[Solved] NURS 3366Patho Test #1 Feedback Spring 2019

NURS 3366Patho Test #1 Feedback Spring 2019 NURS 3366 Patho Test #1 Feedback Spring 2019 Dear Patho Students, Test #1 grades have been finalized. You can look at your grades by going into “Check Your Grade.” Also, please read ALL of the following information carefully, even though it is a very long posting. Please refrain from talking about/sharing information about the tests and/or test-related document with anyone from outside the current Patho class…they may be future Patho students. Also, do not discuss tests AT ALL online. We count on students to maintain high standards of integrity. Some basic explanations: Each question was worth 2.5points. All grades will be carried out only to the second decimal by the computer for your final grade. UTA College of Nursing and Health Innovationdoesn’t allow further rounding (See your syllabus for more info on decimal points, etc.). As you probably already know, the letter grades that go with the numbers are: 90-100 = A, 80- 89.99 = B, 70 – 79.99 = C, 60- 69.99 = D, below 60 = F. The class averagewas ~ 76%, and the grades followed a standard distribution (bell curve). This is consistent with the grades earned in other online courses and in-seat classes where the average ranges from 72 – 78% routinely. The item analysis revealed no “stand-out” questions that were poorly written or understood by only a small number of you. Here is a review of the topics that you may have missed from this exam that you will want to review again for the comprehensive final exam: • Punnett squares and genetics (especially setting up a punnett square for an autosomal dominant vs. an autosomal recessive disease) • The patho of McArdle's disease and the role of glycogen and glucagon • Do you know your “g” words and what they mean? Glycogen, glycogenolysis, gluconeogenesis, etc? • Etiologies and sequela of hypoxia. • sequela of alcoholism and the nutritional deficits that are common to alcoholism and poor nutritional intake. • causes of acid-base imbalances, how to recognize acid-base imbalances using ABG values, understanding the compensation of acid-base imbalances. Do you know your fluid shift vocabulary? • recognizingcauses of fluid shifts and the resulting patient symptoms of edema and dehydration (and how to recognize these in patients- symptoms, using lab values), • sequela of electrolyte imbalances (sodium, potassium, and calcium). Which cause hyperpolarization? Hypopolarization? What symptoms go with each? • Common etiologies of cancer, characteristics of cancerous cells, and the role of free radicals. Can you recognize your cancer and altered cell vocabulary? • Do you know your “basic concepts” vocabulary?Iatrogenic, nosocomial, etiology, etc? Let’s look at these a bit further: • First of all, you will need to get used to “Multiple Answer” questions. You only had two on this test, but you will have a few more with each test that you take. What is the best approach to taking these questions? o Read the stem of the question very carefully. o As you read the answer choices, treat each one as a separate item. Cover all of the answer choices with your hand except the one you are looking at. Ask yourself: “is this “true” or consistent with what I am being asked in the stem of the question? If it is….then you may want to select it as an answer. o Multiple answer questions will appear on tests in nursing school, on HESI examinations, and on the NCLEX. For more information, check out this YouTube video at: • Y’all seemed to have trouble with one of the genetics question. Let’s review an example question. If we choose PKD as the disease, and I give you genotypes for the two parents, and then you will have to decide the percentage possibility of a child having the disease. To do this you MUST know which category PKD falls under. Is it one of the single-gene disorders: autosomal recessive, autosomal dominant, or sex-linked. See page 11 of RRD1 and also the concept map of genetic disorders. Each category has its own behavior. For instance, to figure out possible percentages of children that might have an autosomal dominant disorder, you look at the parents’ genotypes and assign a “big” letter to the gene carrying the dominant mutation and a “little” letter to the normal gene. If one of them is homozygous, for example, her genotype would be RR (using the letter “R” for “random disease” for now). If one of them is heterozygous, his genotype would be Rr. Then you set up a Punnett square: R R R RR RR r Rr Rr Let me ask you some questions: Since this is an autosomal dominant disease, which parent has the disease? Or do both? What is the percent possibility that a child born to them is homozygous? Heterozygous? Has the disease? Lastly, pretend this is an autosomal recessive disease and answer the same questions I just asked above. • Picture an alcoholic that hasn’t eaten in a while and is very underweight, confused, and you notice acetone breath. How can you answer a test question about this scenario? Ask yourself: How do these things go together? What are the links? How can I make a little concept map to help myself understand the concepts that will help with finding the right answers? o Ok, let’s see, a person who is alcoholic usually doesn’t eat properly and is therefore likely hypoglycemic, right? His body is most likely trying to compensate for this state of hypoglycemia—in other words, his body will try to find a source of glucose. Is glycogenesis (part of one of the possible answers) going to help? Why or why not? Will gluconeogenesis (part of another answer) help? Why or why not? • And then there is another question about anaerobic metabolism causing accumulation of HCO3? What is fundamentally wrong about this answer? Is HCO3 a byproduct of anaerobic metabolism? What IS a byproduct of anaerobic metabolism? • There was another question whose answers can be found by understanding the metabolic pathway and its disorders: If you are told a person is having trouble breaking down glycogen (glycogenolysis),(like what happens in McArdle’s) what medication would HELP them? Look at the concept map and see what hormone helps you to begin glycogenolysis. Some of you chose a hormone that would make this situation a lot worse. Hint: When will your body need to be able to break down stored glycogen as a compensatory response…if you are hyperglycemic or hypoglycemic? What hormone would make things worse if you are hyperglycemic? If you are hypoglycemic? • All right, now let’s relate some of the above to acid/base balance & ABGs… If too much HCO3 was indeed a byproduct of anaerobic metabolism, would you expect a person in anaerobic metabolism to have a pH of 7.55 or a pH of 7.25? Would he be in alkalosis or acidosis? What if instead, a byproduct of anaerobic