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DIAG 2735 Hematology Cases 11-20

DIAG 2735 Hematology Cases 11-20 - Hematology Case Study#11...

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Unformatted text preview: Hematology Case Study #11 Discussion Points Arthur Findings: pancytopenia The total loss of red and white blood cetls implies that the bone marrow is no longer functioning due to destruction of the stem cells. Due to the complete lack of precursor calls this is calied aplastic anemia. Aplastic anemia effects mostly adolescents or young adults. Roughly half the cases are idiopathic; however some causative agents haye been identified: benzene. arsenic, radiation. antineuroplastics. antibiotics, NSAIDS, and anticonyulsants. The onset of the disease is usually insidious in the weeks or months foilowing exposure. Signs will vary but usually appear as a very bad case of anemia, with waxy pallor of the skin and mucous membranes. The patient will also experience thrombocytopenia and possibly spontaneous bleeding (particularly in the optic fundus]. Agranuiocytosis may be fatal due to secondary infection. Splenomegaly is usually absent unless caused secondary to the cure. The cure for aplastic anemia is bone marrow transplant from a compatible donon Hematology Case Study #12 Discussion Points Bjorn Findings: Spherecytes The spherecyte morphology is an inherited dominant trait, usually in northern eurepeans. The anemia it causes has been called: chronic familial icterus, congenital hemelyticjaundice. familial spherecytesis, er spherecytic anemia. The disease is characterized by hemelysis of the sperical red blood cells.‘ The disease has been known to skip generations as a result of variation tn the expression of the gene. The spherical nature of the cell alters the surface area to inside ratio. The cells carry less ex gen due to less surface area and the spherical nature means that the cel s get destroyed in the spleen filters. due to lack of flexibi ity. The symptoms of the disease are mild and often asymptomatic. the obvious anemia signs and jaundice (and increased urebilinegen in the urine} will show in the more serious cases. Splenomegaly is nearly always present. The patient may also demonstrate gall stones and the signs associated (+ Murphy's sign, referral pain to right scapula}. The hematology of spherecytesis is that the hematecrit ma be low. due to the smaller spherical cells. Fieticulecytesis (immature REC may be up to 15-30% of circulating red blood cells. Leukocyte numbers may also be elevated. There is a somewhat milder form called elliptecytesis which demonstrates evalecytes. This form does not entail hemelysis er iaundice, but does have spienomegaly. The medical treatment is to vaccinate the patient {with a serious case) the perfrem splenectemy. The result is that the filter which destroys the red blood cells is gone and the cells last longer. The red bioed cell count rises. the reticulecyte goes down and the symptoms abate {especially the splenemegaly]. H ematclogy Case Study #13 Discussion Points Melba Findings: Macrocytes, slight elevation in hematocrit and hemoglobin The patient has complaints consistent with anemia. Hematology reveals normal white blood cell numbers and percentages, with normalplatelet count. The red blood cell morphology is suggestive of immaturity in the red blood cells. Vitamin B12 is the essential nutrient required to mature the red blood cells. Vitamin B12 is only found in animal food products. Vegans must either supplement _B12 in the diet, eat meat occasionally, or suffer the megaloblastic anemia presented. Another form of this anemia is called pernicious anemia. This form results from the inabilityr of the patient to absorb vitamin B12. Vitamin 812 is bound in the stomach to intrinsic factor (IF) manufactured in the lining of the stomach. There are cases where parasitic infection, such as tropical sprue, or autoimmune conditions. like nentropical sprue, cause the gastric mucosa to atrophy. The lack of intrinsic factor makes it impossible to absorb B12, therefore unlike our vegan patient above, the pernicious patient is unable to supplement his wayr to health. In cases of pernicious anemia the patient must receive intramuscular injections of 812. The injections handily dispach the anemia, however this patient should explore the cause of the gastric atrophy and resolve that situation. The development of the anemia is insidious, the liver contains a 3&5 1year supply of B12. Neurologic signs may present in the absence of anemia. The neurologic signs present first as loss of vibration sense {apaliesthesia}, the symptoms may progress to weakness and absence of reflexes. In later stages there is spasticity, and pathological reflexes. Loss of proprioception leads to sensory ataxia. The patient may also experience yellow-blue color blindness and in extreme cases