| The difference between the coagulation disorders Hemophilia A and Hemophilia B lies in: | View Page |
| Coagulation Disorders - Inherited Inherited disorders are those which are considered to be inborn, and have some familial linkage. Hemophilia A is a deficiency of coagulation factor VIII. It is the most commonly encountered hereditary based coagulation disorder. Found almost exclusively in males, its pattern of inheritance is sex-linked recessive. This disorder presents clinically with hemorrhagic events ranging in severity from mild to severe. Patients often present with spontaneous bleeding into their joints, a classic symptom of this affliction. The treatment of Hemophilia A often involves the administration of commercial factor VIII products. | View Page |
| Coagulation Disorders - Inherited Hemophilia B is a deficiency of coagulation factor IX. Found almost exclusively in males, its pattern of inheritance is sex-linked recessive. This disorder presents almost identically to Hemophilia A in terms of symptoms, and has a very similar pattern of inheritance. Be sure to keep in mind that while similar, Hemophilia A and B are caused by a deficiency in different coagulation factors. The treatment of Hemophilia B involves therapeutic administration of Factor IX concentrates. | View Page |
| Coagulation Disorders - Acquired Disseminated Intravascular Coagulation (DIC) is best described as a disorder of consumption, because clotting factors are depleted from the blood. Basically, clotting occurs randomly throughout the body, as opposed to just in the localized areas where vascular damage has occurred, consuming clotting factors and other components such as platelets in the process. Symptoms may range from a mild bleed, to severe, profuse bleeding, primarily dependant upon the availability of clotting factors. As more and more coagulation factors and components are consumed, the disorder progresses and symptoms worsen. Most heavily impacted are the levels of factors I, V, and VIII as well as the number of available platelets. Clinically, DIC is detected via an elevated (positive) FDP, positive D-dimer test, a prolonged PT and APTT, plus the manifestation of hemorrhagic episodes. DIC is diagnosed as two primary types, acute and chronic. Acute DIC manifests in a few hours or a few days, has a high mortality rate, and is seen in infections, obstetric complications, liver disease, and tissue injury. Chronic DIC is a secondary condition to some other disease state. Once you treat the primary disease, this type of DIC will go away. Treatment is often factor replacement therapy through the use of fresh frozen plasma and/or cryoprecipitate. | View Page |
| Introduction Hereditary hemochromatosis (HH) is a disorder of iron regulation that results in excessive dietary iron absorption through the gastrointestinal tract. Over time, the resultant iron overload and its deposition in tissue may lead to widespread organ damage, a variety of chronic disorders, and even death. Although it is a genetic disorder, clinical symptoms most typically become apparent in middle aged adults. Iron overload occurs in a variety of hereditary and acquired forms, known as iron storage diseases. HH is the most common cause of inherited iron overload. (1) Due to lack of awareness, HH often goes undetected or unrecognized by health care providers. Early detection to prevent the serious complications associated with iron overload has important consequences for reducing morbidity and mortality. Laboratory tests that assess iron levels and molecular assays for genetic mutatations are essential for both its detection and diagnosis. | View Page |
| Development of Iron Overload The amount of time needed for iron to increase to levels causing organ damage is variable and may be partially dependent on gender, dietary or other environmental factors, and unknown genetic factors. Blood loss through menstruation and pregnancy are thought to delay the onset of iron overload, and therefore symptoms of HH, in women. Similarly, regular blood donation may confer some degree of protection. The loss of hemoglobin within intact erythrocytes reduces the amount of iron available for recycling.As levels of storage iron increase, clinical features of iron overload, including hepatic dysfunction or failure, diabetes, hypogonadism, arthritis, cardiomyopathy, hyperpigmentation, and fatigue, may become evident.Symptomatic patients typically present in middle age between the ages of 30 and 60, although this is quite variable. Persons as young as 20 may show clinical signs and symptoms of HH.(6) In the US, males are more than twice as likely as females to be diagnosed with HH, and the majority of cases are found in Caucasians. | View Page |
