NURS 3366 PATHO ASSIGNMENT #1 (GRADED A) ANSWERS & RATIONALES | Download To Score A

1 Basic Concepts of Pathophysiology & Implications for Nursing Questions 1 & 2 below refer to the following situation: A 55-year-old man with emphysema (a type of chronic lung disease) who has sm oked 2 packs of cigarettes per day for 40 years is hospitalized for acute onset of cough productive of bloody sputum (sputum=secretions from deep in the lungs). After a few days of testing and treatment, the patient’s nurse reads a physician’s note on the chart: “I have told the patient that the etiologies of his hemoptysis are: 1) exacerbation of his chronic emphysema and 2) the new diagnosis of lung cancer. The onsets of both were contributed to by his longstanding smoking.” 1. The patient asks the nurse for more information. Which of the following explanations to the patient best indicates a full understanding of the patient’s situation? a. “You have a disease process that was iatrogenically caused by cigarette smoking.” Incorrect: “iatrogenically” means caused by a medical person. b. “You have a sudden onset of a chronic lung disease that was brought on by lung cancer.” Incorrect: the chronic lung disease was part of the medical history of the patient; the term “chronic” means a long-standing disease, not a “sudden onset.” c. “The coughing up of blood is caused by a worsening of a disease you’ve had for a long time plus a new problem-- lung cancer.” d. “These diseases have been creeping up on you for probably 20 years; it just goes to show that you should never have taken up smoking.” Incorrect: no evidence in the scenario to support this sentence. (Besides, it sounds very judgmental.) 2. Based on all the information you have on the patient, which statement is most likely correct? a. The patient has a poor prognosis because of the comorbidities of lung cancer and cigarette smoking. Incorrect: Smoking is a risk factor not a disease that would fit the term “comorbidity.” b. Lung cancer was a sequela of the bloody sputum. Incorrect: the bloody sputum was part of the S&S of cancer; this answer implies the bloody sputum caused the cancer. c. A precipitating factor for the acute hospitalization was overexertion when the patient started an exercise class. Incorrect: no evidence in the scenario to support this sentence. d. Heavy cigarette smoking was a risk factor in the patient’s developing emphysema and lung cancer. 2 Questions 3 & 4 refer to the following situation: An 80-year-old patient is in shock from loss of blood following an accident. His vital signs are: BP 80/50 (normal ~ 120/80), HR 120 (norm = 60-100), RR 20 (norm = 12 to 20), T 98.6 (norm ~ 98.6). 3. In assessing this patient, the nurse understands that the abnormal HR is a. probably the etiology for the patient’s low BP. Incorrect: the shock is due to the “loss of blood.” A state of shock has a “big picture” of low BP, high HR, cool hands, weakness, feeling faint, and/or passing out. In this context the high HR doesn’t CAUSE the low BP. b. due to the patient’s heart compensating for low blood volume by pumping faster. c. the normal compensatory response of shunting blood volume to the periphery. Incorrect: shunting blood to the periphery IS a compensatory response, but it is a “co-response” with high HR; one doesn’t cause the other. d. due to multiple risk factors. Incorrect: no evidence in the scenario to support this sentence. (TIP: when you are deciding on answers, plug them each into the stem of the question & ask yourself if it makes sense. Ex—does this sentence make sense? “In assessing this patient, the nurse understands that the abnormal HR is due to multiple risk factors.” Hopefully you see that no, it doesn’t make sense.) 4. The patient would also most likely have all of the following EXCEPT a. S&S of cool feet and hands from the body’s compensatory response to shock. b. S&S of feeling faint and weak from blood loss. c. a risk factor of shock. In an except question, remind yourself that 3 things go together. The 4th one is the one you choose—it doesn’t fit. d. a more guarded (ie, “poorer”) prognosis because of his age. 5. A young, otherwise healthy patient is admitted to the hospital with a diagnosis of heart failure of unknown cause. The etiology of the heart failure would be termed a. iatrogenic. b. idiopathic. c. nosocomial. d. acute. 6. To do well in this course, a student should a. memorize the notes thoroughly. Incorrect: memorize only a few things that are unavoidable. Otherwise, study concepts and contexts! b. be able to apply concepts to different situations. c. begin each assignment Wednesdays at 7am. Incorrect: you should begin and try to finish assignments way before an hour before they are due! d. hurriedly take tests one hour before their stop-time. Incorrect: you should begin and finish tests way before an hour before they are due! Questions 7-10 refer to the following situation A 55 year old male is in the ER having a myocardial infarction (heart attack, AKA “M.I.”), which is caused by coronary arteries that are clogged with fat and narrowed so that not enough oxygen–rich blood is getting to his heart. He admits that his daily nutrition is poor, consisting mainly of high-fat fast food. He has a family history of cardiac disease-- his father had a heart attack at age 46. The patient is obese and is a heavy cigarette smoker-- 2 PPD (packs per day). The patient said he had decided to take up jogging today and after a few minutes began having chest pain, nausea and shortness of breath. He went to the ER and was noted to have profuse diaphoresis (heavy sweating), tachycardia (rapid heart rate), and significant changes on his electrocardiogram (ECG or EKG). The patient recovers from this acute heart attack but his heart is so damaged that subsequently he has many episodes of congestive heart failure and many hospitalizations. 3 7. Without even having further knowledge of course material related to MI’s, you can tell a lot about the scenario from careful reading and knowledge of basic patho verbiage. Example: The paragraph above suggests that the direct pathophysiologic etiology of the heart attack (MI) is most likely related to a. not eating green vegetables. Incorrect: not eating nutritiously is not a DIRECT patho etiology; we do have a hint that he has a risk factor of eating unhealthily (fast food), but don’t “overthink.” b. congestive heart failure. Incorrect: heart failure is a sequela in this context. c. lack of oxygen that narrows the coronary arteries. . Incorrect: the scenario tells you that the MI is “caused by coronary arteries that are clogged with fat and narrowed so that not enough oxygen–rich blood is getting to his heart.” It doesn’t say that oxygen causes the narrowing, which is what this answer says. d. oxygen not reaching tissue that is distal to narrowing of the coronary arteries. See sentence above… also, you are asked to use the knowledge from the RRD about what the term distal means. (See top of page 5 of RRD 1 for reviewing that info) 8. In reading the paragraph above, it is easy to find 4 risk factors—things that “set the stage” for this patient to have a heart attack. They include all the following EXCEPT a. being a heavy cigarette smoker. b. having profuse diaphoresis. This is the correct choice, because it is one of the S&S, not a risk factor. c. a parent with heart disease. d. high-fat diet. 9. Which mini-concept map do you think best describes accurate linkage between underlying pathophysiology and signs and symptoms (S&S) described in this scenario? a. Jogging increased heart rateblood pumped throughout body fastertissues (including lungs and stomach) receive too much bloodpatient complains of shortness of breath and nausea. Incorrect: there is nothing about this situation that implies that “too much blood” is being pumped to the organs. b. History of heart disease in familypatient worries about it constantlybecomes anxioussmokes too muchnicotine causes narrowing of all arteries in body, including coronariesheart attack from narrowed coronaries. c. High levels of fat in the blood from high-fat dietclogs in coronary arteries develop over time oxygenated blood cannot get to distal tissues of heartunoxygenated tissues “cry out” (send pain messages to brain)  patient complains of chest pain. d. Obesity increased pressure on diaphragmbreathing becomes more difficultshortness of breathless oxygen EKG changes. 