in blood typing?
  3. What are agglutinins and agglutinogens? Again, why do we care about these for blood typing?
  4. How do RBC’s differ in the antigens (agglutinogens) they express in each of the ABO blood types?
  5. How is blood typing done? (Also see Lab Exercise)
  6. Which types are compatible for transfusion? Explain this in terms of agglutination reactions.
  7. What is “Rh factor?” Is it another antigen/agglutinin? Why do we care about it in blood typing? T/F-People with A positive blood can receive blood from other A positive blood donors AND A negative blood donors. Could we say the same for A negative recipients?
  8. Does a person ALWAYS have Rh antibodies? Will a person who is Rh- have antibodies present if they are naïve? If they have been exposed to Rh+ blood once, twice, or three times prior?
  9. What iserythroblastosis fetalis or HDN? What causes HDN to occur? What are the dangers of HDN before and after birth? What is Kernicterus?
  10. When, during a pregnancy, could a mother become sensitized to her baby’s blood type? I thought mom and baby had different blood supplies and they don’t mix, so how does sensitization occur?
  11. Are there times when HDN can occur and it’s not because of Rh factor? When? Are these HDNs more or less severe than Rh-HDN?
  12. How can Rh-HDN be prevented? What do we inject? To whom do we give this injection? What does this antibody do? In what time frame must it be used and why?
  13. My baby was born with Rh-HDN, what will the doctors do to my baby once it’s born? What type of blood is transfused, and why should it be of the “negative" type?

White blood cells and the Immune system—Chapter 33 and 34

  1. What are Leukocytes and how are they different from erythrocytes.
  2. Of the WBC’s, which are classified as granulocytes, agranulocytes?
  3. Cite the major roles for each type of WBC and their descriptions. What is the relative frequency of each type of WBC in circulation? (Answer: use the mnemonic “Never Let Monkeys Eat Bananas”)
  4. Which of the leukocytes are phagocytes?
  5. What is inflammation? What is cell-mediated response to inflammation? What happens when these signals reach the multipotent stem cell in bone marrow?
  6. What is leucopenia? What is leukocytosis and leukemia? What could lead to these conditions? How is the patient treated?
  7. What is meant by immunogenicity and antigens?
  8. What are specific vs. non-specific defenses?
  9. Can one particular B or T cell fight many DIFFERENT types of antigens?
  10. What is cell mediated vs. humoral immunity?
  11. What are active vs. memory cells? Why are memory cells important in a secondary response to the same antigen?
  12. What are some physical characteristics of antibodies? What types of antibodies are there?
  13. What can antibodies do?
  14. How do T-cells help with immunity?

Thrombocytes and Hemostasis (notice, not “homeostasis”)

  1. What are platelets derived from? How many are there per ul/ whole blood? Where are they made?
  2. What are the major steps in the overall process of hemostasis? Differentiate between plug formation and coagulation (clot formation.) Are they the same?
  3. Is there homeostasis in the hemostatic balance? That is, is there a balance between clotting factors and anti-coagulants?
  4. What happens in the vascular phase? What prostaglandin is released that helps with vasoconstriction?
  5. What factors can activate platelets? What do platelets look like when activated? What is the role of thrombocytes (= platelets) in hemostasis? What important chemicals are contained within platelets?
  6. What happens in the coagulation phase? What two pathways could be activated in the coagulation phase? How does the extrinsic pathway get activated? What about the intrinsic? Which one is faster? Slower? Which one generates more PAS? What is the final common pathway of the cascade pathways?
  7. Notice the way enzymes are named. What can you say about enzymes whose names begin in “pro-” or end in “-ogen?” What is the enzymatic role of thrombin?
  8. Where are most clotting factors made? What vitamin is essential for synthesis of some of them?
  9. What is the action of factor XIII (fibrin stabilizing factor)? How does it work?
  10. What is the role of platelets in clot retraction?
  11. What is serum vs. plasma?
  12. Once a clot forms, then what must occur? How do we get clot removal? What is the role of plasminogen/ plasmin? On what does molecule does it act?
  13. What is the action of citrate, oxalate, coumarin and heparin? How do they differ in their mechanism of action? What would happen with vitamin K deficiency? Why does aspirin and NSAIDS cause more bleeding?
  14. What is a normal range of platelet counts? What is thrombocytopenia? What is the disorder “idiopathic thrombocytopenia purpura?” What physical symptoms develop in this condition?
  15. What is hemophilia? Discuss its mode of genetic transmission with regard to factors VIII and IX. What is meant by the term “carrier?”
  16. What is a thrombus? An embolus? How can they be treated clinically?
  17. What are the tests used to determine if someone’s intrinsic or extrinsic pathways are compromised?

Learning to Master “Relationship” problems