| General Clinical Considerations Hereditary hemochromatosis (HH) is frequently discovered only during management of associated illness or routine health evaluations. It has been estimated that only a small percentage of all affected persons are actually diagnosed. Individuals with HH may be symptomatic for several years prior to diagnosis and may have consulted multiple health care providers.Under-diagnosis of HH is thought to occur due to:• Lack of specificity of early signs and symptoms• Asymptomatic status of some patients until damage to organs and tissues has occurred• Confusion with liver disease due to other causes• Insufficient awareness and knowledge of HHEarly identification of persons with HH is essential to prevent serious and irreversible complications associated with severe iron overload. A classic triad of skin hyperpigmentation (bronzing), type 2 diabetes, and hepatic cirrhosis has long been recognized as evidence of advanced iron overload. However, persons with HH may present with a much wider variety of signs and symptoms, particularly if they are seen before significant iron accumulation has occurred. Age of presentation and disease severity are highly variable. A diagnosis of HH is based on laboratory evidence of iron overload, genetic mutations associated with HH, and presence of clinical signs and symptoms consistent with HH.(10) | View Page |
| Which of the following does NOT contribute to the under-diagnosis of hereditary hemochromatosis (HH)? | View Page |
| Signs and Symptoms of HH Early signs and symptoms of hereditary hemochromatosis (HH) are vague, nonspecific, and variable. As iron overload progresses (late HH), signs and symptoms become more severe and are related to damage of specific organs. | View Page |
| Which of the following characterizes the early signs and symptoms of hereditary hemochromatosis (HH)? | View Page |
| Secondary Disorders of Iron Overload In addition to hereditary hemochromatosis (HH), there are other conditions of iron overload that must be considered in a differential diagnosis. Disorders such as sickle cell disease, thalassemia, sideroblastic anemia, congenital dyserythropoietic anemia, and liver disease may also cause iron overload. Transfusion-dependant patients and persons who abuse iron-containing vitamin supplements are also at risk. These conditions are usually described as secondary iron overload, in contrast to the primary iron overload of HH.Patient history, clinical signs and symptoms, biochemical and hematologic laboratory analyses, and possibly results of a liver biopsy may be needed to establish a diagnosis of a condition causing secondary iron overload. DNA tests for common HFE mutations are very likely the most important diagnostic tool for identifying HH as the cause of iron overload. In some patients, both secondary causes and HH may be contributing to iron overload. Differentiating the secondary causes of iron overload from HH is heavily dependent on the results of laboratory assays, but a complete discussion is beyond the scope of this course. | View Page |
| Diagnosing HH The diagnosis of hereditary hemochromatosis (HH) is made through a combination of laboratory tests and medical evaluation of a patient's signs and symptoms. Iron overload is identified by tests that evaluate iron metabolism, while molecular assays are needed to document mutations in the HFE gene or others such as hepcidin, hemojuvelin, or transferrin receptor. Individuals with documented iron overload who exhibit signs and symptoms consistent with HH and who possess HFE or other mutations are considered to have HH. Other causes of secondary iron overload may need to be ruled out.An example of a testing algorithm is shown. | View Page |
| Which of the following is (are) needed for a diagnosis of hereditary hemochromatosis (HH)? | View Page |
| What is the major determinant of prognosis for patients with hereditary hemochromatosis (HH)? | View Page |
| Molecular Tests DNA tests for HFE mutations associated with hereditary hemochromatosis (HH) are available in some clinical laboratories and reference laboratories. Testing for the presence of the C282Y is essential, although most labs also test for H63D and S65C mutations. Molecular testing is most appropriate for confirmatory testing of symptomatic individuals with altered iron studies (increased TS and SF), in pre-symptomatic individuals (increased TS, normal SF and liver function tests), and in family members of individuals diagnosed with HH. The use of genetic tests alone for routine screening of asymptomatic persons is not recommended for several reasons. A positive test indicating the presence of HFE mutations does not guarantee that an individual will develop clinically significant iron overload or predict severity of symptoms. A