NURS 3365 BB ASSIGNMENT 3 answers and rationaleS

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 takes time. But the question asked should he go ahead and get a vaccination? Yes, he should. No, it won’t help him NOW, but it will help him if he ever gets a tetanus microbe inside his body in the future—his antibodies can THEN kill the microbe swiftly. 4. A microbe invades the body for the first time. Which statement is most likely about the processes that follow? a. Plasma cells (a type of B-lymphocyte) will immediately secrete T-cells specific to that microbe. Wrong. Plasma cells secrete antibodies, not T-cells. b. CD4 cells will introduce remnants of the microbe to the plasma cells, which directly phagocytize the remnants. Wrong— plasma cells are not phagocytes. They are a form of B lymphocyte. c. Antigens will be created from the memory cells of immunocytes. Wrong—doesn’t make sense. Don’t confuse the word antigen with the word antibody. d. Immunocytes will begin the process of developing memory to that microbe. Correct— During the inflammatory process, if a microbe is involved, the T-cells and/or B-cells are “called in” and begin to develop microbe-specific memory. Especially let’s focus on the antibodies… the Bcells will begin the memory process, and as a result, antibodies that are specific to that particular microbe will be formed and will be on hand for the next time the body “sees” that microbe. (Tcells do similar process, but don’t create antibodies.) 5. A patient has a systemic inflammation. All the following are likely associated with his condition EXCEPT a. increased acute phase reactants. True – acute phase reactants have the job of increasing inflammation as needed—“fuel on the fire”; especially they increase circulating in the blood when there is a systemic inflammation. b. lab results showing a high C-reactive protein (CRP). True—CRP is one of the acute phase reactants. c. lab results showing leukopenia. False, so this is CORRECT answer. During systemic inflammation, leukocytes will increase in number so as to participate in the various parts of the inflammatory response, especially neutrophils, which act as phagocytes (see concept map). So leukocytosis and neutrophilia are part of inflammation, not leukopenia (PENIA= “lower numbers than normal”). d. increased pro-inflammatory prostaglandins. True – remember that prostaglandins have two subcategories—the duty of INCREASING inflammation is called “pro-inflammatory.” The other types of prostaglandins are “protective”—they bolster certain aspects of body function 6. A baby who has received immunoglobulins against the “XYZ” virus via its mother’s milk now has a. natural active acquired immunity. Wrong—an example of this is getting chicken pox. b. natural passive acquired immunity. Correct—natural (from mom); passive = baby did NOT make its own antibodies. c. passive innate immunity. Wrong—mixed up terms. Remember that when we are talking about immunoglobulins, we are automatically thinking of the third line of defense – ACQUIRED immunity, not innate. (Innate involves first and second line of defense) d. active innate immunity. Wrong—see above about acquired vs innate. 7. The baby in the previous question will . a. have lifelong immunity to the XYZ virus because of receiving the immunoglobulins that are specific to that particular microbe. Wrong—can’t get lifelong immunity from receiving SOMEONE ELSE’s antibodies. b. develop temporary immunity to the XYZ virus due to receiving Mom’s antibodies that are specific to that particular microbe. Correct—passive acquired immunity is ok for right NOW, but the antibodies will disintegrate within a short time—hence “temporary.” c. now have complete 2nd line of defense protection, having received it in the breast milk. Wrong— remember that when we are talking about immunoglobulins, we are automatically thinking of the third line of defense d. develop alphabetophobia due overdose of anti-XYZ immunoglobulins.  