4 10. A sequela of the MI was a. having to be hospitalized frequently because of problems associated with the damaged heart. b. having to be hospitalized frequently with repeat heart attacks. c. needing to jog more often. d. continuing to smoke 2 PPD. 11. The most likely sequela of not submitting a weekly assignment by Wednesdays at 8am is a. being allowed to submit the assignment later because you had a bad cold during the days leading up to the assignment due date. Incorrect: if a student waits till the last minute to submit an assignment, there is increased risk of something going wrong, such as not feeling well. b. getting a zero on that assignment. (If there are special, urgent contingencies, especially ones that have documentation, a student may email before the due date to explain why he or she cannot get the assignment in on time. The excuse may or may not be accepted and extra time may or may not be allowed, depending on the circumstances.) c. instructor’s lack of concern, because you will be able to drop the lowest assignment grade. Incorrect: no assignment grades are dropped d. being allowed to submit the assignment later because you thought it wasn’t due till the next day. Incorrect: In this course there are many reminders of due dates and consequences of not getting assignments and tests in on time. To be considered for late submission, a student needs a documented, urgent excuse. 12. At the end of the semester, a student has a total assignment average grade of 100% and a 69.7% total test average grade. What grade did the student make for this semester (see syllabus)? a. 84.85% (B) b. 69.7 % (D) (See box on last page of Course Overview or look in your syllabus) c. 71.43% (C) d. 93.03% (A) 13. Student Katniss Everdeen has been submitting her assignments and tests before the deadlines and making good grades. One day during an unexpected storm, her internet connection goes down in the middle of a test. Since she is a consistently focused and dedicated student, what action do you think she will take? She will a. email her coach that “A pack of wolfmutts attacked and ate my computer. Can I take the test tomorrow?” b. resign herself to getting a zero, since she didn’t read the procedures in the syllabus and Course Overview. c. take the test the next day, since she knows that multiple test entry and submission is allowed. d. immediately email her coach, instructor, and tech support with a detailed report of what happened. 5 14. After not eating since breakfast 6 hours ago, a student taking a test notices a period of hunger and fatigue. He doesn’t have access to food because he is taking the test. About 10 minutes later, though, he begins to feel ok again and finishes the test with flying colors. What has happened in his body? a. A compensatory response called glycogenolysis allowed him to access stored glucose for energy. b. A decompensatory response occurred, in which adrenalin increased and caused more blood flow to the brain. c. Since his blood sugar was likely low, the heart underwent a compensatory response known as hypertrophy in order to increase blood flow to central organs. Incorrect: An acute hypoglycemia will not cause the heart to increase in size. Hypertrophy is a compensatory response that usually occurs over time. d. Using a control mechanism known as hyperventilation, the student was able to “blow off” excess CO2 and thus have a clearer thinking process. Incorrect: Often if a person hyperventilates, acid/base balance is thrown off (causing respiratory alkalosis) and this certainly would not help the thinking process. 15. Which sets of sentences match each other correctly? a. After several days of little sleep a student’s cold turns into pneumonia. Insomnia is a precipitating factor for the change. b. A person with a chronic lung disease gets pneumonia. The pneumonia is considered an acute illness. c. Freshly oxygenated blood flows from the aorta through coronary arteries to various parts of the heart muscle. Blockage in the coronaries would cause decreased oxygenation in the cardiac muscle tissue proximal to the blockage. Incorrect: The correct answer would have said “distal” to the blockage, meaning “beyond” the blockage. d. A and B. Genetic Influence in Disease 16. A child is born to a couple, one of whom is heterozygous for an autosomal dominant disease. The other parent is homozygous normal. What would be the child’s chances of having the disease? (Use a Punnett square to figure this out). a. 0% b. 25% c. 50% Heterozygous for autosomal DOMINANT: Dd (with the “big D” being the BAD gene). Homozygous normal: dd (normal gene in these disorders is the “little,” recessive gene—just the opposite of autosomal recessive diseases.) So do Punnett square and the possible kids’ genotypes are: Dd Dd dd dd. With homozygous dominant disorders, if you have a “big letter” in the genotype, you WILL have the disease. d. 75% 6 17. A child is born to a couple, one of whom is a carrier for a sex-linked recessive disease. The other parent has the disease (“having” the disease means the phenotype is seen—ie, S&S). What would be the chances that the couple has a child with the disease? (Use a Punnett square to figure this out.) a. 0% b. 25% c. 50% In sex-linked diseases, ONLY the woman can be a carrier, so you know that it is the mom that has the genotype of XGXg (in any kind of recessive disorder, the “little” letter—the recessive gene—is the BAD gene and the big letter is the NORMAL gene, so this woman does not HAVE the disease, since the “big” dominant NORMAL gene is overcoming the recessive BAD gene). The dad, then, HAS the disease, so we know he MUST have the little recessive, BAD gene on his X chromosome (part of the definition of a sex-linked disease is that it is interchangeable with “X-linked”). So his genotyped is XgY. Punnett square: XGXg (female carrier—won’t have disease). XgXg—female WITH the disease (a bit unusual—stats show males get the disease much more often), XGY (male with normal genotype), XgY (male WITH the disease). d. 75% 18. In the question above, what are the chances that the child will be a carrier? a. 0% b. 25% (see explan. above) c. 50% d. 75% 19. An RN is taking care of a cocaine addict who has just given birth to a baby with a teratogenic defect. A student nurse asks him what the probable etiology was. The RN shows understanding of genetic disorders when he says a. “It’s hard to know the exact cause, but it’s likely that fetal chromosomal development was impaired by the mom’s intra-pregnancy cocaine ingestion.” b. “The baby inherited a structural chromosomal defect that resulted in a problem called aneuploidy.” Aneuploidy is a problem of numbers, not structure. Also, this question is linking teratogenic defect to intra-pregnancy issues, not inherited one such as suggested in this answer. c. “The baby inherited a gene that caused a defect called trisomy 21.” A single gene doesn’t cause trisomy 21—an extra chromosome does. Also, this question is linking teratogenic defect to intra-pregnancy issues, not inherited one such as suggested in this answer. d. “Since the little guy was born with the Philadelphia chromosome, he will be a life-long Phillies fan.” 20. A child with sickle cell anemia presents with pain all over, especially the joints. Which of the following best links the patho with S&S? a. Cyst formation in the kidneys leads to blood spillage from the circulation into the urine, thus causing anemia. This sentence might be correct if we were talking about PKD. b. A single-gene mutation causes malfunction of genetic coding for clotting properties, leading to bleeding and ischemic pain of the joints. This sentence might be correct if we were talking about hemophilia. c. Chromosomal aberrancy causes malformation of RBCs in the blood supply to the joints and subsequent pain due to lack of oxygen. This is kind of a hodge-podge answer that is incorrect. d. A single-gene mutation causes malfunction in RBC O2-carrying capacity, leading to ischemic pain in the joint tissues. 