negative result (no HFE mutations present) does not rule out a diagnosis of iron overload because of genetic heterogeneity. Compared to biochemical analyses for iron, molecular assays are expensive. Finally, molecular testing may result in the diagnosis of a genetic disease, thus opening up the possibility for discrimination in health insurance coverage. Using molecular methods, DNA is extracted from leukocytes in whole blood samples or from buccal cells and analyzed for specific HFE mutations using polymerase chain reaction (PCR) with melt curve analysis. Currently there are no FDA-cleared products for HFE testing, and testing laboratories are using "home brew" reagents. This situation is expected to change as manufacturers submit products for FDA approval. | View Page |
| Initial Treatment Phlebotomy is considered the treatment of choice for patients with iron overload due to hereditary hemochromatosis (HH). Each unit of blood contains approximately 200 to 250 mg of iron. As erythrocytes are removed by phlebotomy, iron stores are mobilized and utilized in the production of new, circulating erythrocytes. Through periodic phlebotomies, stored iron is removed until iron-deficient erythropoiesis is induced. The initial, or iron reduction, phase of treatment typically consists of removing one unit (450 mL) of whole blood once or twice weekly. Prior to beginning phlebotomy, the patient’s hemoglobin and hematocrit must be checked to ensure that the patient is not anemic. A sample for serum ferritin is also collected at this time.Initial treatment goals include inducing iron deficient hematopoiesis without the development of debilitating symptoms of anemia. A hemoglobin concentration of 10.0 to 12.0 g/dL is often used as a target range. The initial treatment phase continues until excess stored iron is removed and ferritin levels decrease to approximately 50 ng/mL. (13) Ferritin and hemoglobin levels are periodically monitored during this phase. The number of phlebotomies needed to reduce iron levels and induce anemia is related to the degree of initial iron overload. Patients may be referred to a hematologist or gastroenterologist during the initial treatment phase. Many patients receive therapeutic phlebotomy services in a hospital or doctor’s office, but patients may also undergo phlebotomy at a blood center. Blood collected from persons with HH may be used for transfusion or as blood products if it has been collected from a facility with an approved variance from the US Food and Drug Administration. Not all blood centers have applied for or been granted this variance.(14)The initial treatment phase continues until excess stored iron is removed and ferritin levels decrease to approximately 50 ng/mL. Removal of excess stored iron may take from one month to three years. | View Page |
| Rationale for Treatment Treatment for hereditary hemochromatosis (HH) is typically indicated for iron overload in symptomatic patients. The goal of therapy is to reduce stored iron which may result in reversal or resolution of some symptoms and improve prognosis. Causes of death in patients with HH include serious medical conditions such as hepatocellular carcimoma, cirrhosis, cardiomyopathy, and diabetes. Ideally, treatment should begin before these conditions develop. The earlier HH is detected, before the onset of severe organ damage, the lower the risk of mortality. | View Page |
| The general signs and symptoms of smallpox include: | View Page |
| The early symptoms of anthrax include: | View Page |
| Agent: Smallpox (Virus) Most likely means of dissemination: As an aerosolPrimary route of entry: InhalationGeneral signs and symptoms: High fever, extreme lethargy, severe headache, severe backache, severe abdominal pain, with a rash that starts as red bumps but quickly develops into small, itchy blisters. Photo courtesy of the CDC archives. | View Page |
| Agent: Anthrax (Bacterium) Most likely means of dissemination: In a solid state Primary route of entry: Inhalation (also ingestion and absorption) General signs and symptoms: Early symptoms are flu-like—chills, fever, nausea, and swelling of lymph nodes. | View Page |
| Agent: Pneumonic plague (Bacterium) Most likely means of dissemination: AerosolPrimary route of entry: InhalationGeneral signs and symptoms: High fever, chills, headache, coughing up of blood (hemoptysis), and toxemia, progressing rapidly to difficulty in breathing (dyspnea), and bluish discoloration of the skin and mucous membranes (cyanosis).There is another form of the disease called “bubonic plague”. While it is caused by the same organism, it is not transmissible through human contact. Pneumonic plague is transmissible through human contact. | View Page |