8. A person starts Jazzercise for the first time and becomes very sore all over. The most appropriate self-treatment for this person is to , because . a. take an NSAID such as Aleve : it powerfully suppresses phospholipase enzymes in the arachidonic pathway. Wrong—steroids suppress phospholipase. NSAID are non-steroidal antiinflammatories that work further down in the arachidonic pathway. See page 19 of RRD. b. take an NSAID such as Advil : it is an effective suppressor of certain levels of pro- inflammatory prostaglandin activity. Correct c. go in for a CRP test: it will determine the degree of pain. Wrong --CRP is an acute phase reactant that will increase when you have an inflammation but it is very non-specific—you can’t judge degree of pain by that (besides that, FYI—everyone’s pain is different—not something that can be generically measured.) d. take an antihistamine: it will suppress steroidal influence. Wrong—we haven’t discussed antihistamines, but we have talked about histamine, which you know to be a substance that is part of the inflammatory response. So in a sense an anti-histamine suppresses a certain part of inflammation. Steroids also, in a much different way, suppress inflammation—you know this too— via suppressing prostaglandins. So antihistamines suppressing steroids doesn’t make sense. 9. A patient has been in the hospital for treatment of an infection. One day his BP drops to 80/50 (normal ~ 120/80), he has a fever of 102, and he becomes restless and confused. All the following are correct about this situation EXCEPT a. a likely diagnosis is septic shock, partly because his BP is low, and he has S&S related to low blood volume to the brain. True – the definition of shock is low BP that causes S&S. And since he has an infection, it makes sense that sepsis has become involved (sepsis— the inflammatory response to a systemic infection) b. a good mini-concept map would be: infection goes systemic (sepsis) increases circulating acute phase reactantssystemic vasodilationless blood centrally low BP. True—this is exactly how septic shock works. It is the massive vasodilation from massive, systemic inflammatory response that causes the BP go become so low that the patient can’t get enough blood to the brain restless, confused. c. a good mini-concept map would be: local infection gets worse invades lining of blood vessels in the arealocal sepsis develops chronic inflammation results in hypotension. False, so this is the CORRECT answer. The term “local sepsis” is an oxymoron—by definition, sepsis is not local but systemic. d. the patient’s blood work will show leukocytosis, neutrophilia, and high CRP as part of the high degree of inflammatory response in his body. True. See the table on the next page. It is numbered I-XIV. In the right column are words and phrases that link in some way with each of the numbered items on the left. In other words, this is a typical “matching” exercise. Fill out the table, and use it to answer questions 10-15 directly below. ONLY ONE ANSWER TO EACH LEFT- HAND TERM, AND DO NOT CHOOSE THE SAME ANSWER MORE THAN ONCE— CHOOSE THE BEST FIT. 10. Granuloma (#I) a. I b. N--local chronic inflammatory tissue reaction c. A d. F 11. Example of qualitative defect of “not enough” inflammatory function (#IV) a. K-- chemotactic defect – without chemotaxis, certain important cells (phagocytes, immunocytes) wouldn’t be “called” in to help at the site of a defense breach. b. L c. G d. N 12. Leukopenia (#V11) a. D b. E --example of quantitative defect of “not enough” inflammatory function—leukopenia means less numbers of WBCs than usual, making this a quantitative defect. c. K d. O 13. Part of inflammation in which vasomotor tone of capillaries “relaxes” (#X) a. H b. N c. A vasodilation d. J 14. Steroidal suppression of protective prostaglandins (#XII) a. B b. F c. M d. G –Remember that steroids do what you WANT them to do when they suppress the pro-inflammatory side of prostaglandins. So if someone gets a course of steroids for an acute back injury, and the patient feels better, it’s because the steroid is suppressing the inflammation that causes pain. If that person were to STAY on steroids for a long time, though, the side effects could include problems such as stomach ulcers. This risk is related to the fact that steroids are non-specific—as they are suppressing inflammation, they are also suppressing the “protective” aspect of prostaglandins, including protecting the stomach lining from stomach acid. So, long-term steroids use (such as for someone with chronic inflammatory diseases like autoimmune diseases) sometimes has bad side effects. This is an important concept. See RRD 3, page 14. 