Module 7: Women’s and Men’s Health, Infections, and Hematologic Disorders

Literature, cinema, and other cultural references have long examined differences between women and men. These observations extend well beyond obvious and even inconspicuous traits to include cultural, behavioral, and biological differences that can impact pathophysiological process and, ultimately, health.

Understanding these differences in traits and their impact on pathophysiology can better equip acute care nurses to communicate to patients of both sexes. Furthermore, APRNs who are able to communicate these differences can better guide care to patients, whatever their gender.

This week, you examine fundamental concepts of women’s and men’s health disorders. You also explore common infections and hematologic disorders, and you apply the key terms and concepts that help communicate the pathophysiological nature of these issues to patients. 

Buy a Plagiarism Free Paper Here

Learning Objectives

Students will:

• Analyze concepts and principles of pathophysiology across the life span
• Analyze processes related to women’s and men’s health, infections, and hematologic disorders
• Identify racial/ethnic variables that may impact physiological functioning
• Evaluate the impact of patient characteristics on disorders and altered physiology 

Week 10: Concepts of Women’s and Men’s Health, Infections, and Hematologic Disorders

In this exercise, you will complete a 10- to 20-essay type question Knowledge Check to gauge your understanding of this module’s content.  

Possible topics covered in this Knowledge Check include:

• Sexually transmitted diseases
• Prostate
• Epididymitis
• Factors that affect fertility
• Reproductive health
• Alterations and fertility
• Anemia
• ITP and TTP
• DIC
• Thrombocytopenia

Complete the Knowledge Check by Day 7 of Week 10

Knowledge Check: Women’s and Men’s Health, Infections, and Hematologic Disorders

Question 1

A 28-year-old woman presents to the clinic with a chief complaint of hirsutism and irregular menses. She describes irregular and infrequent menses (five or six per year) since menarche at 12 years of age. She began to develop dark, coarse facial hair when she was 14 years of age, but her parents did not seek treatment or medical opinion at that time. The symptoms worsened after she gained weight in college. She got married 3 years ago and has been trying to get pregnant for the last 2 years without success. Height 66 inches and weight 198. BMI 32 kg.m². Moderate hirsutism without virilization noted.  Laboratory data reveal CMP within normal limits (WNL), CBC with manual differential (WNL), TSH 0.9 IU/L SI units (normal 0.4-4.0 IU/L SI units), a total testosterone of 65 ng/dl (normal 2.4-47 ng/dl), and glycated hemoglobin level of 6.1% (normal value ≤5.6%). Based on this information, the APRN diagnoses the patient with polycystic ovarian syndrome (PCOS) and refers her to the Women’s Health APRN for further workup and management.  

Question 1 of 2: What is the pathogenesis of PCOS?

Answer: The pathogenesis of PCOS has been linked to altered luteinizing hormone (LH) action, insulin resistance, and a possible predisposition to hyperandrogenism. One theory maintains that underlying insulin resistance exacerbates hyperandrogenism by suppressing synthesis of sex hormone–binding globulin and increasing adrenal and ovarian synthesis of androgens, thereby increasing androgen levels. These androgens then lead to irregular menses and physical manifestations of hyperandrogenism. The hyperandrogenic state is a cardinal feature of PCOS but glucose intolerance/insulin resistance and hyperinsulinemia often run parallel to and markedly aggravate the hyperandrogenic state, thus contributing to the severity of signs and symptoms of PCOS.

Question 2

A 28-year-old woman presents to the clinic with a chief complaint of hirsutism and irregular menses. She describes irregular and infrequent menses (five or six per year) since menarche at 12 years of age. She began to develop dark, coarse facial hair when she was 14 years of age, but her parents did not seek treatment or medical opinion at that time. The symptoms worsened after she gained weight in college. She got married 3 years ago and has been trying to get pregnant for the last 2 years without success. Height 66 inches and weight 198. BMI 32 kg.m². Moderate hirsutism without virilization noted.  Laboratory data reveal CMP within normal limits (WNL), CBC with manual differential (WNL), TSH 0.9 IU/L SI units (normal 0.4-4.0 IU/L SI units), a total testosterone of 65 ng/dl (normal 2.4-47 ng/dl), and glycated hemoglobin level of 6.1% (normal value ≤5.6%). Based on this information, the APRN diagnoses the patient with polycystic ovarian syndrome (PCOS) and refers her to the Women’s Health APRN for further workup and management.  

Question 2 of 2: How does PCOS affect a woman’s fertility or infertility? 

Answer: Ovulation problems are usually the primary cause of infertility in women with PCOS. Ovulation may not occur due to an increase in testosterone production or because follicles on the ovaries do not mature. Due to unbalanced hormones, ovulation and menstruation can be irregular. A hyperandrogenic state is a cardinal feature in the pathogenesis of PCOS. Excessive androgens affect follicular growth, and insulin affects follicular decline by suppressing apoptosis and enabling follicle to persist. There is dysfunction in ovarian follicle development. Inappropriate gonadotropin secretion triggers the beginning of a vicious cycle that perpetuates anovulation.