| Agent: Botulism (bacterium) Most likely means of dissemination: Aerosol (eating contaminated food)Primary route of entry: Inhalation (oral)General signs and symptoms: Difficulty with speaking, swallowing, or blurred or double vision, drooping eyelids (ptosis), dilated pupils, dry mouth, decreased gag reflex, weakening of the reflexes (hyporeflexia), abnormal sensations such as numbness, prickling, tingling, and arm or leg weakness.Botulism is caused by a neurotoxin and technically could be classified as a chemical WMD. For our discussion it is placed under biological agents because the toxin is derived from a bacterium. Botulism is potentially life-threatening, producing a characteristic clinical picture of muscular paralysis leading to respiratory failure. Photo courtesy of the CDC archives. | View Page |
| Agent: Tularemia (bacterium) Most likely means of dissemination: Solid or aerosolPrimary route of entry: Inhalation, absorption, or ingestionGeneral signs and symptoms: Sudden fever, chills, headaches, muscle aches, joint pain, dry cough, progressive weakness, and pneumonia.The disease is not transmissible through human contact. When used as a WMD, infection would be acquired by handling infected material, eating or drinking contaminated food or water or by breathing in the bacterium. | View Page |
| Agent: Viral hemorrhagic fevers (Ebola, Marburg, Lassa and Argentine) Most likely means of dissemination: Solid, liquid or aerosolPrimary route of entry: Absorption, inhalation, ingestionGeneral signs and symptoms: Vary by type of viral hemorrhagic fever (VHF), but initial signs and symptoms often include marked fever, fatigue, dizziness, muscle aches, loss of strength, and exhaustion. Severe cases of VHF often show signs of bleeding under the skin, in internal organs, or from body orifices like the mouth, eyes, or ears. Photo courtesy of the CDC archives. | View Page |
| Early symptoms of inhaled Anthrax include | View Page |
| Blood Agents Example: Hydrogen cyanidePhysical Properties: Highly volatile gas with a bitter almond odor.General Signs and Symptoms: Violent convulsions, stoppage of breathing, cardiac failure.Relative Rate of Action: Incapacitation within minutes and death within 15 minutes. | View Page |
| Lung-damaging or Choking Agents Example: Phosgene Physical Properties: Heavy gas, smells like fresh cut hay. General Signs and Symptoms: Coughing and choking, followed by tightness in chest, nausea, vomiting and headache. Death is due to the accumulation of fluid in the lungs. Relative Rate of Action: Immediate in high concentrations to several hours in low concentrations. | View Page |
| Blister Agents Example: MustardPhysical Properties: Oily liquid that may or may not have a garlic odor.General Signs and Symptoms: Initial redness of skin followed by blister formation, irritation to eyes, hoarseness or hacking cough, possibly nausea and vomiting.Relative Rate of Action: Usually 4 to 6 hours before onset. Photo courtesy of the Wikimedia Commons. | View Page |
| Nerve Agents Examples: Tabun, SarinPhysical Properties: Colorless liquid, usually odorless, but may have a fruity smell.General Signs and Symptoms: Difficulty in breathing, contraction of the pupils, blurred vision, headache, nausea, convulsions, and eventually death.Relative Rate of Action: Rapid, within minutes. Photo courtesy of the Wikimedia Commons. | View Page |
| In Case of a Biological Attack Listen to the radio for instructions from authorities on whether to evacuate or stay put. If told to stay inside, seek shelter in an internal room or a room with as few doors and windows as possible. Turn off all ventilation and as best as possible seal all openings in windows and doors. Continue to monitor the radio. Some biological attacks may be more immediately apparent than others. Monitor your radio, television, or medical alert for instructions from authorities regarding disease symptoms and how and where to seek medical attention. If you do come in contact with a visible, potentially infectious substance, you should remove and bag your clothes and personal items, wash yourself with warm soapy water immediately, and seek medical assistance. | View Page |