megalobiastic madness (paranoia, dementia, confusion and irritability}. Hematology Case Study #14 Discussion Points Giuseppi Findings: Nucleated Fted blood cells. target cells, hypochromic rmcrocytes, and basophilia The aptient presents with signs of a gall stone, with complaint of fatigue and muscle weakness. Fatigie and waekness are signs of anemia and the fact that the patient demonstrates gall bladder signs implies that the anemia rnaydbe hemolytic. Othe signs that may be present are: splenomegaly and jEiLIi'l ice. The radiographic findings of honeycomb trabeculae. and a hair on and appearance top the skull [looks like spiky hair on x—ray} are classic sign of thalessemia anemia. This is also called Mediterranean anemia (people that live in along the Mediterranean sea} or Cooley's anemia. The problem with thalessemia is that the patient does not develop all four of the hemoglobin chains at the same rate. The slower growing chain destabilizes the whole hemoglobin molecule and therefore the red blood cells. The red blood cells are weaker and break down faster. Heterozygotes have only one thalessemia gene and therfore have a mild or assymptomatic form. This is called thalessemia minor. Hom ozygotes have the major form and of these beta major is the worst (named for the beta chain of hemoglobin]. The symptoms of beta major are those of severe anemia. bone marrow expansion. gall stones, and ulceration {Particularly in the lower extremity]. Growth rate is slowed as is the onset o puberty. The life expectancy of patients with thalessemia minor is normal. With major forms some of the patients may actually live up to and through puberty. These patients will require multiple transfusions; however there comes a risk of iron overload. Therefore the transfusion must be balanced with the iron overload risk or the patient must undergo an iron reduction therapy via chelation. Splenectomy may help in patients with severe splencmegaly. Hematology Case Study #15 Discussion Points Martin Findings: low red blood cell count, low platelet count, blueberries The most common malignancy in chiidren is acute lymphocytic leukemia ALL. The peak occurence is age 3-5 years old. ALL has the signs of acute leukemia: anemia. with bleeding tendency, and decreased immunity. The leukemic lymphocytes often invade the bone marrow, the testicles, and the CNS. CNS si as are those of increased intracranial pressure: papilledema, constant ead ache, projectile vomiting, cranial nerve paisy, and neurological deficit. The signs are nonspecific including fatigue, fever, malaise. bleeding and bruising tendency, hematuria and GI bleeding, and with ALLjoint pain is common. With this form cure is a realistic goal. The younger the patient the more likely the cure. The first step is to regain normal blood values. Then the patient must be immunologically stabilized, often with broad spectrum antibiotics to wipe out opportunistic infection. The drugs of choice are meihotexate and mercaptopurine with a duration of therapy between 2 and 3 years. The risk of relapse is about 20% and usually within the first year of ending therapy, therefore when most patients complete chemotherapy the disease is over. In most cases of remission the time period is short and it is easy to cure again. When remission occurs one of the chief concerns is marrow infiltration and in this case it helps to have a compatible donor nearby for bone marrow transplant. Homatology Case Study #115 Discussion Points Jacob Findings: Lots of atypical lymphocytes, with extreme white blood cell or ieyation The extreme white blood cell elevation is suggestiye of either leukemia or lymphoma. The elevation of lymphocytes places it in the lymphocytic leukemia or lymphoma category, and the atypical nature of the lymphocytes indicates lymphocytic leukemia. The patient’s age will suggest that it is chronic iymphocytic leukemia CLL. The patient experiences the same nonspecific symptoms as pallor, sfienornegaly, fatigue, anorexia, abdominal discomfort, and night sweats, a lot insidious onset. as many other disorders (anemia. yiral infection}. The progression is that the bone marrow begins to fill with the lymphocytes and causes shut down of granulocyte production, erythrocyte production and thrombocyte production. Additionally the abnormality of the lymphocytes leads to decreased immunoglobulin production. The diagnosis is often made incidentally while doing a lymph node biopsy, or in perfroming routine blood work. There are multiple types of CLL with yagring iife expectancies from 3-4 years up to 20 years. Treatments inclu e chemotherapy, radiation therapy, and corticosteroid therapy. |-|emat+:tlegyr Case Study #1? Discussion Peints John Findin 5: Elevated white bleed celi ceunt, decreased red bleed cell ceunt, ruising tendency, nen-differentiated granulecvtes, Hf.