7 Questions 22-26 are based on this scenario: A 25-year old pregnant women voices concerns about the genetic health of her fetus because she has sickle cell disease. Her husband has been genetically tested and has a heterozygous genotype. Tips: The questions assume that you are taking the following critical thinking steps: • You read the question and by knowing (from your readings) that sickle cell disease is an autosomal recessive disease and thus has a certain pattern of inheritance (do your Punnett square work below) • You know that in most genetic diseases, the gene that has been mutated will not code properly for certain proteins that are important for certain normal functions. You will ask yourself, in sickle cell, how does the mutation lead to the phenotype, ie, the signs and symptoms? First figure out the Punnett square for this couple (blue highlight) & then the possible kids’ genotypes (yellow) — (use the letter “s” for the parents’ genotypes—stands for sickle cell; see pgs 50-51 as needed): s 21. Mom’s genotype is a. ss b. Ss c. SS d. none of the above. 22. Which is true about the dad? a. His genotype is ss. b. He is a carrier of sickle cell. c. He likely has the typical S&S of sickle cell. d. All of the above. 23. What is the percent possibility of this couple’s child having a completely normal genotype? a. 0% (“SS” would be completely normal in this situation and it is not possible with these parents) b. 25% c. 50% d. 100% 24. What is the percent possibility of this couple’s child having sickle cell trait? a. 0% b. 25% c. 50% Having the trait means that the genotype is exactly the same as a carrier, but normally when you are a carrier, you have NO S&S of the disease. Rarely, the “small, bad guy” gene “peeks out” and the person will have some S&S which are usually milder than that of the full blown genotype, ss. d. 75% 25. What is the percent possibility of this couple’s child having the disease, sickle cell anemia? a. 0% b. 25% c. 50% (“ss”) d. 75% 8 26. The parents of a new baby with Down’s syndrome ask their nurse what to expect. She bases her answer on her understanding that the child will have a. developmental problems brought on by a sex-linked monosomy. This answer has several things wrong, including that Down’s is a chromosomal polysomy, not a single gene disorder. b. developmental problems brought on by the pathologic interaction of 3 chromosomes where there should be only two. c. a phenotype based on defective mitochondrial protein synthesis that created aneuploidy. This answer has several things wrong, including that Down’s is a nucleic problem, not mitochondrial. d. the phenotype of diminished IQ and physical differences that are caused by a single-gene disorder. The first part matches; the second part doesn’t. 27. A person has hemophilia. Which is the correct genotype? a. HH This would be a normal genotype in the context of an autosomal (not sex-linked) recessive disorder. b. XHY This would be a normal genotype in the context of sex-linked disorders. c. XhY This is a classic genotype for a sex-linked single-gene disorder, which hemophilia is. d. hh This would be the correct genotype for someone who has an autosomal (not sex-linked) recessive disorder. 28. The phenotype of the person in question 27 includes having ________ because _. a. joint pain : the gene that codes for coagulation factors is defective, causing easy bleeding into the joints. b. joint pain : the joint tissue is oxygen-starved due to deformed hemoglobin in the RBCs. This would be correct if we were talking about sickle cell anemia. c. simian facial features : hemophilia is a teratogenic disorder caused by maternal alcohol abuse. d. severely shortened arms and legs : a drug called thalidomide caused the mutated genotype. Intracellular Function and Disorders Questions 29-31 apply to this scenario: The parents of a five year old girl complain anxiously to her pediatrician that in the last couple of weeks, no matter how much she eats, she keeps losing weight. She appears quite thin, well below her normal weight. Her blood sugar is 300 (normal range 75-110). She is diagnosed with Type I diabetes mellitus (DM 1). 29. In this scenario, the explanation that bests links pathophysiology with S&S in this child is that in DM1, the pancreas a. quits producing glucagon so that glycogen stores are inaccessible, thus causing weight loss. b. increases insulin production so that glucose stays in the blood, causing hyperglycemia. c. quits producing insulin so that glycogenolysis is stimulated and too much glucose enters the blood. Glycogenolysis is stimulated by the hormone glucagon when the body in HYPOglycemic. In DM & in this scenario, the patient is HYPERglycemic. d. quits producing insulin so that glucose cannot be used as energy in the cells, thus causing the body to burn up fat and protein for energy. 9 30. If ABGs were done on this patient, you would expect all the following EXCEPT: a. a blood pH of 7.32 because sustained gluconeogenesis causes acidic byproducts to accumulate. b. a HCO3 of 20 because the high numbers of acids in her body “take over” and “overcome” the HCO3, which then diminishes in number. c. a HCO3 of 30 because the low numbers of acids in her body stimulate increase in HCO3. If you chose this one you were likely overthinking. The others all fit metabolic acidosis. d. this acid/base imbalance to be called metabolic acidosis because it is an acidotic state caused by a metabolic disorder. 31. This girl’s body needs to compensate for the acid/base imbalance noted above. Knowing that the lungs will compensate when the “metabolic” side is “sick” and the kidneys will compensate when the lungs are “sick,” which compensatory response would you expect? a. Hyperventilation --increased respiratory rate (RR)-- to “blow off” CO2; this is the lungs’ way to get rid of acids. b. Hypoventilation—decreased RR-- to “hold onto” CO2, since CO2 is an alkali that will counteract the acidosis. CO2 is an acid… it will make acidosis worse. c. Kidneys will excrete more HCO3 into the urine to get rid of acidic byproducts. Remember the kidneys are considered “sick” in metabolic problems and therefore cannot help. d. By hyperventilating and blowing off CO2, the body will bring the pH down to normal range. The lungs will indeed blow off CO2, and acid, which will bring pH UP to normal range, not DOWN. Ex—it will bring 7.32 up to 7.38. 32. A child accidentally ingests an insecticide with the ingredient cyanide. Knowing that cyanide suppresses the actions of cytochrome oxidase in the electron transport chain, what signs might an RN expect and why? (see page 2 of metabolic pathway concept map) a. Ketonuria due to increased glycogenesis. Gluconeogenesis has byproducts of ketones; glycogenesis does not. But neither have anything to do with this scenario. b. Confusion due to glycolysis. Glycolysis is the normal first step inside a cell of all glucose molecules in the metabolic pathway, so it’s a normal process & doesn’t cause confusion. c. Mild euphoria due to enhanced production of ATP. Anything that suppresses cytochrome oxidase will also SUPPRESS, not ENHANCE ATP. d. Shortness of breath due to decreased ATP to use for the work of breathing. 33. A patient with a serum calcium of 6.0 (norm = 8.5- 10.5) is most likely to because . a. be lethargic: the cells are hypopolarized. b. have muscle spasms: more Na+ has entered the cells. The state of being hypocalcemia causes cells to be more permeable to INFLUX of Na+ increases cations in cell increased positivity of the RMP moves RMP electrical setting closer to the “goal pole” of +30mV hypopolarization pathologically less time/distance to reach depolarization cells are hypersensitive & may spasm. c. be weak: more Na+ has left the cells. d. have hyperirritable muscles: the cells are hyperpolarized. 