Homolytic Anemia Essay

DIAGNOSTIC DATA: White count was 13.4, hemoglobin and hematocrit 15.4 and 45.8, platelets 206, with an 89% shift. Sodium 133, potassium 3.7, chloride 99, bicarb 24, BUN and creatinine are 18 and 1.1, respectively. Glucose 146, albumin 4.3, total bilirubin 1.7. The remainder of the LFTs is within normal limits. Urinalysis reveals trace ketones with 100mg per decilitre protein and a small amount of blood. CT scan was performed revealing evidence of acute appendicitis with pericecal inflammation, as well as, dilatation of the appendix and

A 20-year old male presented to the hospital with: nausea; diarrhoea and fever. Upon examination he had abdominal pain and a tender liver. The patient admitted to eating wild mushrooms, of which he had collected himself, the afternoon before attending the hospital. Laboratory analysis at the time of admission revealed elevated serum ALT (665 U/L) and AST (880 U/L), increased total bilirubin (4.9mg/dL) and an increased prothrombin time (3.11 seconds). Laboratory tests were repeated six hours later and all levels, except AST, were elevated even further; with ALT and bilirubin doubling in concentration and the prothrombin time also doubling. Albumin concentration was also tested and presented normal at both times. The patient was administered a haemodialysis with N-acetylcysteine.

A 49 year old Afro-Cuban male with a history of chronic alcoholism and hypertension presented with a three day history of fever (106ᵒ F), change in mental status, and body aches in August, 2016. On admission, he was febrile 103.1ᵒ F, with a heart rate of 137 beats per minutes, blood pressure of 156/79 mm of Hg, and respiration rate of 32 breaths per minute. The patient’s laboratory results on admission included white cell count 9.2 x 103/microL, platelets 71 x 103/microL , PT 28 seconds, PTT 43 seconds, INR 2.62, albumin 3.1, Tblb (total bilirubin) 13.6 mg/dl , AST (aspartate transaminase) 133, and ALT (alanine transaminase) 56. Lactic acid was 6.2 mmol/L, and blood alcohol level checked the next day was less than 10 mg/dl. In addition, he

A 7-year-old, intact, male thai mixed breed dog named Jum-bo was refer to Prasu-Arthorn animal Hospital for blood transfusion. The clinical sign shown weakness, depress and petechial hemorrhage at ventral area of the body. The dog also had jaundice and pale mucous membrane. On physical examination, the animal showed tachypnea and abdominal discomfort with a heart rate of 98 bpm, normal heart sound, increase lung sound and 5% dehydrate. Hematological analyses revealed leukocytosis (40,440 cell/mm3; normal range 6,000-17,000 cell/mm3), thrombocytopenia (9,000 cell/um3 ; normal range 200,000-500,000 cell/um3) and severe anemia (Hematocrit 15.6% ; normal range 35-55%, RBC 2.18 x106cell/mm3; normal range 5-9 x106cell/mm3 ). Serum biochemical showed

We measured a panel of prothrombotic risk factors (Table 1) and detected hyperhomocysteinemia, and 4 heterozygous gene mutations, including MTHFR C677T and A1298C, glycoprotein GP3A and Fibrinogen- β G/A-455. Electrocardiogram and chest x-ray were normal, as well as the remaining routine laboratory tests, including differential blood cell count, protrombin and partial thromboplastin times, serum glucose, creatinine, electrolytes, liver enzymes, calcium, vitamin B12 and folate. Anti-nuclear, anti–single-stranded DNA, anti–double-stranded DNA, anti-cardiolipin, anti–SS-A/B antibodies were negative. She was treated with dexamethasone 5mg twice daily and LMW heparin (enoxaparin 60 mg twice

After careful review of the patient’s labs, WBC elevated and symptoms of low grade fever reflect that there is some sort of organism growth or inflammatory response in the body possible at the surgical site. The patient’s immature neutrophils(segs) elvateted indicative sign of inflammation or infection. Patients hemoglobin of 8.6 is considerably fair for a patient with chronic kidney disease. Low hemoglobin a indicative marker for severity of kidney disease (Leeder et al., 2006). The kidney is responsible for making erythropoietin a hormone that stimulate the bone marrow to make red blood cells, if the kidney is not working well we expect the RBC production to decrease( our text book). The patient elevated PT/INR is reflective on the positive fecal occult blood. Unfortunately Coumadin therapy most resume or continue because of her history of A-Fib. The sedimentation rate elevated is expected for history diagnosis of rheumatoid arthritis.