15. A way of conferring artificial active acquired immunity. (#XI) a. D b. A c. B booster shot—a booster is a vaccination shot that is given periodically to keep stimulating your immunocytes to create antibodies to certain microbes. Because you are stimulated to create your OWN antibodies, this is classified as an ACTIVE acquired immunity. The artificial part is because the microbe did not naturally make its way into your body—it was injected into your body artificially. d. C MATCH up words or phrases that are most appropriately related and then answer questions 10-15 above (10-15 are what you submit electronically). ONLY ONE ANSWER TO EACH LEFT-HAND TERM, AND DO NOT CHOOSE THE SAME ANSWER MORE THAN ONCE—CHOOSE THE BEST FIT. I. granuloma N A. vasodilation II. erythema I B. booster shot III. decrease in phagocytic functions J C. steroid IV. example of qualitative defect of “not enough” inflammatory function K D. oncogenic event resulting in defective creation of multiple cells V. breach of first line of defense M E. example of quantitative defect of “not enough” inflammatory function VI. serosanguinous exudate H F. degranulation releases histamine, prostaglandins, leukotrienes VII. leukopenia E G. stomach ulcers VIII. benign neoplasm of the bone O H. wound fluid leakage contains serous fluid and blood IX. mast cells of tissue F I. reddened, inflamed appearance of skin X. part of inflammation in which vasomotor tone of capillaries “relaxes” A J. results in decreased inflammatory response and less healing ability K. chemotactic defect XI. a way of conferring artificial active acquired immunity B L. can have negative effect on normal bowel flora, resulting in breach of body’s defenses XII. steroidal suppression of protective prostaglandins G M. Sjogren’s syndrome XIII. suppresses pro-inflammatory aspects of prostaglandins C N. local chronic inflammatory tissue reaction XIV. antibiotics L O. osteoma 16. A patient has just had a liver transplant and is beginning to display S&S consistent with rejection. The following is most likely a true statement about the situation: a. The patient is undergoing an autoimmune hypersensitivity. Wrong—no evidence of self- attack, so no autoimmune problem. b. The patient is undergoing an IgE-mediated hypersensitivity reaction. Wrong—IgE- mediated hypersensitivities are basically allergic reactions—doesn’t fit scenario. c. The donor’s immunoglobulins are attacking the HLA’s on the patient’s RBCs. Wrong— RBCs don’t have HLAs; HLAs are found on almost all tissue cells’ cell membranes ESCEPT RBCs— RBCs instead have ABO & Rh. d. The recipient’s immunoglobulins are attacking the HLA’s on the donor liver. Correct— rejection is a type of alloimmune hypersensitivity. Questions 17-19 refer to the following scenario: A woman has just been diagnosed with SLE (lupus). 17. In educating the patient about her disease, the nurse shows complete understanding of the pathophysiology of SLE when he tells the patient: a. “Unfortunately, you will need to be on a gluten-free diet.” Wrong—would apply to celiac disease b. “You should expect to have swelling in the area of your thyroid.” Wrong—would apply to Grave’s disease. c. “Fortunately SLE only affects one area, usually the joints in your hands.” Wrong—SLE is a systemic disease; hand joints MAY be involved, but usually other areas are too. d. “You may have a variety of symptoms that come and go.” Correct—this is true of most autoimmune diseases—have waxing and waning of their symptoms. 18. Some labs are done. Which of the following is a likely finding? a. Test results that indicate hemolytic anemia. b. A low CRP. Wrong—in almost any inflammatory situation such as an autoimmune disease, there is SOME inflammation and therefore high likelihood that the CRP (an acute phase reactant) would be HIGH, not low. c. A positive ANA. Correct—ANA stands for anti-nuclear antibody. So this test “looks” for a molecule that is an antibody against nucleic (DNA) material. The immune complex formed in SLE is exactly that—an autoantibody coupled to a piece of random DNA. A positive test indicates likelihood of having SLE. d. Test results that indicate a low ANA. 19. The pathophysiology related to the above test is best described by which of the following? a. Vasculitis caused breakdown of RBCs, resulting in anemia that the lab test detects. Wrong—SLE does involve vasculitis (inflammation of the blood vessels that the immune complex irritates), but vasculitis doesn’t cause hemolysis—breakdown of RBCs. b. SLE is a hypersensitivity disorder in which autoantibodies attack nucleic acids and form detectable complexes that circulate in the blood. Correct—the complexes then “land” in the lining of tiny blood vessels within organs and other body parts vasculitis inflammation S&S. c. SLE is a hypersensitivity disorder in which autoantibodies attack DNA form detectable complexes that migrate to one type of tissue. Wrong—SLE is systemic, doesn’t just affect one tissue. d. Immune complexes invade CD4 cells, a phenomenon which is detected by lab tests as a low ANA. Wrong—this is a mix references to