Question 3

A 20-year-old female college student presents to the Student Health Clinic with a chief complaint of abdominal pain, foul smelling vaginal discharge, and fever and chills for the past 4 days. She denies nausea, vomiting, or difficulties with defecation. Last bowel movement this morning and was normal for her. Nothing has helped with the pain despite taking ibuprofen 200 mg orally several times a day. She describes the pain as sharp and localizes the pain to her lower abdomen. Past medical history noncontributory. GYN/Social history + for having had unprotected sex while at a fraternity party. Physical exam: thin, Ill appearing anxious looking white female who is moving around on the exam table and unable to find a comfortable position. Temperature 101.6F orally, pulse 120, respirations 22 and regular. Review of systems negative except for chief complaint. Focused assessment of abdomen demonstrated moderate pain to palpation left and right lower quadrants. Upper quadrants soft and non-tender. Bowel sounds diminished in bilateral lower quadrants. Pelvic exam demonstrated + adnexal tenderness, + cervical motion tenderness and copious amounts of greenish thick secretions. The APRN diagnoses the patient as having pelvic inflammatory disease (PID).  

Question: What is the pathophysiology of PID? 

Answer: Pelvic inflammatory disease (PID) is an infectious and inflammatory disorder of the upper female genital tract, including the uterus, fallopian tubes, and adjacent pelvic structures. Infection and inflammation may spread to the abdomen, including perihepatic structures.

PID is initiated by infection that ascends from the vagina and cervix into the upper genital tract. Chlamydia trachomatis is the predominant sexually transmitted organism associated with PID. Of all acute PID cases, less than 50% test positive for the sexually transmitted organisms such as Chlamydia trachomatis and Neisseria gonorrhea. Other organisms implicated in the pathogenesis of PID include, Gardnerella vaginalis (which causes bacterial vaginosis (BV), Haemophilus influenzae, and anaerobes such as Peptococcus and Bacteroides species.  Inflammatory responses in the fallopian tubes and uterus causes swelling and sometimes necrosis of the area. This inflammation leads to scarring of the fallopian tubes and causes infertility. N gonorrhoeae is no longer the primary organism associated with PID, but gonorrhea remains the second most frequently reported sexually transmitted disease, after chlamydial infection.

Question 4

A 27-year-old male comes to the clinic with a chief complaint of a “sore on my penis” that has been there for 3 days. He says it burns and leaked a little fluid. He denies any other symptoms. Past medical history noncontributory. Social history: works as a bartender and he states he often “hooks up” with some of the patrons, both male and female after work. He does not always use condoms. Physical exam within normal limits except for a lesion on the lateral side of the penis adjacent to the glans. The area is indurated with a small round raised lesion. The APRN orders laboratory tests, but feels the patient has syphilis.  

Question: Describe the 4 stages of syphilis.

Answer: Syphilis is an infectious venereal disease caused by the spirochete Treponema pallidum. Syphilis is transmissible by sexual contact with infectious lesions, from mother to fetus in utero, via blood product transfusion, and occasionally through breaks in the skin that come into contact with infectious lesions. If untreated, it progresses through 4 stages: primary, secondary, latent, and tertiary.

Primary: A chancre, or hard lesion develops at the site of the treponemal entry after exposure. In acquired syphilis, T pallidum rapidly penetrates intact mucous membranes or microscopic dermal abrasions and, within a few hours, enters the lymphatics and blood to produce systemic infection. Incubation time from exposure to development of primary lesions, which occur at the primary site of inoculation, averages 3 weeks but can range from 10-90 days. Secondary syphilis develops about 4-10 weeks after the appearance of the primary lesion. During this stage, the spirochetes multiply and spread throughout the body.

Secondary syphilis lesions are quite variable in their manifestations. Systemic manifestations include malaise, fever, myalgias, arthralgias, lymphadenopathy, and rash. Even if untreated, the immune system is usually able to suppress the infection and spontaneous resolution of skin lesions occurs.

Latent syphilis is a stage at which the features of secondary syphilis have resolved, though patients remain seroreactive. Some patients experience recurrence of the infectious skin lesions of secondary syphilis during this period. About one third of untreated latent syphilis patients go on to develop tertiary syphilis, whereas the rest remain asymptomatic.

Tertiary syphilis disease is rare. When it does occur, it mainly affects the cardiovascular system (80-85%) and the CNS (5-10%), developing over months to years and involving slow inflammatory damage to tissues. The 3 general categories of tertiary syphilis are gummatous syphilis (also called late benign), cardiovascular syphilis, and neurosyphilis.

Question 5

A 19-year-old female presents to the clinic with a chief complaint of “fluid filled bumps” and intense pruritis of her vulva. She states these symptoms have been present for about 10 days, but she thought she had a yeast infection. She self-medicated with over the counter (OTC) metronidazole (Flagyl™) intravaginally but the symptoms got worse. No other complaints except for fatigue out of proportion to her activity level. Past medical history noncontributory. Social history: sexually active with several men and did forget to use a condom during one sexual encounter. Physical exam negative except for pelvic exam which revealed multiple fluid filled (vesicular) lesions on the vulva and introitus. Positive lymph nodes in inguinal areas. The APRN diagnoses the patient with herpes simplex virus-type 2 known as genital herpes. 

Question: What is the pathophysiology of HSV-2? 

Answer: After the initial exposure and entry of the virus at mucocutaneous sites, the virus replicates locally in the dermis. This leads to cell destruction, transudation and vesical formation. The virus spreads and eventually enters the sensory nerves. Neurovirulence (the capacity to invade and replicate in the nervous system) occurs and leads to a systemic inflammatory immune response.