- The elevatien ef white bleed cells and decrease et whrtfe bleed cells and platelets is suggestive ef leukemia. The cemplaint ef the patient ef fatigue, weight less, and bruising are alse censistent with a leukemia. The patient is 35 vears eld, which makes acute Ivmphecvtic leukemia unlikelv {childheed}, it alse makes chrenic lymphecvtic leukemia unlikelv [eld age}, and chrenic mvelecvtic leukemia unlikely {median age 45). Remissien and reductien in this disease is in the 50-85% range, the younger the patient, the better the pregnesis. There is alse a likeliheed that the patient will experience disseminated intravascular ceagulatien {DIG} as the leukemic cells lvse and release preceagulants. Hernatelegvr Case Study #13 Discussien Peints David Findings: Very high WBC eeunt, elevatien ef basephils and eesinephils, and many immature white bleed sells in eireulatien. David presents with nenspeeifie svmptems ef fatigue, and neek pain, with seme abdeminal swelling. The bleed werk is the kev te revealing the patient is suffering frem leukemia. This may eeeur in either sex and at any age; hewever the median age is 45 veers eld. Tvpieal svmptems are: fatigue, weakness, anerexia, weight less, night sweats, and abdeminal fullness {due te splenemegalv}. Paller, bleeding. and bruising tendenev may be eneugh te eause suspleien and bleed werk. Beeause the patient has seme almest nermal leeking sells it is safe te assume his immune system is partially funetiening and the risk ef seeendarv infeetien is lewer. The treatment ef Chrenie Mveleeytie Leukemia is usually palliative, net curative. If the bene marrew can be suppressed such that the white bleed eell eeunt dreps beiew 25,000 the svmptems usually disappear, but life span is shertened. H ematology Case Study #19 Discussion Points Roderick Findings: normal lymphocytes, with way elevated white cell count The patient exhibits multiple lymph node swellings which is consistent with the increased white blood cell count and lymphocyte elevation. The normal appearance of the lymphocytes would tend to suggest the cause is other than a lymphocytic leukemia. The lymphomas are Hodgkins and non Hodgkins. Hodgkins lymphoma signs and symptoms: fever, night sweats, intense itching, and weight loss are some eneral signs. In effected areas drinking alcohol will cause pain. In the ske eton the patient may develop an ivory vertebra {with anterior scalloping). The patient may experience anemia and bleeding disorder with bone marrow infiltration. The other symptoms will be related to which lymph nodes are blocked, for example blockage along the hepatic nodes results in jaundice. in the femoral triangle results in leg swelling. There will be some degree of immune compromise since the immune system is multiple processes happening together, here one gets way out of range and the others suffer. Non Hodgkins lymphoma differs from the Hodgkins in that swelling of the head and face are common symptoms, and ureteral compression leads to renal failure. Both of these are very rare in Hodgkins lymphoma. Most non Hodgkins patients will also develop anemia from marrow infiltration. The difinative diagnosis of both is via lymph node biopsy. Survival rates are decent with treatment which includes radiation and chemotherapy. Hematology Case Study #20 Discussion Points Michelle Findings: Burr cells, absent platelets The first finding to jump out in this presentation is that the patient has almost completely stopped urinating and experiences kidney pain distribution. This is suggestive of kidney failure. The resulting uremia would explain the burr cells evident in the blood specimen. The lack of platelets is consistent with the bleeding tendency. There is a condition which involves excessive formation of thrombi in the vessels. The formation uses up all the available platelets. The thrombi will result in ischemic damage to multiple organs. In this patient, as many others, the kidneys are subject to that damage. The lack of platelets leads to bruising tendecy called purpura. The uremia results in hemolysis of red blood cells, which leads to a fluctuating jaundice, elevation of both direct and indirect bilirubin levels, and liver failure. The patient will demonstrate proteinuria and hematuria when actually able to urinate. The picture is complete for a condition known as thrombotic- throm bocytopenic-purpuric-hemolyticwuremic syndrome (“FTP-HUS). This condition in children will resemble E. Coli infection. In adults there is a loose association with pregnancy, but in most cases it is idiopathic. The condition if untreated is almost always fatal. The patient will usually respond to treatment but require constant monitoring over the next few years, since relapse is possible. Treatment consists of daily palsma injections until signs of the disease abate. Corticosteroids and antiplatelet drugs have also been used with success. ...
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