SLE (immune complexes) and invasion of CD4s (HIV/AIDS) 20. A patient tells his nurse practitioner (NP) that he had rheumatic fever as a child. Knowing the pathophysiology behind this disease, the NP will need to assess the patient for a. angioedema. Wrong—this is a swelling that is related to anaphylaxis. b. S&S of immunodeficiency. Wrong—rheumatic fever increases risk for an autoimmune disease, as disease of “too much” inflammation, whereas immunodeficiency falls in category of “too little” immunocyte response. c. heart valve problems. Correct—following a strep throat infection, sometimes the antibodies to strep become autoantibodies and attack our own tissue, such as our kidneys and our heart valves, giving S&S known as rheumatic fever. If the heart valves were attacked, there might be lingering problems and malfunctions of the heart valves in adulthood. d. urticaria. Wrong—this is medical term for hives, which occurs in anaphylaxis. 21. A patient who receives blood with an incompatible blood type may develop a. an alloimmune reaction. Correct—alloimmune means self against another person’s tissue b. an opportunistic infection. Wrong—an opportunistic infection is likely with a suppressed immune system; opportunistic infections are the result of immunodeficiency rather than a hypersensitivity situation such as this. c. a humoral autoimmune reaction. Wrong—“autoimmune” has to do with self against self. d. a cell-mediated hyposensitive reaction. 22. Which of the following compatibility situations is most likely? A patient who is a. B positive and receives B negative blood will have a transfusion reaction. Wrong—the “B” part is the same. Re: the Rh part: the donor RBCs have no Rh antigen on their RBCs, so whether the recipient is + or neg, Rh negative blood can be given. NO transfusion reaction will occur. b. AB positive and receives B negative blood will do fine. Correct—AB recipients have no A or B antibodies in their plasma that will attack the B antigen on a donor’s RBCs. c. A negative and receives A positive blood will do fine. Wrong—if an Rh negative recipient gets Rh pos blood, he will begin creating antibodies to that Rh factor. He may not have a problem THIS time, but if he ever receives Rh pos blood again, there will be a reaction. So things are not “fine.” d. A negative and receives O negative blood will have a transfusion reaction. Wrong— the O donor has no A or B antigens on the RBCs & the AB recipient has no A or B antibodies in its plasma, so this is a double “OK.” It is even a TRIPLE ok, because the recipient is receiving blood without the Rh antigen (the “negative” part). So NO transfusion reaction. 23. A patient presents with generalized itching, urticaria, and wheezing. She says it started after she was stung by a bee. The patient is most likely experiencing a. the effects of complement system opsonization of an invading microbe. b. localized effects of mast cell degranulation. Wrong—the scenario is a systemic problem (“generalized”) c. a cell-mediated response. Wrong—allergic reactions MUST be humoral because they involve an immunoglobulin – IgE. d. anaphylaxis. Correct 24. The wheezing in the patient scenario above is at least partly caused by a. bronchoconstriction due to leukotriene over-release from mast cells throughout the body. Correct—this is one of the rare situations where you see the term “constriction” in the same mix with inflammation, since usually with inflammatory situations there is dilation of blood vessels. But here we are talking about actual bronchial muscle constriction—not blood vessels. In asthma there will ALSO be blood vessel dilation of the capillaries in the bronchi, but over-abundance of leukotrienes in this case specifically cause bronchial tightening—like trying to breathe from a thin straw. b. over-active response to immune complex deposition in the lung tissue. Wrong—this might be true if this question was about SLE. c. bronchoconstriction from humoral immunodeficiency. Wrong—see answer c in #8. d. vasoconstriction from the effect of autoimmune over-degranulation. Wrong—much mixing of different processes here: autoimmunity is a different kind of hypersensitivity than allergic; also, any kind of inflammatory response, whether as part of an allergy or autoimmunity will involve vasodilation, not CONSTRICTION. Questions 25-28 refer to the following scenario: Upon his yearly physical a 68 year old male patient was found to be HIV positive. Six months later he had a CD4 count of 400 and for many years it stays at this level. Now the patient presents to his NP with complaints