| Repetitive Motion Injuries Repetitive motions can cause a variety of disorders that affect nerves, tendons, and muscles. Symptoms can include tingling or numbness in the fingers or hands, decreased range of motion, decreased grip strength, sleep interupted by numbness or discomfort in the hands, pain in fingers, hands, or wrist, or pain shooting up into the forearms or arms.Some common afflictions that could affect laboratory workers due to the nature of their jobs are listed in the table below. Condition Symptoms Cause Carpal tunnel syndrome Pain that radiates up the arm, numbness or tingling in the thumb, index, or middle finger and weakness in the wrist and hand Compression of the median nerve that runs from the forearm into the hand Thoracic outlet syndrome Numbness and tingling in the hand, intensified with overhead activities Compression of the nerves and blood vessels between the neck and shoulder Radial tunnel syndrome Elbow pain, pain near the base of thumb, or pain anywhere in between. A common symptom is wrist weakness. Compression or entrapment of the radial nerve; may be caused by repetitive wrist and finger extension or repetitive forearm turning. Tendinitis Stiffness, tightness, and burning sensation; may experience a deep nonspecific pain. Grip impairment. Occurs most often in the tendons of the fingers, thumb, forearm, elbow, and shoulder. Repetitive motions or maintaining an awkward position that stresses tendons beyond their strength. Friction from overuse can cause inflammation. Tenosynovitis Pain, swelling, difficulty moving the joint in the affected area Inflammation of the tendon sheath | View Page |
| Eyestrain Eyestrain is a common problem associated with the prolonged use of computers or microscopes. Symptoms of eyestrain include: Blurred or double vision Itchy, dry, sore, burning, or tired eyes Headaches Color fringes / after images Sensitivity to light | View Page |
| Which of the following is a symptom of a repetitive motion injury? | View Page |
| Light sensitivity and headaches are symptoms of what disorder? | View Page |
| A 20 year-old female was admitted into the hospital complaining of 10 to 15 bloody mucous stools per day, fever, gastrointestinal disturbances, abdominal pain, and nausea. The preliminary O & P report went out as "Probable Entamoeba histolytica trophozoites and cysts, confirmation pending." This patient is most likely suffering from: | View Page |
| Match each organism with its respective associated condition: | View Page |
| A 32 year old male was seen in the emergency room with gastrointestinal discomfort. Upon questioning the patient it was learned that he first began feeling ill after spending a day at the park where he swam and played volleyball barefooted. He first noticed a lesion on his foot. Later, he developed vague respiratory symptoms. Now his largest complaint is severe abdominal pain along with occasional vomiting. This patient is most likely suffering from: | View Page |
| This stool parasite measures 55 µm by 50 µm and is the causative agent of: | View Page |
| This parasite, found in striated muscle, is responsible for which of the following conditions? | View Page |
| Which of the following symptoms are associated with an infection of the parasite pictured below? | View Page |
| Perianal itching is the major symptom of infection with both forms of the organism pictured here. This parasite is the causative agent of: | View Page |
| Arrange the following hookworm symptoms in order of their occurance based on the parasite's migration through the body beginning with human transmission: | View Page |
| A 68-year-old female, who recently vacationed in Brazil, presented to her physician exhibiting overall weakness, fever, and enlarged lymph nodes. Blood was collected for culture and parasitic examination. The culture was negative. This suspicious form was recovered upon examining the Giemsa-stained preparation. This patient is most likely suffering from: | View Page |
| Match each parasite named below with its respective primary symptom: | View Page |
| Label the morphologic structures on this parasite form: | View Page |
| A 21 year old male presented in the emergency room with symptoms resembling a liver infection. The patient complained of abdominal pain, fever, cough, nausea, vomiting and constipation alternating with diarrhea. Further examination revealed the presence of a hepatic abscess. This suspicious form was recovered following parasitic examination of a sample from the abscess and measures 20 µm. What condition is the patient most likely suffering from? | View Page |
| A 55 year old female, who recently returned from an extensive trip to China, presented to her physician complaining of diarrhea and abdominal cramps. The doctor ordered a complete blood count (CBC), chem 21 panel, and stool for culture and parasite examination (O & P). The CBC revealed pronounced eosinophilia. The chem 21 and stool culture were unremarkable. The O & P revealed suspicious forms like the one below that each measured approximately 140 µm by 80 µm. This patient is most likely infected with: | View Page |
| A 27 year old male was seen in the emergency room complaining of diarrhea. He had no other symptoms and was in very good health. The doctor ordered a stool for culture and parasite study. The culture revealed no enteric pathogens. This suspicious form was seen on the wet preparations and the permanent stain. It measured 16 µm. With which of the following parasites is this patient most likely infected? | View Page |