This is a 60 year-old male with a past medical history of hypertension who presented with several week history of recurrent fever accompanied by poorly localized abdominal pain. His physical examination revealed an acutely ill-appearing man with tender hepatosplenomegaly.Routine laboratory workup revealed pancytopenia, transaminitis as well as elevated alkaline phosphatase and

In this case study, I believe that Thomas is experiencing hepatitis A (HAV). His symptoms includes mild jaundice of the sclera and skin, abdominal tenderness with hepatomegaly, as well as dark yellow urine. In hepatitis

Physical examination was normal except the presence of joundice. He had no history of any chronic illness, drugs or chemicals. He stated that he had a sleeve gastrectomy operation 6 months ago for obesity and he was on low caloric intake due to early satiety since sleeve gastrectomy. Preoperative laboratory studies before the gastrectomy were obtained and reevaluated. All were normal except mild indirect hyperbilirubinemia (serum total bilirubin: 1,4 mg/dl, indirect bilirubin: 1,2 mg/dl). On admission to our clinic his laboratory studies were as follows: AST: 14 U/L ALT: 16 U/L ALP: 45 U/L GGT: 28 U/L total bilirubin: 6,58 mg/dl, indirect bilirubin: 6 mg/dl, direct bilirubin: 0,58 mg/dl . Serologic tests for viral hepatitis (HBs Ag, anti HBc Ig G, anti HCV, anti HAV Ig M) were all negative. There were no clinical and laboratory sign of hemolysis; Hb: 15,2 g/dL, Hct: 44,1, Plt: 208.000 /µL and reticulocyte count was %0,5. Abdominal ultrasound showed the presence of multiple stones in the gallbladder. Common bile duct and biliary tree were found to be normal in MRCP and endosonography. Gilbert’s syndrome was diagnosed and phenobarbital 30 mg/day was initiated. Serum bilirubin concentration dropped gradually (total bilirubin: 3,5 mg/dl, indirect bilirubin: 3 mg/dl) in one week and the patient was

A 64 year old male with medical history of hepatocellular carcinoma, liver cirrhosis secondary to chronic hepatitis C was admitted for weakness and failure to thrive. In initial work up it was noted that patient was anemic (Hb 7.9

CASE: 51-years-old male visiting from Guyana with past medical history of hypertension and hyperlipidemia presented with non-obstructive jaundice for 3 weeks. Patient is a former heavy alcohol drinker (15 years), and a former cigarette smoker (15 years). Patient was prescribed INH for latent TB 2 months ago. Also, 7 days prior to admission he was prescribed Gemfibrozil 600mg. Other home medications were Metformin 500mg, Ramipril 5mg, Metoprolol 50mg, and multivitamins. Patient denies Hepatitis A and B vaccination, blood transfusion, family history of liver cancer/chronic disease, drug use, recent sexual activity/STDs. Physical exam remarkable only for scleral icterus, jaundice and bright yellow urine and clay colored stools. Labs revealed AST 1626 ans ALT 1250, trending up form 2 months ago

A 45 years female suffer from ascites five months ago, fatigue, loss of appetite, yellow skin and weight loss. We did for her many laboratory tests to check liver and kidney function. She had high level of certain and bilirubin and that was indicate liver

Sickle cell disease is a hereditary hemoglobin defect that occurs in people of African and Mediterranean decent. “First identified in 1904 by a hospital intern, sickle cell disease became, more than forty years later, the first disease found to be a genetic disease” (Harris 83). This disorder is caused by a recessive allele that changes the structure of hemoglobin. Sickle cell hemoglobin (HbS) differs from normal hemoglobin (HbA) in that of all the 574 amino acids it is made of, just one is different. In the sixth amino acid of the beta chain, HbA has glutamic acid and HbS has valine.

Table 1, displays the densitometic analysis of membrane protein deficiencies in each of the subjects and patients as well as red blood cell counts, Hb density, MCHC, RDW%, RET %, and bilirubin levels. From this data, the subjects were categorized according to their primary

OTHER HEMATOLOGICAL PROBLEMS: Progressive splenomegaly in poorly managed thalassemics leads to secondary thrombocytopenia and leukopenia. Bleeding tendencies may be present with or without associated thrombocytopenia mostly in the form of epistaxis. Dental caries is also common in Indian subcontinent.