of difficult and painful swallowing (dysphagia); upon examination, the NP notes white patchy areas in the mouth and throat. The NP orders a CD4 count, which is 198. (Norm CD4 ct = 600) 25. To establish the diagnosis of being HIV positive, all the following were true of this patient picture EXCEPT that the a. ELISA test showed antibodies to HIV. ELISA is done first. If it is positive, then Western Blot is done. b. Western blot was positive. The Western Blot is confirmatory & is part of establishing HIV+ status. c. CD4 count was 198. A CD4 count is not used to initially establish HIV status. d. ELISA was positive. This answer says basically same thing as “a”—presence of HIV antibodies = a positive ELISA. 26. Which is true? a. A diagnosis of AIDS was established when the patient’s CD4 count was 400. CD4 of 400 is low, but not low enough for AIDS dx, plus no mention of opportunistic infection. b. The patient officially has AIDS because of the opportunistic infection in his mouth and because of his HIV+ status. No—all AIDS patients are HIV+ so that’s a given. c. An AIDS diagnosis is automatic when the ELISA test shows antibodies to HIV. d. The patient officially has AIDS because of the opportunistic infection in his mouth and because of the CD4 count of 198. Once a person is HIV+ (as determined by the ELISA & Western Blot), her or she may or may not ever have AIDS. It usually takes a CD4 count of 200 to make a person completely unable to fight opportunistic infections. So CD4200 PLUS presence of opportunistic infection = AIDS. 27. The patient’s nurse describes to him a couple of opportunistic disease processes that he is at high risk for. Which of the following shows that the nurse has a complete understanding of the link between AIDS and opportunistic infections? a. “You are more likely to get PCP (pneumocystis carinii pneumonia) because your HIV antibody level is so high.” The two parts of this sentence don’t go together. If the second half said “your CD4 cells are so low,” then the whole sentence would be correct. b. “The numbers of your infection-fighting cells is low, so you are more likely to get unusual infections such as CMV retinitis.” Most people with CD4 levels above 200 won’t usually get a “strange” infection like CMV retinitis. But if the CD4 cells fall below 200, you are especially vulnerable to microbes that otherwise wouldn’t have a chance to flourish. “Opportunistic” means taking advantage of a situation that is unusually conducive. c . “The numbers of your infection-fighting cells is low, so you are more likely to get autoimmune diseases such as lupus.” Autoimmunity implies a pathologically “ramped-up” immunocyte system, so it is actually the opposite of immunodeficiency states. d. “Your CD4 count of 198 is ok for now, but when it drops below 50 you will need to avoid people with common infections such as a cold or the flu.” 28. This patient is put on several medications. All the following are steps in the HIV invasion process that a medication might target EXCEPT the a. use of viral protease to make new viral proteins in the CD4 cell. b. insertion of the HIV DNA molecule into the CD4 cytoplasm. HIV is an RNA retrovirus, not a DNA virus. c. use of the viral enzyme reverse transcriptase. d. use of integrase to insert viral DNA into the CD4 nucleus. 29. A patient presents to the ED with fever, chills, myalgia, and a dry cough. He says he has recently traveled to China. He says he got a flu shot a year ago. Which is most likely in this case? a. This disease is pertussis, probably contracted from an unvaccinated contact when he visited China. b. The disease is probably not influenza, since he had a flu shot during last year’s flu season. c. The diagnosis is influenza, probably contracted via fecal/oral route while in China. Flu is transmitted by coughing, sneezing etc, so not by fecal/oral route. d. The diagnosis is influenza, possibly contracted because patient did not have this year’s flu shot. 30 The disease mentioned above has the following characteristic: a. The causative microbe can also cause a membrane across the pharynx. Diphtheria. b. This disease is difficult to treat because of the antigenic drift of its exotoxin. Flu is a virus and thus doesn’t have exotoxins like bacteria. c. New mutations of proteins on its cell membrane cause a variety of types each year. The two cell membrane antigens that undergo antigenic shift each year are hemagglutinin (H) and neuraminidase (N), which give the flu virus its name each year (H1N1, H5N1, etc). d. A later outbreak may include skin lesions in a dermatome pattern. Shingles. 