| A 31 year old male missionary worker recently returned from Africa where he helped a small rural community update their sanitation practices. He presented to his physician weak and complained of recent weight loss, abdominal pain, and diarrhea that was often bloody. The doctor ordered a battery of tests including a complete blood count (CBC) and stool for parasite examination. The CBC revealed eosinophilia and anemia. This suspicious form was seen on the wet preparations. It measured 52 µm by 27 µm. What parasite is mostly likely present? | View Page |
| A 4 year old female from South Carolina was rushed to the emergency room who was suffering from malaise, bloody diarrhea and abdominal pain. Examination revealed rectal prolapse. Stool was submitted for parasitic examination and this suspicious form was seen. It measures 45 µm by 20 µm. Which of the following is the correct identity of this suspicious form? | View Page |
| What term is defined as the presence of arthropods in or upon a human host: | View Page |
| An 8 year old girl is protected from severe hemolytic anemia by an elevated fetal hemoglobin level ( hemoglobin F). | View Page |
| A 5-year-old girl was brought to a physician's office because of fever and viral-type illness symptoms. Her blood pressure was elevated.Hemogram: hemoglobin 9.1g/dL (normal 12.0 - 16.0 g/dL), hematocrit 28% (normal 37 - 48%), MCV 80 fl (normal 86 - 98 fl), RDW 13.1% (normal 11 - 15%), platelets 90.1 X 109/L (normal 150 - 450 X 109/L) WBC 9.6x109/L (normal 4.3 - 10.8 x 109/L).The peripheral blood smear is represented in the photograph.Which of the following are the most likely associated conditions? | View Page |
| Considering the predominance of microspherocytes on the blood smear, and the patient's jaundiced condition, what is the most likely diagnosis? | View Page |
| Atypical smear: Case follow-up The patient whose blood smear is shown in the photograph was a 32-year-old female from Virginia who came to the high country of Colorado to ski. The day after arrival, she experienced shortness of breath, fatigue, and upper abdominal pain. She was seen in a medical center in the mountains where a working diagnosis of altitude sickness was made. A CBC revealed RBCs 5.1 x 1012/L, hemoglobin 12.8g/dL, MCV 60fL, hematocrit 40.9%, and normal total WBC, differential, and platelet count. The RDW was normal. Further questioning revealed a previous diagnosis of heterozygous beta-chain thalassemia. No other abnormal hemoglobins were found on hemoglobin electrophoresis, but HbA-2 was elevated to 5%, supporting the diagnosis of beta thalassemia. The patient's poikylocytosis and anisocytosis may be a clue to an underlying erythrocyte abnormality. Persons with iron deficiency anemia may experience various degrees of hypoxia upon arriving at high altitudes. Those with sickle cell disease and thalassemia minor (as in this case) may experience bone pain or other symptoms of "crisis" and/or alteration in the appearance of their erythrocytes upon sudden high altitude exposure. The classic teaching is that in differentiating iron deficiency anemia from thalassemia, increased RDW would favor iron deficiency; normal RDW favors thalassemia. | View Page |
| Literature and online resources Literature Dutton RP, Shih D, Edelman BB, Hess J, Scalea TM. Safety of uncrossmatched type-O red cells for resuscitation from hemorrhagic shock. J Trauma. 2005 Dec;59(6):1445-9. Johnson ST, Rudmann SV,Wilson, SM. Serologic problem solving strategies:a systematic approach. Bethesda, MD: AABB, 1996.Online resourcesThe following are online examples of good practice. The information should not be used as a substitute for technical and clinical judgment. Medical and technical information becomes obsolete quickly and current sources relevant to the user's location should always be consulted. Urgent requirements for blood (Calgary Laboratory Services, Calgary,Alberta, Canada) Online resource for laboratory's clients Why is there never enough O Rh negative blood? (American Red Cross) Advice for physicians on how to help prevent shortages of O Rh negative blood Transfusion reactions: Transfusion complications (Canadian Blood Services) Education website for CBS's hospital customers REACT (Sunnybrook HSC, Toronto, ON, Canada) Pocket reference card for nurses on signs and symptoms of transfusion reactions Quick cals (online calculator of p values for Fisher's exact test) Use a one-tailed test (since we would expect an antibody to react with red cells that are positive for the corresponding antigen) | View Page |