34. A patient has been vomiting copiously for 3 days. He is probably in because . a. metabolic acidosis : vomiting often leads to hyperventilation. b. respiratory alkalosis : vomiting often leads to hyperventilation c. metabolic alkalosis : vomiting of the normal acidic digestive secretions of the stomach eventually depletes the body’s acids. d. metabolic acidosis : vomiting of the normal acidic digestive secretions of the stomach eventually depletes the body’s acids. 10 Questions 35-37 apply to this scenario: A 78 year old patient with cancer of the esophagus has not been able to eat, has lost 80 pounds and appears cachectic (extremely thin & wasted; the noun is cachexia). He is struggling to breathe, is very weak, and has generalized edema. His breath smells fruity, like acetone. He has an oxygen (O2) saturation level of only 80% (normal is 98 to 100%...less than 95 means patient’s cells are probably becoming hypoxic). His pH is 7.14 and HCO3 18. (normal HCO3 is 24-28) 35. What acid/base imbalance is he in? a. respiratory alkalosis. b. metabolic alkalosis. c. metabolic acidosis. Low ph = acidosis; low HCO3 = metabolic. d. respiratory acidosis. 36. Link aspects of his clinical presentation to the pathophysiology underlying them. a. Patient can’t eat hypoglycemiainsulin secreted from pancreas triggers glycogenolysis as a back-up plan  raises blood sugar but byproducts include ketones. b. Difficulty breathing increased metabolic needsuses up all energy sources body begins to use HCO3 as source of energyHCO3 depleted HCO3 decreases to 18, causing pH to increase from normal to 7.14. Tip: even if you weren’t sure about everything else, the part of the answer that should stand out as wrong is the fact that if HCO3 decreases (ie, “the alkali guy” decreases), then acidity will INCREASE and the pH will go DOWN even more, not INCREASE. c. Chronic illnessincreased stressincrease in counterregulatory hormonesglycogenesis triggeredtoo much glucose being stored rather than being readily availablecachexia. d. Given the description of the patient's debilitated state, he is probably in sustained gluconeogenesisgives energy but also increases accumulation of ketones  body tries to get rid of them via many ways, including as acetone in the breath. 37. A scene in the ER: A CIA operative who has had no previous medical history presents with initial complaints of nausea, vomiting, severe weakness. Now he is also short of breath. His pH is 7.20 and his HCO3 is 17. What is most likely going on in his body? a. Poisoning (by an enemy spy) cellular hypoxiacells must repeatedly go through anaerobic glycolysis to gain some ATPSincreases pyruvatelactic acidosis metabolic acidosis. Normally, when there is plenty of O2, the first step in breaking down glucose is AEROBIC glycolysis. But if there is not enough O2 (hypoxia), the back-up system is ANAEROBIC glycolysis, whose downside is accumulation of acids. This can cause acidosis. Because a metabolic reason caused this (the poisoning) and not a respiratory problem like hypercapnea (retention of CO2), metabolic acidosis would be the end result. Also, as soon as you see that the HCO3 is out of normal range, you KNOW the problem is metabolic. b. Poisoning (by an enemy spy) hypoxiacells must continuously go through aerobic glycolysis instead of continuing down normal metabolic pathway low ATPSrespiratory acidosis. Aerobic glycolysis is normal, so this doesn’t fit. c. Gastrointestinal flu can’t eat low blood sugarglucagon secretedtriggers glycogenolysis glucose released into blood, but also there are acidotic byproducts that must be countered by more HCO3increased alkalinitymetabolic alkalosis. This is a hodge-podge that doesn’t make a lot of sense. d. Job stresslow oxygenation body compensates by increasing respiratory rate (hyperventilation) too much CO2 blown off respiratory alkalosis. A CIA operative would have a lot of job stress, and anxiety does cause respiratory alkalosis, but the low pH and low HCO3 point to metabolic acidosis. 11 38. A patient in the ER is about to get a laceration stitched up. First the ER nurse practitioner (NP) will infiltrate the area with Lidocaine, a drug that will prevent the patient from feeling pain as the stitches go in. The medication’s mechanism of action is to change the permeability of nerve cell membranes so that they decrease the number of Na+ ions that are normally allowed to come into the cell. Using critical thinking and knowledge of RMP issues, what do you think is the next step? a. The nerve cells in the area become filled with anions and the RMP is reset from -90mV to -60mV. b. Because of the increased influx of cations, the local nerve cell membranes become more positively charged. c. Because of the decreased influx of cations, the local nerve cell RMPs will be reset from -90mV to -120mV. Less-than-normal Na+ enter the cell, thus causing the RMP to be more negative (-120) d. The sodium/potassium pump of the cell membranes will cease to work properly, and the cells will become incapable of holding their normal RMP charge. 39. Link the correct answer in question 39 with the effect of numbing the skin in the area to be stitched. a. Since the RMPs of the area nerve cells are now more positively charged, they are hypopolarized and therefore will conduct pain sensations very slowly or not at all. b. Since the RMPs of the area nerve cells are now more negatively charged, they are hyperpolarized and therefore will conduct pain sensations very slowly or not at all. The RMP setting of -120 is now “further away” from the “goal pole” of +30mV. The process of depolarization & “doing its job” is now much slower for the nerve cell, to the point of very sluggish pain signals to the brain…. thus the area is anesthetized. c. Since the RMPs of the area nerve cells are now more negatively charged, they are hypopolarized and therefore will be so hyperactive that pain sensation will be negligible. d. Since the RMPs of the area nerve cells are now more positively charged, they are hyperpolarized and therefore will conduct pain sensations very slowly or not at all. 40. Patho student Haymitch Abernathy spent 4 days in the hospital with pancreatitis. He gets out on a Wednesday evening feeling much better but knows he missed the 8am deadline for weekly assignment submission. What should he do, according to course policy? a. Send an email to the instructor and his coach right away to explain about his hospitalization, understanding that excuses must be offered within 24 hours after the deadline. b. Scan his doctor note and email the copy to his coach and instructor. c. Opt to use this assignment zero score as the one grade he can drop at the end of the semester. d. A and B. Alterations in Fluids and Electrolytes 1. Remember the patient in Assignment #1, with cancer who can’t eat and has lost 80 pounds? Let’s add to his assessment findings: let’s say he has generalized edema and a serum protein of 4gm/dl (normal = 6.0 to 8.3 gm/dl ). Which is the most accurate mini-concept map linking low protein with edema? a. hypoproteinemia concentration in blood is now lower than the normal concentration of fluids inside cells fluid goes from B to T. b. hypoproteinemia concentration in blood is now higher than the normal concentration of fluids inside cells fluid goes from B to T c. hypoproteinemia blood is now hyperosmolar compared to the cells  fluid goes from T to B d. hyperproteinemiablood now has lower oncotic pressure than normal fluid goes from T to B 2. All of the following are accurate possible findings in the patient above EXCEPT that a. he has confusion due swollen brain cells. b. he has crackles in his lungs from fluid in the alveoli (lung tissue). c. his serum osmolality is 302 (norm = 280- 295). d. he will need a hypertonic IV solution to return fluid status to normal. Rationales for questions 1 & 2: After something has changed the concentration status of the blood, figure out which has the higher concentration of solutes. Does blood (B) now have a higher concentration than tissue (T)? Or does T now have a higher concentration than B? Fluids will always move by the principle of osmosis TOWARDS the higher concentration, higher osmolality, higher tonicity, higher oncotic pressure, etc (all these terms have the same PRINCIPLES driving them.) Remember: CONCENTRATION CALLS! and OSMOLALITY ORDERS! In this question, proteins in the blood have diminished, so the blood has become LESS concentrated than normal, ie less concentrated than the tissues, which INITIALLY are normal concentration. But when the CHANGED blood (now HYPOproteinemic compared to the tissues NORMAL protein levels) gets to the tissue, an osmotic shift BEGINS. That shift will be that fluid will be “called in” to the higher concentration—the TISSUE in this case. So with fluid going INTO the tissues, you then develop edema, which explains the next question….