31. A commonality of herpetic organisms that cause diseases like chicken pox and shingles is that a. each is caused by a bacterial organism that penetrates the nervous system. Herpetic organisms are viruses, not bacteria. b. the causative microbe can remain dormant in the nervous system. These diseases are one of a variety of herpes viruses, which have the commonality of invading peripheral nerve system and remaining dormant there for “X” amount of time, depending on individual. c. the causative microbe causes bloody diarrhea. Wrong—this would be true if asked about shigella. d. each is transmitted via vector. Wrong— chicken pox is acquired via airborne transmission. Shingles develops from a harbored chicken pox virus. 32. An otherwise healthy Texas rancher whose water supply comes from a well is more at risk for a infection than a Dallas suburbanite. a. giardia Giardia is a protozoa that is more common in untreated water such as from wells in rural areas. b. trichinosis the state of having a helminth that commonly invades the GI tract via undercooked pork & then migrates to tissues. c. C. diff it is usually a non-pathogen unless antibiotics wipe out intestinal flora competition. d. cysticercosis a version of “b” that walls itself off in cyst-like partitions in the brain 33. A 4 year old patient presents with bloody diarrhea. Possible causes include because a. shigella: the microbe has caused inflammation in the lining of the intestines. Correct— there are many modes of action to give the S&S of infectious diarrhea; when an organism causes a great deal of inflammation of the intestinal lining, this is when there is dysentery-- bloody diarrhea-- (inflammation capillary dilation, leakage of substances from blood to stool); shigella is one of these b. pseudomembranous colitis: C. diff has eradicated normal flora. Wrong—a person gets pseudomembranous colitis when antibiotics eradicate normal flora—that allows C diff invasion. c. giardia: this protozoa invades the intestinal wall and causes necrosis. Wrong—giardia causes decreased absorption of fat, so the S&S include foul, fatty diarrhea, not bloody diarrhea. d. diphtheria: this bacteria causes parotid enlargement. Wrong—mumps virus causes parotid enlargement. 34. After coming home from an overseas assignment a young army officer begins complaining of extreme fatigue and arthralgia. He has a very high fever and shaking chills, and he is anemic. The most likely etiology of his S&S is a. infection with rabies virus. Wrong—rabies has neurologic S&S such as confusion, agitation, dysphagia. b. protozoal invasion of his RBCs Correct—look at the WHOLE picture and link S&S with patho: this is a picture of malaria—protozoa invade RBCs, cause them to rupture  the extreme hemolysis causes anemia & release of acute phase reactants fatigue, fever, arthralgia. c. Staph aureus-related cellulitis. Wrong—scenario has nothing about skin infection. d. Guinea worm infestation—Wrong—guinea worm would not cause the high fever and other classic S&S of malaria. Questions 35-38 refer to the following scenario: A patient presents to the ED with a local skin infection (cellulitis). She says she has no idea how she got it. She is told that it is a staph infection. A penicillin-type antibiotic called Augmentin is prescribed, and she is sent home. A week later, despite taking all her Augmentin, she is back with worsening of the local infection, plus fever and leukocytosis. She is hospitalized. A culture of the wound shows MRSA and she is placed on more appropriate antibiotics. 35. Which best describes the pathology behind the events in this scenario? a. A certain Staphylococcus aureas species developed special bonding affinity with methicillin. Wrong not affinity, but instead, “attack” capabilities. b. The patient likely had a compromised immune system, as evidenced by the leukocytosis. Wrong --leukocytosis is a normal and desired fighting force in people with normal inflammatory capability. c. A certain Staphylococcus aureas species developed beta-lactamase, which destroyed the penicillin molecule. The beta lactam ring is an essential structural part of all penicillins such as methicillin. Certain strains of staph aureas (SA) called methicillin-resistant SA (MRSA) have developed an enzyme called beta- lactamase that can destroy the ring and render the antibiotic ineffective. d. Staphyloccocus areas is an organism that doesn’t respond to any kind of penicillin. Some non-resistant strains of staph still respond to the penicillin class of antibiotics. 