| Follow-up with clinical staff The patient's physician was notified that compatible blood was unavailable and that the patient's antibody was still being investigated.When asked whether or not the patient was experiencing a transfusion reaction due to the transfusion of the two unmatched and incompatible O Rh negative RBC, the nurse in the OR stated that the patient was undergoing surgery and completely sedated. A transfusion reaction was not apparent but they would investigate and closely monitor.Hemolytic Transfusion Reactions (HTR)Before proceeding to the next page, make a short list of signs and symptoms associated with immediate hemolytic transfusions reaction and another list associated with delayed hemolytic transfusion reactions. | View Page |
| Immediate HTR - Signs and symptoms The following signs and symptoms are associated with acute HTR due to ABO incompatibility but can be associated with other blood group incompatibilities. ABO incompatibility typically results from patient misidentification.The more serious symptoms result from intravascular hemolysis (IVH) caused by antibodies such as anti-A and anti-B that can bind complement to C9.Signs and symptoms typically appear within minutes of the transfusion but can occur anytime during the transfusion. They may include: 1. Burning sensation along the vein being transfused (IVH due to complement activation to C9)*2. Lower back pain in the area of the kidneys (renal failure with subsequent oliguria/anuria) *3. Unexplained bleeding/oozing from a surgical site (fibrinolysis following DIC)*4. Hypotension leading to hypovolemic shock (release of vasoactive substances caused by C3a and C5a)5. Tightness in substernal area of the chest (bronchial constriction due to release of vasoactive substances caused by C3a and C5a fragments)6. Other symptoms: fever, chills, skin flushing, dyspnea, wheezing, anxiety, malaise, nausea, headache. * If untreated, these complications may lead to patient death. | View Page |
| Delayed HTR - Signs and symptoms Delayed HTR often go undetected as the symptoms are usually mild and subclinical (death has occurred, but rarely). Symptoms may not occur until days after transfusion when the patient has left the hospital. Donor red cell destruction is usually by extravascular hemolysis (EVH). Signs and symptoms can include: Fever with or without chills Unexplained drop in hemoglobin and hematocrit Transient jaundice due to elevated serum bilirubin | View Page |
| Signs and symptoms - Job Aids Some blood safety standards require that a list of common signs and symptoms of suspected adverse reactions be included in both nursing and transfusion service manuals. Several organizations have developed job aids to help clinical staff recognize the signs and symptoms of various suspected transfusion reactions and to suggest appropriate actions (e.g., see REACT in Online Resources). | View Page |
| Signs and symptoms - Precaution Signs and symptoms are used only as a general guide to the type of transfusion reaction that may be occurring.Lower back pain, for example, would suggest an acute hemolytic reaction, whereas fever is associated with several types of reactions: Hemolytic (immediate and delayed) Febrile Bacteriogenic | View Page |
| Which of the following signs and symptoms is most likely to indicate a severe immediate hemolytic transfusion reaction? | View Page |
| Tuberculosis infection The natural history of TB infection is usually followed by an immune response and latency after exposure. In about 5-10% of cases, the latent period progresses to an active infection.The organism that causes TB infection is Mycobacterium tuberculosis. This organism is pictured in the photograph to the right as observed when stained with acridine orange stain. Infection occurs when a susceptible person inhales droplet nuclei containing Mycobacterium tuberculosis and the organism reaches the alveoli of the lungs.About 2-12 weeks after infection, the immune system limits multiplication of additional bacteria and the immunological test becomes positive.Latent tuberculosis infection (LTBI) is the stage when the viable organism remains in the body, and the patient has no symptoms and is non-infectious.Most infected persons do not experience clinical illness and are noninfectious. About 5-10% of persons infected with Mycobacterium tuberculosis who are not treated will develop TB during their lifetime. The risk for progression is highest during the first several years after infection.TB infects the lungs most often; however, it can infect almost any organ in the body, including bones and joints. | View Page |
| Symptoms Symptoms of active TB include:coughing for more than 3 weeks,loss of appetite,unexplained weight loss,night sweats,bloody sputum,hoarseness,fever,fatigue,and chest pain.