“Swollen” brain cells means edema in the brain; crackles in the lungs means edema in the lung tissue; a hypertonic IV is appropriate to help REVERSE edema (this treatment will quickly change the blood concentration to hypertonicity --B more concentrated than T now—so that water will COME OUT of cells). So, C is the OUTLIER—remember, this is an EXCEPT question, so C, with its HIGH osmolality is the one that doesn’t fit with the rest. Summary: A, B, D all fit with this scenario and C does not, so C is the answer. 3. A 28-year-old man presents with a low blood pressure due to blood loss from a gunshot wound. The regulatory action that will best compensate for this patient’s fluid volume deficit is: a. increased action of the natriuretic peptide system. b. increased action of the RAAS. c. inhibition of renin secretion. d. conversion of aldosterone into angiotensin II. 4. As a result of the action in the previous question, all the following will occur EXCEPT: a. the patient’s body will “hang on” to fluids. b. Na+ will be retained by the kidneys. c. water excretion into the urine will increase. d. blood pressure will increase. Rationale for 3 & 4: When there is a diminished blood volume (fluid volume DEFICIT) sensed by the kidneys, they respond by secreting renin; renin stimulates the secretion of aldosterone from the adrenal cortex aldosterone “tells” the kidneys to hang on to Na by not excreting it in the urine & instead keeping it in the blood stream when the kidneys hang on to Na, H2O follow. As a result of hanging on to H2O in the body, urine output is DECREASED and blood volume is INCREASED. Also, renin stimulates the process of angiotensin II creation; angiotensin II constricts blood vessels in the periphery blood volume that normally circulates out to peripheral vessels is decreased due to the constriction, so that a larger part of the blood volume can be shunted to the central areas where it is most needed—heart, lungs, kidneys. So in essence the main, most important circulatory areas have a compensatory increase in volume (and a much needed increase in blood pressure), whereas the periphery gets a decrease (that’s why this patient probably has cool & pale hands & feet). Answer 3A is wrong because the natriuretic system kicks in when the heart senses an excessive amount of volume returning to it atrial natriuretic peptide or b-type natriuretic peptide is secreted by the heart & the kidneys respond by increasing urination, therefore reducing the fluid volume; a reduction in blood volume is NOT what this person needs! Inhibition of renin secretion (3C) is the opposite of what is needed in this case. 3D is wrong because aldosterone doesn’t convert into angiotensin II (be sure you know the basic steps of the RAAS). The explanation above should answer the “why” of question 4. A,B,D are all applicable to this scenario. C is the outlier, so it is the correct choice (As discussed above, part of the RAAS is to have aldosterone “tell” the kidneys to hang onto Na+, thus ALSO hanging onto water—keeping it in the blood-- instead of excreting in the urine). PEARL OF WISDOM: Any time you have a PROBLEM and then a COMPENSATION for the problem (just like when you are figuring out acidosis/alkalosis & compensations), be sure you clearly separate them in your mind: “Here’s the problem and what caused it. THEN here’s the body’s compensation for that problem. Or if you are given a scenario with the compensation, be sure you can trace it back to the problem… that’s called studying from both the “front door” and the “back door.” See the How-to” manual if you need more study tips like that. (Normal labs: Na+ = 135 to 145; K+ = 3.5 – 5.0; osmo = 280- 295; HCO3 = 22-28). 5. A patient is hospitalized in renal failure. Because of her kidneys’ inability to excrete water, she has generalized edema & a serum sodium of 129. Because the kidneys have also lost the ability to appropriately regulate potassium, she also has a serum potassium of 5.9. These lab results show: a. hypernatremia & hypokalemia. b. hyperkalemia & hyponatremia. c. hyperosmolality & hypernatremia. d. hypoosmolality & hypocalcemia. 6. In the previous question, the edema is most likely due to fluid shifting from the intravascular space into interstitial spaces secondary to all the following EXCEPT: a. hypertonicity of the plasma space. b. hypotonicity of the plasma space. c. hypoosmolality of the blood. d. diminished osmotic pressure of the blood. Rationale for #5: Na levels < 135 = hyponatremia, or “low sodium in the blood,” and K levels > 4.5 = hyperkalemia, or “high potassium in the blood.” Therefore answers A and C cannot be right, since they mention hypernatremia. And D is wrong because nothing in the lab results that I gave you in the scenario relates to calcium, so hypocalcemia is not correct. Pearl: Be sure to read your scenario thoroughly to understand what information you are given. But also don’t read anything MORE into it. Rationale for #6 In the beginning scenario you are told that the Na is low in the plasma space—serum Na of 129 (remember that the plasma space is also called “the blood,” the “intravascular space,” the “vasculature,” the “vascular space,” and so forth), so you already know that the patient is hyponatremic, which correlates with HYPOtonicity, not HYPERtonicity (answer B). When you are given a scenario in which the patient has edema, always correlate this with FLUID VOLUME OVERLOAD—picture a patient who for some reason (in this case “sick kidneys” which aren’t getting rid of H2O properly) has extra water in the blood, thus diluting it & decreasing its concentration—this goes along with decreased osmolality (C) and diminished osmotic pressure (D). Thus B, C, D go together, and will cause fluid to shift into the tissues, causing edema. [Remember, the tissues will initially be NORMAL in their osmolality & tonicity, therefore, their concentration is now greater than that of the blood, so according to the rule – CONCENTRATION CALLS—the tissue cells will pull water into them from the blood (“B to T”), causing edema.] Answer A is the outlier in this EXCEPT question, thus it is the correct answer. Pearl: Draw pictures! Now, did you see the similarities in questions 1,2, 5, & 6? In one way or another they ALL resulted in LESS concentration in the blood, thus the patient pictures were ultimately similar. Same thing with questions 7, 9-11, and some of the ones in question 14. Think about their commonalities and then think about situations that would be the opposite. 7. A patient has advanced liver disease. Blood tests reveal that his serum albumin (albumin is one of the protein molecules found in the blood) level is very low. What eventually happens in this patient situation? a. Water would shift from blood (B) to tissue (T) because of decreased plasma oncotic pressure. b. There would be an increased intravascular volume due to increased plasma oncotic pressure. c. There would be dehydrated brain cells due to fluid shifting from T to B. d. Water would shift from T to B because of increased osmolality of the vascular space. 