Latency is the establishment and maintenance of latent infection in nerve cell ganglia proximal to the site of infection, and in genital HSV infection, the sacral nerve root ganglia (S2-S5) are involved. 

Reactivation: The reactivation and replication of latent HSV, always in the area supplied by the ganglia in which latency was established, can be induced by various stimuli (eg, fever, trauma, emotional stress, sunlight, menstruation), resulting in overt or covert recurrent infection and shedding of HSV. In immunocompetent persons who are at an equal risk of acquiring HSV-1 and HSV-2 both orally and genitally, HSV-1 reactivates more frequently in the oral rather than the genital region. On the other hand, HSV-2 reactivates 8-10 times more commonly in the genital region than in the orolabial regions. Reactivation is more common and severe in immunocompromised individuals.

Cellular immunity is an important defense against herpes simplex. Dissemination of herpes simplex infection can occur in people with impaired T-cell immunity, such as in organ transplant recipients and in individuals with AIDS. Herpes simplex infection can also complicate burn wounds or damaged skin such as in atopic dermatitis or other allergic dermatoses.

Question 6

A 27-year-old male presents to the clinic with a chief complaint of a gradual onset of scrotal pain and swelling of the left testicle that started 2 days ago.  The pain has gotten progressively worse over the last 12 hours and he now complains of left flank pain. He complains of dysuria, frequency, and urgency with urination. He states his urine smells funny. He denies nausea, vomiting, but admits to urethral discharge just prior to the start of his severe symptoms. He denies any recent heavy lifting or straining for bowel movements. He says the only thing that makes the pain better is if he sits in his recliner and elevates his scrotum on a small pillow. Past medical history negative. Social history + for sexual activity only with his wife of 3 years. Physical exam reveals red, swollen left testicle that is very tender to touch. There is positive left inguinal adenopathy. Clean catch urinalysis in the clinic + for 3+ bacteria. The APRN diagnoses the patient with epididymitis.  

Question: Discuss how bacteria in the urine causes epididymitis.  

Answer: In men with bacteriuria, the pathogenic organism usually reaches the epididymis by ascending the vasa deferentia from an already infected urethra or bladder. The presence of bacteria initiates the inflammatory response, causing symptoms of bacterial epididymitis. In patients who have a history of lifting or straining, the is reflux of the urine from the bladder into the vas deferens and epididymis. Urine is extremely irritating to the epididymis and initiates an inflammatory response called chemical epididymitis.

Question 7

A 42-year-old male presents to the clinic with a chief complaint of fever, chills, malaise, arthralgias, dysuria, urinary frequency, low back pain, perineal, and suprapubic pain. He says he feels like he can’t fully empty his bladder when he voids. He states these symptoms came on suddenly about 12 hours ago and have gotten worse. He noticed some blood in his urine the last time he voided. He tried to have a bowel movement several hours ago but could not empty his bowel due to pain. Past medical and social history noncontributory. Physical exam reveals an ill appearing male. Temperature 101.8 F, pulse 122, respirations 20, BP 108/68. Exam unremarkable apart from left costovertebral angle (CVA) tenderness. Rectal exam difficult due to enlarged and extremely painful prostate.  Complete blood count revealed an elevated white blood cell count, elevated C-reactive protein and elevated sedimentation rate. Urine dip in the clinic + for 2+ bacteria.  

Question: Explain the differences between acute bacterial prostatitis and nonbacterial prostatitis. 

Answer: Prostatitis is defined as an increased number of inflammatory cells within the prostate gland. The inflammatory process may be infectious or inflammatory in origin. The most common histologic pattern is a lymphocytic infiltrate in the stroma immediately adjacent to the prostatic acini.

Prostatitis occurs in distinct forms that have separate causes, clinical features, and outcomes. Four clinical entities have been described: acute bacterial prostatitis, chronic bacterial prostatitis, nonbacterial or abacterial prostatitis, and prostatodynia. NIH classification and definition of prostatitis The National Institutes of Health (NIH) classification and definition of the categories of prostatitis are as follows:

• Category I – Acute bacterial prostatitis (ie, acute infection of the prostate) • Category II – Chronic bacterial prostatitis (ie, recurrent urinary tract infection and/or chronic infection of the prostate)
• Category III – Chronic abacterial prostatitis/chronic pelvic pain syndrome (ie, discomfort or pain in the pelvic region for at least 3 mo with variable voiding and sexual symptoms and/or no demonstrable infection; by definition, the syndrome becomes chronic after 3 mo)
• Category IIIA – Inflammatory chronic pelvic pain syndrome (ie, white blood cells in semen and/or expressed prostatic secretions and/or third midstream bladder specimen)
• Category IIIB – Noninflammatory chronic pelvic pain syndrome (ie, no white blood cells in semen and/or expressed prostatic secretions)
• Category IV – Asymptomatic inflammatory prostatitis (ie, evidence of inflammation in biopsy samples, semen and/or expressed prostatic secretions, but no symptoms)

In patients with noninfectious prostatitis, urine reflux may occur with urethral stricture disease, voiding dysfunction, or benign prostatic hyperplasia. Refluxing urine, even when it is sterile, may lead to chemical irritation and inflammation. Tubule fibrosis is initiated, and prostatic stones form and lead to intraductal obstruction and stagnation of intraductal secretions. This obstruction initiates an inflammatory response, and prostatitis symptoms develop.