metabolism was too much pyruvate? Would that person have a pH of 7.60 or 7.30? Would he be in alkalosis or acidosis? Find out which is correct about anaerobic metabolism by looking at the concept map, page 2. Also, look on page 24 of RRD. (Hint: is HCO3 a base or an acid? Is it base or acid that results from anaerobic metabolism?) • In one question, some of you chose aerobic metabolism as related to certain cellular metabolism disorders. Is aerobic metabolism normal / usual or abnormal/compensatory? • Re: hypo & hyper polarization, y’all did ok, but some of you are still obviously confused. Here is a little summary: (see more info starting on page 18 of RRD1) a) Solutes (such as, for our purposes, potassium, sodium, calcium)move by diffusion from an area of high concentration to an area of lower concentration. So if a person is hyperkalemic, for example,that means the blood (“emia” ALWAYS means “in the blood”) has more potassium ions (K ) than usual; so when the blood circulates to a cell, K moves from the blood into the cell, which had the “normal” number of K to begin with (and therefore initially had less K than the newly-altered blood numbers). b) When there are MORE cations than normal in a cell, that cell’s RMP will RESET to become a MORE positive number—say, from -90 mV to -60mV. This new RMP number is now closer to thedesired depolarization goal of ~ 30mV and because that “distance” is smaller than normal, this cell membrane is now HYPOpolarized. The significance in terms of S&S is that the patient’s cells will be hypersensitive—any smaller-than-normal stimulus can cause them to contract. Nutshell: MORE cations in cell = LESS “distance” to contraction point = HYPOpolarized membrane= HYPERactive cell (S&S of muscle spasms, cramping, etc). c) The opposite is true of when you have, say, hypokalemia: the blood has less potassium ions (K ) than usual; so when the blood circulates to a cell, K moves out of the cell into the blood, thusleaving the cell with LESS cations than usual. Nutshell: LESScations in cell = MORE “distance” to contraction point = HYPERpolarized membrane= HYPOactive cell (S&S of weakness, lethargy). • There was one fluid shift question that was an EXCEPT question. I think some of you may have missed it because you didn’t notice the EXCEPT. Always think about what your scenario patient “looks like”—all answers should jibe with that picture. In this case, three of the answers painted the same picture of the patient as being in a state of fluid abnormality, and a certain type of IV fluid should be used to help return the patient to normal. Would you give a bag of 3% NaCl to a patient who has edema and lung crackles, or to a patient with poor skin turgor and oliguria? Would you give a bag of 0.45% NaCl to a patient who has edema and lung crackles, or to a patient with poor skin turgor and oliguria? Hint: normal “salinity” of the blood is 0.9%...a bag of 0.9% NaCl would be isotonic to the blood. In which scenario would you give hypotonic fluid? Hypertonic? Think about what you want as the “helper.” Do you want fluid (H20) to go from blood to tissue or tissue to blood in order to fix this person? • Free radicals… read pgs 13 & 14 in RRD & look at #17 in Assignment 2. Some of you were confused as to: is superoxide good or bad? IE, would we want to give a patient some of it if we could? What about lipid peroxidation? Is that a good thing or a bad one? What about superoxide dismutase? Be sure you know generally what a free radical is, what kind of harm it does, and what we (or our bodies) can do to counteract free radicals. • If a surgeon did a biopsy on a “funny-looking” mole on your skin, what would make you happier when the biopsy report came back? A. “The cells were highly undifferentiated.” B. “The cells were quite well-differentiated.” What is the significance of differentiation of cells? (See RRD2). Now, here are some words of advice to consider If you made a grade from a 0% (because you missed the test) to a 50%, I strongly recommend you consider talking to your advisor about dropping the course.Earning a failing grade in patho carries significant consequences if you are eventually admitted to the CONHI, because a failing grade in patho is counted as one of the only two course failures you can have in the program. For more information, please speak with your advisor. If you did not do well on this test, I STRONGLY encourage you to re-assess your methods of studying and/or taking tests. Consider a CHANGE PLAN of some sort.Plan to be spending 12- 15 hours a week on learning the patho content. Carefully look for patterns in your studying and test-taking approaches that you can apply from here on. Move right along to studying the current material that will be on test 2… don’t dwell on test 1 material too much for now. You do need a general understanding of its concepts, as they appear again & again throughout the semester, but you will not actually be tested on specific test 1 material again until the final. However, do try to figure out what you can change about how you take the next tests. I always receive post-test emails asking about ways to improve success at studying and taking tests, ie, how to go about making a CHANGE PLAN. Much of what I have to offer in the form of advice is in the "How-to Manual" that was given to you on the first day & is also available to download, if you have lost your original copy. If you have not read that document, I suggest that you do so. A review of some key points: 1. Get started on each week's RRDs right away. Look over any concept maps that are posted and concurrently review the prep for any A&P info you may not understand, especially info that has special relevance and/or emphasis in the notes. Listen to the podcasts. 2. Answer your RRD Assignments as if they were a test (rather than concurrently as you read the RRDs). Enter your answers on the BB assignment page and check your score. Review the A&Rs when they are sent out. Make more CTQs for yourself by turning the given ones around in various ways. Have a study buddy make some more CTQs & vice versa and quiz each other. 3. Verbalize concepts out loud; link concepts together as much as possible; approach “ from the front door” and then “from the back door.” 4. Make concept maps for each lecture topic or section. After studying the concept map you made for the current lecture, go back to previous ones you made and review them too--that way you are constantly refreshing yourself on previous information. 5. Consider using Q or the Cornell 5 day study plan to help you get ready for the next exam: A last word: if you did badly on this test, DO NOT GET DISCOURAGED. Just find out what went wrong and try to fix it. I have seen many, many students who make a 65 or greater on the first exam rally very successfully.