8 The physiologic process underlying fluid shifts in the patient situation above is that a. “concentration calls” fluid into hypoosmolar compartments from hyperosmolar ones. b. the principle of diffusion results in albumin molecules going from lower to higher concentration. c. “concentration calls” fluid into compartments with higher oncotic pressure from compartments with lower oncotic pressure. The tissues initially have normal oncotic/osmotic pressure, but compared to the blood that has become hypoosmolar, the tissues are the higher concentration so fluid is “called into” the tissue compartment from the lower-concentrated blood compartment. d. the proteinemia means that protein molecules will diffuse throughout the blood and tissue. 9. A patient who just came out of general anesthesia has lab work done. The serum osmo is 165. The nurse taking care of this patient suspects that the is due to . a. hyperosmolality: dehydration. b. hypoosmolality: syndrome of inappropriate ADH (SIADH). c. hypertonicity: SIADH. d. high oncotic pressure: a state of hyperpolarization inside the cells. 10. The nurse in the previous question (9) would expect all the following S&S EXCEPT: a. signs of cerebral edema such as irritability. b. signs of cerebral cell dehydration such as headache. c. pitting edema d. crackles in the lungs upon auscultation. 11. Re: the patient in the previous two questions (9 & 10): As an intervention to return the patient to normal serum osmolality, the nurse is likely to be ordered to hang an IV bag of because once the fluid is distributed in the blood it will and help return fluid compartment status to homeostasis. a. 0.45 NaCl: cause water to shift from tissue (T) to blood (B). b. 3% NaCl : cause water to shift from T to B. c. 0.25 NaCl : shift water from B to T. d. NS : shift water from B to T. Rationales: #9-- A low serum osmolality (165) means the patient is HYPOosmolar. B is correct, since the more ADH you have being secreted, the larger the volume the fluid in your circulation, which causes blood concentration to be diluted, thus giving rise to blood that is LESS concentrated than usual—hypoosmolality, hypotonicity, etc, would go along with this, NOT the “hypers” that you see as part of the rest of the answers. Pearl: After you figure out a CTQ like this, turn it around in various ways to help you expand your studying. For instance, you could ask yourself, “how could I change the question to make answer A the correct answer?” #10 Three of the answers in an EXCEPT question “go together.” In this case, A, C, & D paint a picture of someone with fluid overload, which is the sequela for SIADH. Too much ADH = too much volume being “held onto” & less volume of urine that is more concentrated (higher specific gravity)  decreased osmolality in the vascular compartment water is “pulled” into the next door compartment, ie, the surrounding tissue that has normal osmolality edema signs of cerebral edema such as irritability (headache is also a definitive sign of cerebral edema, but in this case not due to cerebral dehydration). Pearl: A good example of critical thinking is to realize that headache and irritability are both examples of altered cerebral cell status, but the underlying mechanism can be different, depending on the scenario. #11 NS—normal saline—is isotonic fluid, meaning it is the same tonicity (and osmolality) as the blood). One way to think of tonicity, especially in nursespeak, is in terms of sodium traveling in the blood as NaCl. The normal tonicity (isotonic) of the blood is 0.9% NaCl. Any IV fluid lower than that—answers A & C—would further dilute the blood & cause worse edema. Giving NS (D) might eventually help the problem, but the best answer in terms of quickest way to get fluid to come back from T to B is to give a hypertonic fluid such as 3%NS (B). 12. A patient who is having hyposecretion of ADH (antidiuretic hormone) would MOST LIKELY have the following sign: a. serum osmolality of 270. b. oliguria (low urine output). c. serum osmolality of 300. d. edema. Rationale: Hyposecretion of ADH is the OPPOSITE picture of SIADH, in which one would have HYPERsecretion of ADH, low osmolality due to fluid overload, decreased urine output, and edema. Not enough ADH results in S&S of fluid volume deficit, which would include a high osmolality. (FYI--This state, the opposite of SIADH, is called diabetes insipidus (DI)…we will have info on DI later in the semester, but as you can see, you don’t need a particular name to figure out fluid shifts, if you are provided certain info and go step by step). Pearl: Again, be sure that all parts of your patient picture are consistent, that taken together it all makes sense. As corrected above, A, B & D paint a picture of ADH hypersecretion. C is the only one that fits with hyposecretion of ADH. 13. If you had a patient whose labwork showed that he was hyperproteinemic, what would you know about that patient? a. He has a low osmotic pressure. b. He has a low blood oncotic pressure. c. His blood is more concentrated than usual. d. You may need to hang an IV bottle of albumin. Rationale: If there are more than normal protein molecules in the blood, a person would have high oncotic pressure, high osmolality, higher concentration than normal blood—all the “highs” go together and all the “lows” go together. Certainly you wouldn’t want to give them MORE protein (D). 14. You have two patients whose serum osmolality results are as follows: Albus Dumbledore (Mr. D.) has a serum osmolality of 263. Minerva McGonagall (Ms. M) has a serum osmolality of 326. (normal serum osmo = 280- 295). Based on understanding the links between fluid imbalances, lab results, and S&S, you will expect that a. Ms. M. will have an overall puffy appearance. b. Mr. D will have poor skin turgor and dry mucus membranes. c. Ms. M. will need a hypertonic IV to get her fluid status back to normal. d. Mr. D will have generalized pitting edema. 15. On a more cellular level, which is true regarding the two patients in question 14? a. Mr. D’s tissue cells are likely shrunken from fluid being pulled from tissue to blood. b. Ms. M’s tissue cells are likely shrunken from fluid being pulled from tissue to blood. c. Ms. M has more dilute blood than Mr. D. d. Mr. D’s blood is hyperosmolar compared to normal. Rationale: Mr. D: serum osmo of 263 = hypoosmolar--means blood is more dilute, AKA LESS concentrated than usual, so when it flows to normal-concentrated tissues, “concentration calls” water from B to T and Mr. D becomes edematous (edema is “extra fluid in the tissues than normal”). A hypertonic (ie, hyperconcentrated) IV fluid like 3%NaCl can help return homeostasis. Ms. M: serum osmo of 326 = hyperosmolar--means blood is more concentrated than usual, so when it flows to normal- concentrated tissues, “concentration calls” water from T to B and Ms. M’s tissues are “sucked dry.” A hypotonic IV fluid like 0.45%NaCl can help return homeostasis. 16. A diabetic patient has pathological changes to his arteries that result in narrowing and blockage. He is diagnosed with gangrene of the toes (gangrene is when LOTS of cells die).. Lab work is drawn and shows an elevated CK. Which pathological process accurately explains this type of occurrence? a. necrosisgangreneischemia creatine kinase spillage into blood. b. infarct cellular differentiation release of urea. c. ischemia cell injuryswellingspillage of cellular enzymes into blood. d. metastasis superoxide dismutase release of free radicals. Rationale: C is the only answer that follows the general correct steps: in this case there has been ischemia from a blocked artery. Ischemia leads to hypoxia, which leads to loss of ATP for energy to drive processes like Na/K pump, which then fail and allow Na & water to freely come into the cell. This process culminates with swelling & leakiness and/or rupture of the cell membrane. The final step is leakage of intracellular substances (enzymes like CK) into the blood. 