Question 8

A 32-year-old woman presents to the clinic with a chief complaint of pelvic pain, excessive menstrual bleeding, dyspareunia, and inability to become pregnant after 18 months of unprotected sex with her husband. She states she was told she had endometrioses after a high school physical exam, but no doctor or nurse practitioner ever mentioned it again, so she thought it had gone away. She has no other complaints and says she wants to have a family. Past medical history noncontributory except for possible endometriosis as a teenager. Social history negative for tobacco, drugs or alcohol. The physical exam is negative except for the pelvic exam which demonstrated pain on light and deep palpation of the uterus. The APRN believes that the patient does have endometriosis and orders appropriate laboratory and radiological tests. The diagnostics come back highly suggestive of endometriosis.    

Question: Explain how endometriosis may affect female fertility

Answer: While the link between endometriosis and infertility is strong, the exact mechanism for infertility is unknown. The inflammation and irritation caused by the endometriosis can affect fertility. Inflammation of the fimbria, which pick up the egg and transport it into the fallopian tube, causes swelling and scarring so the egg may not reach its destination. Endometriosis can also block the fallopian tubes preventing the egg from being fertilized. The uterine endometrium in women with endometriosis appears to have an overactive response to estrogen and an under active response to progesterone, impairing the endometrial receptivity to blastocyte implantation, decreasing the chances of successful pregnancy.

Question 9

An APRN working in an anticoagulation clinic has been asked by the local college to present a lecture on platelets and their role in blood clotting to the graduate pathophysiology nursing students.  

Question: What key concepts should the APRN include in the presentation? 

Answer: Platelet activation is primarily under the control of the endothelial cells lining the blood vessels. Damage to the vessel causes platelets to fill in the endothelial gaps. Platelet adhesion is initiated by the loss of endothelial cells (or ruptures or erosions of atherosclerotic plaque) which exposes adhesive glycoproteins.

Platelets adhere to the subendothelium through receptors that bind to the adhesive glycoproteins. Platelet activation begins after platelet adhesion and undergoes an activation process that leads to changes in receptors, resulting in their ability to bind adhesive proteins. There are changes in the platelet shape, formation of pseudopods and activation of arachidonic pathways.

Platelet aggregation is induced by the release of thromboxane A2 (TXA2). Adhesive glycoproteins bind simultaneously on 2 different platelets. Stabilization of the platelet plug (blood clot) occurs by activation of coagulation factors, thrombin, and fibrin. Heparin neutralization factor enhances clot formation.

Platelet plug formation occurs when red blood cells and platelets become enmeshed in fibrin. Clot retraction and clot dissolution -clot retraction, using large numbers of platelets, join the edges of the injured vessel. Clot dissolution is regulated by thrombin and plasminogen activators.

Question 10

A 36-year-old woman presents to the clinic with complaints of dyspnea on exertion, fatigue, leg cramps on climbing stairs, craving ice to suck or chew and cold intolerance. The symptoms have come on gradually over the past 4 months. The only thing that make the symptoms better is for her to sit or lie down and stop the activity. She denies bruising or bleeding and states this is the first time this has happened. Past medical history noncontributory except for a new diagnosis of benign uterine fibroids 6 months ago after experiencing heavy menstrual bleeding every month. Social history noncontributory and she denies alcohol, tobacco, or drug use. Physical exam: pale, thin, Caucasian female who appears older than stated age. Physical exam remarkable for a soft I/IV systolic murmur, pallor of the mucous membranes, spoon-shaped nails (koilonychia), glossy tongue, with atrophy of the lingual papillae, and fissures at the corners of the mouth. The APRN suspects the patient has iron deficient anemia (IDA) secondary to excessive blood loss from uterine fibroids. The appropriate laboratory tests confirmed the diagnosis.  

Question: Discuss iron deficiency anemia and how the patient’s menstrual bleeding contributed to the diagnosis. 

Answer: Iron deficiency anemia develops when body stores of iron drop too low to support normal red blood cell (RBC) production. Inadequate dietary iron, impaired iron absorption, bleeding, or loss of body iron in the urine may be the cause. IDA is a hypochromic-microcytic anemia. With either excess bleeding or loss of body iron, there is no intrinsic dysfunction in iron metabolism. But both conditions deplete iron stores and reduce hemoglobin synthesis. Either diminished absorbable dietary iron or excessive loss of body iron can cause iron deficiency. Diminished absorption usually is due to an insufficient intake of dietary iron in an absorbable form. Hemorrhage is the most common cause of excessive loss of body iron, but it can occur with hemoglobinuria from intravascular hemolysis. Malabsorption of iron is relatively uncommon in the absence of small bowel disease (sprue, celiac disease, regional enteritis) or previous GI surgery. Iron contributes to immune function by regulating immune effector mechanisms (cytokine activities [interferon gamma], nitric oxide formation and T-cell proliferation. Acquired hyperemia may be part of the body’s response to infection. Bleeding for any reason produces iron depletion. If sufficient blood loss occurs, iron deficiency anemia ensues. A single sudden loss of blood produces a post-hemorrhagic anemia that is normocytic. The bone marrow is stimulated to increase production of hemoglobin, thereby depleting iron in body stores. Once they are depleted, hemoglobin synthesis is impaired and microcytic hypochromic erythrocytes are produced. The patient’s excess menstrual bleeding was most likely the cause of her anemia.