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| A Word of Caution Symptoms of TB can mimic other diseases and the physician must consider the patient's history as well as physical symptoms before making a final diagnosis. | View Page |
| Health Care Worker Tuberculosis Screening All HCWS receive baseline TB screening upon hire, using either the two step skin test or BAMT. Annual screening varies depending on setting risk. In low risk settings, screening is not necessary unless an exposure occurs. In a medium risk setting, all HCWS are screened for symptoms and HCWs with negative baseline results are tested.In a potential ongoing transmission setting, HCWs receive testing every 8-10 weeks until lapses are corrected. | View Page |
| Match the recommended frequency for TB screening of a healthcare worker with the risk category of the healthcare setting from the drop-down box: | View Page |
| Protect Yourself Healthcare workers must be alert for signs and symptoms of TB to protect themselves from inadvertent exposure.Help protect yourself, coworkers, patients, and visitors by: Having current TB screening according to the risk classification of your setting, Understanding the risks of TB in your work area, Practicing good infection control at work and at home. | View Page |
| A peripheral blood smear is submitted for morphology review. The patient is a 10 year-old boy with symptoms suggesting appendicitis and an appendectomy is being considered. The total WBC is 18.5 X 1000/uL, RBC's = 5.45 X 1M/uL, hemoglobin = 16.0 g/dL, hematocrit 48.2%;wbc differential: Segs = 53%, bands = 42% (two of which are shown in the photograph), monocytes = 2%, and lymphocytes= 2%. These findings support the diagnosis of appendicitis. | View Page |
| Case Follow-up Illustrated in the upper and lower photographs are two-lobed, eye glass ("pince nez") nuclei of neutrophils typical for patients with Pelger-Huet anomaly. In addition to the characteristic two lobes connected by a delicate bridge, the dense, homogeneous nuclear chromatin helps to define Pelger-Huet anomaly. Since the peripheral blood smear did not support the diagnosis of appendicitis in this patient, and since abdominal pain localized to the right lower quadrant never developed, the boy was hydrated with intravenous fluid and observed. After hydration, his constitutional symptoms improved and the abdominal pain subsided. In fact, the lad was back on the ski slopes the next afternoon. People entering high altitude where the humidity may be very low are susceptible to dehydration and may experience symptoms related to mountain sickness. Therefore, close observation and hydration may be the best practice in monitoring patients with stories and findings similar to this one. A further lesson here is that technologists must be alert to the possibility of Pelger-Huet anomaly if a high white blood cell count with a high percentage of band neutrophils with strikingly uniform morphology and without toxic granulation are found. Inappropriate therapy or an invasive procedure as was contemplated here may be avoided by a proper smear assessment and clinical corroboration. | View Page |
| Case history A 14 year-old boy came to the physician's office with a sore throat that progressively worsened over a three day period. His posterior pharynx was swollen ,shiney and erythematous. The boy complained of pain on swallowing. His temperature was 98.5F. A rapid direct streptococcal antigen test was positive. However, his symptoms did not subside over the next two days while on antibiotic therapy. Anorexia and nausea were persistent and compounded by a frontal headache. Cervical lymph nodes became noticeably enlarged. The results of the CBC were: WBC 11.9/mm3 with 17% segmented neutrophils, 5% bands, 72%(60% atypical--see photograph)lymphocytes and 6%monocytes. All red cell findings were normal. A monospot test was positive. This is a case of group-A streptococcal infection superimposed on infectious mononucleosis. Symptoms subsided in 3 weeks following completion of the antibiotic therapy. | View Page |