17. A patient says she has read that free radicals might be partly responsible for the development of her disease process. She wants to know more information and if there is anything that can counteract free radicals. The nurse’s explanation will be based on understanding that all of the following statements are true EXCEPT a. an example of a free radical is cytochrome oxide. b. free radical molecules initiate harmful reactions such as lipid peroxidation, which damages the lipids of cell membranes. c. the body’s way to counteract free radicals include enzymes such as superoxide dismutase. d. free radicals are molecules that are in a highly reactive state and can be calmed by taking certain vitamins. Rationale: Remember that this is an except question, so 3 things go together and are true. Free radicals are highly reactive and out-of-control molecules that can damage cells in several ways, including by destroying cell membranes (B, D). Our body can “calm” free radicals by using defusing enzymes (C) and vitamins (D). Answer A is wrong. Superoxide is an example of a free radical; cytochrome oxide is a made-up mix of a couple of terms (cytochrome oxidase is the enzyme that facilitates ECT reactions.) Pearl: You are looking for 3 correct pieces of information about free radicals, which are B, C, & D. Answer A is the outlier, the incorrect piece of information & therefore the correct answer. 18. A patient who smokes expresses concern to his nurse about the metaplastic changes of the bronchi that were seen during his bronchoscopy. The nurse bases her response on the knowledge that this type of cellular change is a. an irreversible cellular adaptation pattern. b. considered a precancerous cellular change. c. reversible if the change agent is removed. d. due to a physiologic hyperplasia. Rationale: To correctly answer this you must understand the different adaptive processes; atrophy, hypertrophy, hyperplasia, metaplasia—are all considered reversible if the irritant or change agent is removed. Therefore answer A can be eliminated. B is wrong because it is dysplasia that is considered to be a precancerous change. D is wrong because a metaplasia (change in type of cell) is not the same as any type of hyperplasia (increased number of cells). 19. Which sets of information are correctly linked? a. a patient with decreased RBC production: erythropoietin injections are needed to counteract overproliferation of red blood cells. b. arterial embolus blocks blood flow: decrease in venous circulation to tissue with resultant hypoxia of cells. c. gout: caused by diet high in urea. d. carbon monoxide: binds to Hgb in oxygen’s place. Rationale: Answer A is wrong because erythropoietin actually helps to increase proliferation of RBCs (not counteract) in patients such as those with kidney disease (since erythropoietin is made by the kidneys, a person in kidney failure would have less erythropoietin made & therefore be anemic from less RBCs). B is wrong because the second half implies that VEINS bring oxygen to the tissue; if a person has blockage in an artery, then the distal tissue becomes ischemic/hypoxic because of lack of arterial flow. (Veins carry deoxygenated blood.) C is wrong because gout is caused by a diet high in uric acid, a by-product of purine breakdown. Urea is a byproduct of other protein breakdown. Questions 20-23 refer to this scenario: A large bookcase falls upon an elderly man in his home. His left leg is pinned and he cannot move for 2 days until his neighbor finds him. He is hospitalized with massive trauma to his left leg, with resultant rhabdomyolysis (rhabdomyo means striated muscle tissue; lysis means “break down”). His pulses in that foot are unpalpable and the foot is pale and cool. Eventually his foot must be amputated. 20. Which mini-concept map, showing one event leading to the next, best fits with the scenario above? a. Massive mechanical trauma to leg distal arterial flow blocked ischemia to foot infarction of foot tissue amputation. b. Rhabdomyolysis damage to striated cells spreads to arteries proximal to the trauma ischemia infection amputation. Several things are wrong in this answer, one of them being that if there is any type of blockage of arterial flow, the tissue at risk is DISTAL to the blockage, as in correct answer A, not proximal. If you don’t understand this concept relating to how arteries flow, and the concepts of proximal and distal, be sure to review it until you understand it, and/or ask for help. c. Mechanical trauma interrupt cell membrane functions such as Na/K pump solute imbalance leg edema amputation. Swelling would occur in any kind of trauma, but the mechanisms have more to do with inflammatory response rather than direct solute imbalance. And edema isn’t a clear enough reason for amputation. It is not emphasized in the scenario in the way that arterial flow problems is emphasized. d. Cool foot tissues become too cold to conduct metabolic pathway functions cells become dormant distal arterial flow increases pathologically amputation. This is a hodge-podge of info… The foot is cool & pale because the arterial flow is decreased (not Increased), thus not bringing warm blood to the area. The cells will THEN not get O2 and have metabolic pathway problems. But the problems don’t BEGIN with a cool foot (as opposed to, say, frostbite). 21. Initial lab work is drawn that show a CK of 100,000 (normal serum CK is 0 to 200). Why is it so high? a. As a compensatory response, the production of the enzyme creatine kinase (CK) is increased in the cells and then is excreted to “clean up” the cellular debris. CK production doesn’t increase, per se; the level of it increases in the blood because injured cells are leaking it. b. As a result of injury, the striated cell membranes lose integrity and there is leakage of intracellular substances such as CK into the surrounding tissue bed. CK is an enzyme that is normally found INSIDE cells and in very small amts in the blood, so when it increases in the blood, we know there is cellular injury somewhere. c. Creatine kinase (CK) is only found in striated muscle cells, so it makes sense that rhabdomyolysis would result in greater release of CK. CK is a generic cellular substance found in many types of cells. When its blood levels rise, you only know there is injury, but it doesn’t tell you exactly what tissue is injured. d. Local tissue response to injury includes release of toxic, lytic substances such as CK. Very large amounts of CK can be problematic for the kidneys to deal with, and in that way it could in a way be considered toxic at high levels. But it is not normally considered toxic nor lytic. 22. Because of massive cellular injury, myoglobin leaks from cells into blood. The patient develops kidney failure from this myoglobinemia. All the following are true about this situation EXCEPT a. the patient may need injections of erythropoietin because of the kidney failure. b. myoglobinuria will likely be present. c. erythropoietin will be dangerously high in the blood secondary to kidney involvement. In the long run, a person with kidney failure often gets anemic because of LOW levels of erythropoietin, not HIGH levels of it. d. the etiology of the kidney failure is the inability of the kidneys to process such high amounts of myoglobin. 23. After many months the patient finally has recovered enough to be able to get up and have some physical therapy. What change of the musculature will the therapist have to deal with in the injured leg (besides loss of a foot)? a. Presence of decubiti because of scarring. b. Muscle cell shrinkage called atrophy. This is sometimes called disuse atrophy, because as the cells are not used & stimulated, they shrink in size. c. Increase in numbers of muscle cells, called hyperplasia d. Hypertrophy of the striated muscle cells. 