Question 11

A 67-year-old woman presents to the clinic with complaints of weakness, fatigue, paresthesias of the feet and fingers, difficulty walking, loss of appetite, and a sore tongue. These symptoms have been present for several months but the patient thought they were due to her recent retirement and geographic move from the Midwest to New England. The symptoms have gotten worse over the past few weeks and she has noticed that she is much more forgetful. This is of great concern as she worries she might have the beginning stages of Alzheimer’s Disease. Past medical history significant for Hashimoto thyroiditis that she developed in her early 20s. The rest of PMH and social history non- contributory. Physical exam reveals an average sized female whose skin has a sallow appearance. BP 128/74, Pulse 120, respirations 18 and temperature 99.0F orally. Examination of the head and neck reveals a smooth and beefy red tongue. Abdominal exam negative for hepatomegaly or splenomegaly.   

The APRN recognizes these symptoms and physical exam indicate the patient has pernicious anemia. After appropriate laboratory data received, the definitive diagnosis of pernicious anemia was made. 

Question 1 of 2:  How does pernicious anemia develop? 

Answer: Megaloblastic anemia resulting from vitamin B12 deficiency due to lack of intrinsic factor (IF). Impaired IF production can occur in adults due to autoimmune destruction of parietal cells, which secrete IF. Gastrectomy can significantly reduce the production of IF. A rare congenital autosomal recessive disorder can result in deficiency of IF without gastric atrophy. Early in the disease process the gastric submucosa becomes infiltrated with inflammatory cells, including autoreactive T cells. It appears that the T cell response initiates gastric mucosal injury and triggers the formation of autoantibodies. Several conditions other than impaired Intrinsic Factor production can cause a megaloblastic anemia such as: folic acid deficiency, altered pH in the small intestine, and lack of absorption of B12 complexes in the terminal ileum. Thus, pernicious anemia must be differentiated from other disorders that interfere with the absorption and metabolism of vitamin B-12.

Pernicious anemia probably is an autoimmune disorder with a genetic predisposition. The disease is more common than is expected in families of patients with pernicious anemia, and it is associated with human leukocyte antigen (HLA) types A2, A3, and B7 and type A blood group. Antiparietal cell antibodies occur in 90% of patients with pernicious anemia but in only 5% of healthy adults. Similarly, binding and blocking antibodies to IF are found in most patients with pernicious anemia. A greater association than anticipated exists between pernicious anemia and other autoimmune diseases, including thyroid disorders, type 1 diabetes mellitus, ulcerative colitis, Addison disease, infertility, and acquired agammaglobulinemia. An association between pernicious anemia and Helicobacter pylori infections has been postulated but not clearly proven.

Question 12

A 67-year-old woman presents to the clinic with complaints of weakness, fatigue, paresthesias of the feet and fingers, difficulty walking, loss of appetite, and a sore tongue. These symptoms have been present for several months but the patient thought they were due to her recent retirement and geographic move from the Midwest to New England. The symptoms have gotten worse over the past few weeks and she has noticed that she is much more forgetful. This is of great concern as she worries she might have the beginning stages of Alzheimer’s Disease. Past medical history significant for Hashimoto thyroiditis that she developed in her early 20s. The rest of PMH and social history non- contributory. Physical exam reveals an average sized female whose skin has a sallow appearance. BP 128/74, Pulse 120, respirations 18 and temperature 99.0F orally. Examination of the head and neck reveals a smooth and beefy red tongue. Abdominal exam negative for hepatomegaly or splenomegaly. The APRN recognizes these symptoms and physical exam indicate the patient has pernicious anemia. After appropriate laboratory data received, the definitive diagnosis of pernicious anemia was made. 

Question 2 of 2: How does pernicious anemia cause the neurological manifestations that are often seen in patients with PA? 

Answer: Patients with severe Vitamin B12 deficiency over a period of time begin to exhibit neurological changes such as peripheral and optic neuropathy, encephalopathy, and myelopathy. Nerve demyelination is the main pathophysiological feature of the neurological changes. That may produce neuronal death with subsequent disability. The posterior and lateral columns of the spinal cord may be affected and causes a loss of position (proprioception) and vibration sense.

Question 13

A 49-year-old man with a 22-year history of severe rheumatoid arthritis (RA) presents to clinic for his preadmission testing (PAT) and medical clearance for a planned right total hip arthroplasty. The patient had been severely limited in ambulation due to the RA. Current medications include prednisone 20 mg po qd and methotrexate 7.5 mg Thursdays, 5mg Fridays, and 7.5 mg Saturdays.  The patient had a complete blood count (CBC) with manual differentiation and red blood cell indices, complete metabolic panel (CMP) and coagulation studies (prothrombin time [PT], international normalized ratio [INR] and activated partial thromboplastin time [aPTT]). All the laboratory studies come back within normal limits except for the red blood cell indices. The hemoglobin and hematocrit were low along with mean corpuscle volume, plasma iron and total iron binding capacity, and transferrin also being low. There was a normal reticulocyte count, normal ferritin, serum B₁₂, folate and bilirubin. The APRN in the PAT clinic recognizes that the patient has anemia of chronic disease (ACD).  