36. The fever and leukocytosis a. are evidence that the staph infection may have become systemic. Local infections don’t usually cause systemic responses like leukocytosis and fever. b. show that the patient is unable to mount an appropriate inflammatory response to the infection. c. show that the patient’s third line of defense is not needed. d. are evidence that the patient likely has VRE. VRE—vancomycin-resistant enterococcus— is a different microbe and is not related to this scenario. 37. After three of weeks of being on strong antibiotics, the patient develops chronic diarrhea. Her stool is cultured. In THIS context, what organism would you expect the stool culture to grow? a. MRSA. b. VRE. c. Salmonella. d. C. diff. Clostridium difficile—C. diff—is usually a non-pathogen that can live in the gut of many people without causing problems. However, if anything wipes out the competition of the normal “friendly” flora in the GI tract, C. diff can fall into the category of opportunistic infection and take over, causing diarrhea. 38. Choose the mini-concept map that best describes the links from the events and pathophysiology to the diagnosis. a. 3 weeks on antibiotics normal bowel flora wiped out Clostridium difficile has no competition and flourishespseudomembranous colitis. C. diff microbial infection causes diarrhea that is also associated with the development of a membranous coating on the inner wall of the intestines. This gives the condition its name—pseudomembranous colitis. b. 3 weeks on antibiotics normal bowel flora proliferate bowel walls are irritated inflammationantibiotic-associated diarrhea. Antibiotics destroy normal flora, not cause it to proliferate. c. vancomycin destroys enterococcus in bowel other bowel flora have no competition and flourish pseudomembranous diarrhea. The term pseudomembranous is associated with C. diff infection, not enterococcus infection. d. iatrogenic antibiotics normal bowel flora wiped out giardia invades bowel inflammation nosocomial diarrhea. Giardia is a protozoa that invades via tainted water and doesn’t need normal flora to be wiped out to cause diarrhea. Also, “nosocomial” refers to something hospital- caused. There is nothing here to suggest a patient was in the hospital. 39. A patient who is undergoing a course of chemotherapy for cancer contracts chicken pox and almost dies. What is the most likely reason for this severe response to a fairly mild disease? a. Because of the cancer, the patient likely has neutropenia, which is a state of overabundance of nonfunctional WBCs. “Neutropenia” means lower-than-usual-numbers of neutrophils, not “overabundance,” which would be the word “neutrophilia.” b. Because of the chemotherapy, the patient likely has acquired combined B-cell and T-cell immunodeficiency. Correct—essentially, the chemo wiped out all (or most) of the leukocyte growth (see RRD 3 and concept map). c. The patient developed shingles, which is a secondary infection that is harder to treat. No mention of shingles in scenario. d. The patient probably has severe combined immunodeficiency syndrome (SCIDS). This is a congenital disease and was not mentioned in the scenario. 40. A woman whose blood type is AB+ is pregnant with a baby who is B- (B negative) Which is true about getting a Rhogam shot? a. Mom would not need a Rhogam shot, since the baby’s RBCs have a B antigen, which is compatible with mom’s AB blood. The baby’s RBCs do indeed have a B antigen—that is what gives the baby the blood type “B.” But Rhogam has to do with the Rh factor, so the first part of this answer doesn’t match with the second half. b. Mom will always need a Rhogam shot following pregnancies in which the baby is Rh negative, such as this baby. Only one situation sets up the possibility of the mom needing a Rhogam shot: when a mom is Rh negative and her fetus is Rh positive, because the mom’s body will see the Rh factor of the baby as being a foreign substance and will develop antibodies to it. With the next Rh+ baby, her antibodies will attach that baby’s RBCs. A Rhogam kills any antibodies she has developed, prior to the next pregnancy. This mom is Rh+, so her body will never see an Rh factor as being “foreign” and so there will never be a need for Rhogam, no matter what Rh type the fetus is. c. The baby will need Rhogam; otherwise he will develop Rh-antibodies that will attack the Rh antigen on the mom’s RBCs. Rhogam is for the mother, as needed, not the baby. d. Mom will never need a Rhogam shot with any pregnancy; she will never develop antibodies to Rh antigens on an Rh+ baby’s RBCs. Correct—see explanation for B.