24. Which correctly links the picture below with its name and an example? a. D = dysplasia. Example: pre-cancerous cells on a biopsy. The cells are not completely wild & undifferentiated, like cancer cells are (E) but there is enough deviation from normal to cause worry. b. C = hypertrophy. Ex: the heart undergoes hypertrophy when stressed. The heart does undergo hypertrophy when stressed, but the definition of hypertrophy—individual cells that enlarge—goes with picture B, not C. c. E = cancer cells. Ex: increased cellular differentiation of the skin after sun exposure. Picture E is of cancer cells, but they are DEcreased in their differentiation, not INcreased. Remember that the more differentiated a cell is, the more specialized and complex it is; cancer cells are the opposite—they grow via a process called anaplasia— lack of differentiation. d. B = hyperplasia. Ex: BPH—benign prostatic hyperplasia. Hyperplasia is when cells multiply, so picture C (not B) is hyperplasia. Notice the cells aren’t bigger—just more of them than normal. Tissue cells Normal A. B. C. D. E. 25. A patient that has been recently diagnosed with a neuroma on the sole of his foot is very anxious. Of the following, which information shows that the nurse understands the nomenclature of neoplasms when explaining the situation to the patient? a. “You should have the neuroma removed, as this is a cancer that will spread to other parts of the body.” b. “This is most likely a malignancy that will metastasize to your lymph nodes.” c. “Neuromas are benign growths that usually will not spread.” d. “You will soon have the irresistible urge to put on tap shoes and dance in a Broadway musical.” Rationale: If this were a cancerous growth, the name would be neuroblastoma. Pearl: Note that A & B are essentially saying very close to the same thing, so it wouldn’t have made sense to choose one of them. You can rule out D too in this case (even though neuromas are not a form of cancer, they are still painful & certainly wouldn’t trigger the desire to tap dance—ouch! ) So that leaves C. 26. A family nurse practitioner (FNP) tells a patient that her biopsy shows leiomyosarcoma staged at T2N2M0. This patient has a a. benign tumor of the endometrium. b. smooth muscle malignancy that has spread to the lymph nodes. c. a malignancy of the uterus that has spread to distant sites. d. muscle cell tumor that is a carcinoma. Rationale: The “T” of staging means “is there a malignant tumor?” The fact that it is staged at T1 automatically gives you the answer “yes,” so you can rule out A. N2 means lymph node involvement but M0 means no distant metastasis, so rule out C. The nomenclature of the growth means (sarcoma) that it is a malignant connective tissue growth, not an epithelial growth (carcinoma). So you are left with B, which fits with all the information given in the stem of the question. 27. Which mini-concept map has correct linkage in describing cancer genesis? a. angiogenesiscachexialack of nutritioncellular starvationcancerous changes b. growth factor signalsincreased cellular differentiationanaplasiacancer. c. oncogeneclonal proliferationincreased cellular differentiationcancer. d. oncogeneclonal proliferationanaplasiacancer cells. 28. A 59 year old man is diagnosed with CML—chronic myelocytic leukemia. All of the following help to explain the genetic etiology of the CML EXCEPT a. a chromosomal structural defect called translocation occurs. b. pieces of two chromosomes are exchanged. c. a chromosomal aneuploidy defect called translocation occurs. An aneuploidy is a chromosomal problem of numbers. For instance, trisomy 21—Down’s syndrome—is a problem of too many chromosomes, so it is an aneuploidy (specifically it is a polysomy, and even MORE specifically, a trisomy). A translocation is a structural problem, so you have two words that shouldn’t be in the same sentence. d. a short, defective chromosome called the Philadelphia chromosome develops. 29. Link CML etiology with its S&S: a. Genes on a defective chromosome malfunction and code for extreme leukocytosis. b. Myelocytic leukocytes attack cells in the blood and cause changes known as The Philadelphia Story.  c. A genetic defect causes cancerous changes in the blood vessels, producing hemangiosarcomas. Correct in general, except doesn’t apply to CML. d. Genes on an extra chromosome malfunction and cause defects in leukocyte development, resulting in leukopenia. Leukopenia means “less than normal leukocytes.” CML is a problem of leukocytosis—“too many” leukocytes. 30. All of the linkages below are correct EXCEPT a. cancer-related angiogenesis leaches nutrition from our cells cachexia, weakness. b. cancer injures prostate cells release into blood of high levels of a tumor marker called PSA (prostate-specific antigen) c. ingestion of foods high in preservatives increase genetic “hits” increased risk of cancer. d. age-related wear and tear of cells increased risk of cancerous lesions such as lipomas. This sentence is correct until “lipomas,” which are NON-cancerous lesions. Questions 1-3 refer to this scenario: A man presents to an ER with a large laceration sustained at a construction site a few hours before. The area around the laceration is erythematous, painful, and swollen. 1. The erythema and swelling can be explained at a cellular level by all the following EXCEPT a. mast cell degranulation and release of histamine. True (see concept map) b. pro-inflammatory prostaglandins released. True c. increased vasomotor tone (tightening) of the capillaries in the area. False statement, so this is the CORRECT answer. Any inflammatory response involves some degree of DECREASED vasomotor tone—ie, capillaries in the area must VASODILATE (relax, have less tone) in order for substances to “ooze out”-- leak out of the blood to go “help” healing in the tissue. So usually we equate “dilation and leakage” with inflammation. This is why you often see swelling with inflammation—the swelling is caused by the dilated blood vessels and accumulation of leakage. d. local reaction to acute phase reactants. True 2. The patient is given a TIG (tetanus immunoglobulin) injection because the wound is high risk for tetanus exposure and he doesn’t remember ever having a tetanus vaccination. The purpose of the TIG is to a. prevent any tetanus bacteria from activating the inflammatory system. Wrong—inflammation will be activated as soon as any cell in the body is irritated and/or injured. Giving antibodies (immunoglobulins)– the “IG” in TIG— doesn’t prevent inflammation. b. introduce tetanus bacteria so that the immunocyte system can create antibodies to tetanus. Wrong— TIG is antibodies, not the microbe itself. c. give the patient natural active acquired immunity. Wrong—the word “natural” implies that a person contracted tetanus (HAD the disease) and created their own antibodies as a result of the active disease. d. provide tetanus antibodies to fight any tetanus bacteria that might be present. CORRECT—just in case this person’s body was invaded by a tetanus bacteria, giving them antibodies NOW will help them fight the microbe NOW. This is called conferring artificial passive acquired immunity. 3. The patient (should or should not) be instructed to also get a tetanus vaccination, because . a. should: he needs protection against future tetanus exposure. CORRECT : passive immunity (when you DON’T make the antibodies in your own body, but are given them) is very short-lived. The antibodies that are GIVEN to you, that you DON’T create on your own, will disintegrate within a few weeks. So you WILL need a vaccination, which confers artificial ACTIVE immunity— having a weak tetanus injected in you will make you create your OWN antibodies, which are long-lived. b. should: the vaccination will provide additional passive immunity. Wrong—see above (vaccination and PASSIVE shouldn’t be in the same sentence; vACcination = ACtive) c. should not: the TIG is enough, as it will provide long term active acquired immunity Wrong—see above d. should not: the vaccine will do nothing for the current exposure. Wrong—see above. Look at this answer closely. The last part is true. A vaccination WILL NOT help a person RIGHT NOW, because creating your antibodies