Question 1 of 2: What is ACD and how does it develop? 

Answer: Anemia of chronic illness traditionally encompassed any inflammatory, infectious, or malignant disease of a long-standing nature. The modern definition includes rheumatoid arthritis, severe trauma, heart disease, diabetes mellitus, and inflammatory bowel disease. In these conditions, there is primarily a decreased availability of iron, relatively decreased levels of erythropoietin, and a mild decrease in the lifespan of RBCs to 70-80 days (normally 120 days).

Hepcidin, an endogenous antimicrobial peptide secreted by the liver, has been identified as controlling the level of plasma iron by regulating the intestinal absorption of dietary iron, as well as the release of iron from macrophages and the transfer of iron stored in the hepatocytes. Increase in hepcidin level in the course of inflammatory disease may be a significant mediator of the accompanying anemia

During chronic inflammation cytokines, such as interleukins (IL-1 and IL-6) and tumor necrosis factor (TNF-alpha) are released. These are believed to cause the destruction of RBC precursors and decrease the number of erythropoietin receptors on progenitor cells.

Question 14

A 49-year-old man with a 22-year history of severe rheumatoid arthritis (RA) presents to clinic for his preadmission testing (PAT) and medical clearance for a planned right total hip arthroplasty. The patient had been severely limited in ambulation due to the RA. Current medications include prednisone 20 mg po qd and methotrexate 7.5 mg Thursdays, 5mg Fridays, and 7.5 mg Saturdays.  The patient had a complete blood count (CBC) with manual differentiation and red blood cell indices, complete metabolic panel (CMP) and coagulation studies (prothrombin time [PT], international normalized ratio [INR] and activated partial thromboplastin time [aPTT]). All the laboratory studies come back within normal limits except for the red blood cell indices. The hemoglobin and hematocrit were low along with mean corpuscle volume, plasma iron and total iron binding capacity, and transferrin also being low. There was a normal reticulocyte count, normal ferritin, serum B₁₂, folate and bilirubin.  

The APRN in the PAT clinic recognizes that the patient has anemia of chronic disease (ACD).  

Question 2 of 2: Why do patients with chronic kidney disease (CKD) develop ACD?

Answer: Anemia of chronic illness traditionally encompassed any inflammatory, infectious, or malignant disease of a long-standing nature. The modern definition includes rheumatoid arthritis, severe trauma, heart disease, diabetes mellitus, and inflammatory bowel disease. In these conditions, there is primarily a decreased availability of iron, relatively decreased levels of erythropoietin, and a mild decrease in the lifespan of RBCs to 70-80 days (normally 120 days). In patients with advanced stages of CKD, the etiology of anemia tends to be multifactorial and include the following: decreased RBC production due to lack of erythropoietin, increased RBC destruction due to hemolysis (intravascular or extravascular), and increased blood loss due to multiple venipunctures for an array of indications. When the kidneys are damaged, they fail to produce adequate amounts of erythropoietin in response to decreased numbers of erythrocytes. The kidney is frequently affected by chronic inflammatory processes caused by circulating immune complexes and other factors that deposit in the kidneys and activate secondary inflammatory mechanisms. Damage to the kidneys affects the secretion of erythropoietin which is a necessary hormone for production of erythrocytes in the bone marrow, thus resulting in diminished bone marrow erythropoiesis. Uremic toxins that increase in the blood secondary to renal failure may suppress bone marrow function and damage erythrocytes. Platelet function may also be defective, and this results in chronic bleeding and loss of erythrocytes

Question 15

A 14-year-old female is brought to the Urgent Care by her mother who states that the girl has had an abnormal number of bruises and “funny looking red splotches” on her legs. These bruises were first noticed about 2 weeks ago and are not related to trauma. Past medical history not remarkable and she takes no medications. The mother does state the girl is recovering from a “bad case of mono” and was on bedrest at home for the past 3 weeks. The girl noticed that her gums were slightly bleeding when she brushed her teeth that morning. Labs at Urgent Care demonstrated normal hemoglobin and hematocrit with normal white blood cell (WBC) differential. Platelet count of 100,000/mm3 was the only abnormal finding. The staff also noticed that the venipuncture site oozed for a few minutes after pressure was released. The doctor at Urgent Care referred the patient and her mother to the ED for a complete work up of the low platelet count including a peripheral blood smear for suspected immune thrombocytopenia purpura (ITP). 

Question: What is ITP and why do you think this patient has acute, rather than chronic, ITP? 

Answer: Immune thrombocytopenia (ITP) is a syndrome in which platelets become coated with autoantibodies to platelet membrane antigens, resulting in splenic sequestration and phagocytosis by mononuclear macrophages. The resulting shortened life span of platelets in the circulation, together with incomplete compensation by increased platelet production by bone marrow megakaryocytes, results in a decreased number of circulating platelets. Acute ITP is usually secondary to infections, particularly viral, or other conditions that lead to a large number of antigens in the blood, such as drug allergies or systemic lupus erythematosus. In these cases, the antigen usually forms immune complexes with circulating antibody, and it is believed that the immune complexes bind to Fc receptors on platelets, leading to their destruction in the spleen. In this patient, a recent severe case of Epstein-Barr virus probably was the initiating factor, which is common in acute ITP.

Question 16

A 22-year-old male is in the Surgical Intensive Care Unit (SICU) following a motor vehicle crash (MVC) where he sustained multiple life-threatening injuries including a torn aorta, ruptured spleen, and bilateral femur fractures. He has had difficulty maintaining his mean arterial pressure (MAP) and has required various vasopressors. He has a triple lumen central venous catheter (CVC) for monitoring his central venous pressure, administration of medications and blood products, as well as total parenteral nutrition. Per hospital protocol, he is receiving an unfractionated heparin 1:1000 flush after administration of each of the triple antibiotics that have been ordered to maintain patency of the lumens.  Seven days post injury, the APRN in the SICU is reviewing the patient’s morning labs and notes that his platelet count has dropped precipitously to 50,000 /mm³ from 148,000/mm³ two days ago. The APRN suspects the patient is developing heparin induced thrombocytopenia (HIT).  

Question 1 of 2: What is underlying pathophysiology of heparin induced thrombocytopenia? 

Answer: Heparin-induced thrombocytopenia (HIT) is caused by antibodies that bind to complexes of heparin and platelet factor 4 (PF4), activating the platelets and promoting a prothrombotic state. HIT is more frequently encountered with unfractionated heparin (UFH) than with low molecular weight heparin (LMWH). It is an immune mediated adverse drug reaction caused by IgG antibodies against the heparinplatelet factor 4 complex leading to platelet activation through platelet FcyIIa receptors. The release of additional platelet factor 4 from activated platelets and activation of thrombin lead to increased platelet consumption and a decrease in platelet counts beginning 5-10 days after administration of unfractionated heparin.

Buy a Plagiarism Free Paper

Question 17

A 22-year-old male is in the Surgical Intensive Care Unit (SICU) following a motor vehicle crash (MVC) where he sustained multiple life-threatening injuries including a torn aorta, ruptured spleen, and bilateral femur fractures. He has had difficulty maintaining his mean arterial pressure (MAP) and has required various vasopressors. He has a triple lumen central venous catheter (CVC) for monitoring his central venous pressure, administration of medications and blood products, as well as total parenteral nutrition. Per hospital protocol, he is receiving an unfractionated heparin 1:1000 flush after administration of each of the triple antibiotics that have been ordered to maintain patency of the lumens.  Seven days post injury, the APRN in the SICU is reviewing the patient’s morning labs and notes that his platelet count has dropped precipitously to 50,000 /mm³ from 148,000/mm³ two days ago. The APRN suspects the patient is developing heparin induced thrombocytopenia (HIT).  

Question 2 of 2: The APRN assesses the patient and notes there is a decreased right posterior tibial pulse with cyanosis of the entire foot. The APRN recognizes this probably represents arterial thrombus formation. How does someone who is receiving heparin develop arterial and venous thrombosis? 

Answer: Platelet activation results in the release of procoagulant platelet microparticles, platelet consumption, and thrombocytopenia. Marked generation of thrombin, activation of monocytes and other inflammatory cells, and endothelial injury and activation follow, producing the characteristic venous and arterial thromboses of HIT. The risk of HIT is highest with prolonged use of heparin for postoperative thrombophylaxis. However, case studies have also demonstrated the possibility of developing HIT with minimal heparin exposure via intravascular flushes to maintain the patency of indwelling arterial or venous catheters. The platelets aggregate in the microcirculation, leaving to systemic thrombocytopenia but the platelets clump together and form thrombi and emboli. Arterial emboli usually form in the larger arteries of the upper and lower extremities and if not identified quickly, limb necrosis occurs. Treatment is not warfarin which could lead to skin necrosis but rather withdrawal of the heparin and the use of thrombin inhibitors such as argatroban.

Question 18

A 33-year-old female is brought to Urgent Care by her husband who states his wife has gotten suddenly confused and complains of a severe headache. He also noticed large bruises on her legs which were not there yesterday. Only significant past medical history is that the patient developed herpes zoster 2 weeks ago and was given acyclovir for treatment. Physical exam revealed well developed female who is only oriented to person. Large areas of ecchymosis noted on both arms and legs. Stat CBC revealed a platelet count of 18,000/mm^3, hemoglobin of 8 g/dl and hematocrit of 24%. The patient was immediately transported to the Emergency Room by Emergency Medical Services (EMS) where further work up demonstrated idiopathic thrombotic thrombocytopenic purpura (TTP).  

Question: What is the pathophysiology of TTP? 

Answer: The underlying mechanism in idiopathic TTP typically involves antibodies inhibiting the enzyme ADAMTS13. TTP is caused by spontaneous aggregation of platelets and activation of coagulation in the small blood vessels. Platelets are consumed in the aggregation process and bind von Willebrand Factor (vWF). These platelet-vWF complexes form small blood clots which circulate in the blood vessels and cause shearing of red blood cells, resulting in their rupture and formation of schistocytes. These microemboli cause severe organ damage by reducing blood flow to the organ.

The classic presentation of TTP, which occurs in less than 10% of people, includes five major signs. These are:

• Fever
• Changes in mental status
• Thrombocytopenia
• Reduced kidney function
• Microangiopathic hemolytic anemia

The treatment at this time is through plasma exchange but some newer monoclonal antibody has shown some positive results. Some patients may require splenectomy.

Question 19

A 64-year man is recovering from a transurethral resection of the prostate for treatment of benign prostate hyperplasia. The patient is receiving intravenous antibiotics for the urinary tract infection that was found on the preoperative urine culture and sensitivity (C & S). The post-operative course has been smooth and the APRN is removing the 3-way Foley catheter when there is a sudden release of bright red blood with many blood clots in the Foley bag. The patient becomes hypotensive, tachycardic and the APRN notes new ecchymoses on the patient’s arms and legs. The patient was immediately transferred to the surgical intensive care unit (SICU) and a stat hematology consult was conducted. Stat CBC, d-dimer, peripheral blood smear, partial thromboplastin time, Prothrombin time/international normalization ratio (INR), and fibrinogen labs were drawn. Results were:  

CBC with markedly decreased platelet count, peripheral blood smear showed decreased number of platelets and presence of large platelets and fragmented red cells (schistocytes), prothrombin time prolonged as was the partial thromboplastin time. The d-dimer was markedly elevated, and fibrinogen level was low. The diagnosis of disseminated intravascular coagulation (DIC) was made based on clinical picture and laboratory data.  

Question 1 of 2: What is DIC and how does it develop? 

Answer: Disseminated intravascular coagulation (DIC) is characterized by systemic activation of blood coagulation, which results in generation and deposition of fibrin, leading to microvascular thrombi in various organs and contributing to multiple organ dysfunction syndrome (MODS). Consumption of clotting factors and platelets in DIC can result in life-threatening hemorrhage. Derangement of the fibrinolytic system further contributes to intravascular clot formation, but in some cases, accelerated fibrinolysis may cause severe bleeding. Therefore, a patient with DIC can present with a simultaneously occurring thrombotic and bleeding problem, which obviously complicates the proper treatment. The hematologic derangements seen in DIC result from the following 4 simultaneously occurring mechanisms ,Tissue factor (TF)–mediated thrombin generation, dysfunctional physiologic anticoagulant mechanisms (eg, depression of antithrombin and protein C system), which cannot adequately balance this thrombin generation, impaired fibrin removal due to depression of the fibrinolytic system – This is mainly caused by high circulating levels of plasminogen activator inhibitor type 1 (PAI-1); however, in exceptional forms of DIC, fibrinolytic activity may be increased and contribute to bleeding, and inflammatory activation. Hepatic dysfunction in sepsis results in decreased anti-thrombin synthesis and extravascular leakage of this protease inhibitor because of capillary leakage. The amount of thrombin produced during DIC exceeds the ability of the body’s naturally occurring anticoagulants to regulate it.

Question 20

A 64-year man is recovering from a transurethral resection of the prostate for treatment of benign prostate hyperplasia. The patient is receiving intravenous antibiotics for the urinary tract infection that was found on the preoperative urine culture and sensitivity (C & S). The post-operative course has been smooth and the APRN is removing the 3-way Foley catheter when there is a sudden release of bright red blood with many blood clots in the Foley bag. The patient becomes hypotensive, tachycardia and the APRN notes new ecchymoses on the patient’s arms and legs. The patient was immediately transferred to the surgical intensive care unit (SICU) and a stat hematology consult was conducted. Stat CBC, d-dimer, peripheral blood smear, partial thromboplastin time, Prothrombin time/international normalization ratio (INR), and fibrinogen labs were drawn. Results were:  

CBC with markedly decreased platelet count, peripheral blood smear showed decreased number of platelets and presence of large platelets and fragmented red cells (schistocytes), prothrombin time prolonged as was the partial thromboplastin time. The d-dimer was markedly elevated, and fibrinogen level was low. The diagnosis of disseminated intravascular coagulation (DIC) was made based on clinical picture and laboratory data.  

Question 2 of 2: What factors contribute to the development of DIC?  

Answer: Several disease states may lead to the development of DIC, generally via one of the following two pathways: A systemic inflammatory response, leading to activation of the cytokine network and subsequent activation of coagulation (eg, in sepsis or major trauma). Release or exposure of procoagulant material into the bloodstream (eg, in cancer, crush brain injury, or in obstetric cases). Infectious causes include: Bacterial (eg, gram-negative sepsis, gram-positive infections, rickettsial), Viral (eg, HIV, cytomegalovirus [CMV], varicella-zoster virus [VZV], and hepatitis virus), Fungal (eg, Histoplasma), Parasitic (eg, malaria).

Malignancy causes include: Hematologic (eg, acute myelocytic leukemia), metastatic (eg, mucin-secreting adenocarcinoma). Obstetric causes include amniotic fluid embolism, abruptio placentae, acute peripartum hemorrhage, preeclampsia/eclampsia/hemolysis, elevated liver enzymes, and low platelet count (HELLP) syndrome, retained stillbirth, septic abortion and intrauterine infection, acute fatty liver of pregnancy

Traumatic causes include burns, motor vehicle accidents, snake envenomation. Transfusion related: hemolytic reactions of transfusion. In general, if the underlying condition is self-limited or can be appropriately handled, DIC will disappear, and the coagulation status will normalize. A patient with acute hemorrhagic DIC that is associated with metastatic gastric carcinoma likely has a lethal condition that does not alter patient demise, regardless of treatment. On the other hand, a patient with acute DIC associated with abruptio placentae needs quick recognition and obstetric treatment; the DIC will resolve with the treatment of the obstetric catastrophe.