Haemoglobin Case Study

Anemia is a disorder of the blood. It occurs when your body does not produce enough erythrocytes or red blood cells (RBCs). Without the erythrocytes oxygen can not be adequately delivered to the tissues and organs throughout the body. This will cause you to become weak and tired. A person may also experience headaches, skin pallor, and faintness. Your body may attempt to compensate for these symptoms by speeding up the heart rate and respiratory rate. This is the body’s attempt to return oxygen levels to normal(Thibodeau and Patton, 2005).

As a provider, one will care for many patients that have different types of anemia. Anemia is not so much as a disease as a symptom of an underlying issue. Although there can be particular signs and symptoms associated with anemia, the basis of a diagnosis is from laboratory data. For the purpose of this discussion, I will evaluate a case study and give a differential diagnosis. I will also assess how patient history, physical exam, and lab reports support my diagnosis. I will explain the pathophysiology of the type of anemia and give causes and treatment options available.

Also known as normocytic anemia. This is the most frequent type of anemia most often happening to males over 85 years old. It is a common problem that occurs to men and women over 85 years old. Symptoms include and are caused by: a reduced production of normal-sized red blood cells even though presence of hemoglobin in the red blood cells is within the standard range; an increased production of HbS as is seen in sickle cell diseases; greater destruction and loss of red blood cells; an increase in plasma volume that is not compensated by anything else; a B2 (riboflavin) deficiency; and a B6 (pyridoxine) deficiency. (Brill & Baumgardner 2000).

Binding of CO to hemoglobin is greatly affected to anemic and smoking individuals. Hemoglobin plays a major role in our body to transport oxygen. Since hemoglobin has a higher affinity for oxygen, it binds to an oxygen molecule and increases its oxygen concentration. Thus, when the blood cells are at a different part of the body where the oxygen concentrations are low, the oxygen will leave the hemoglobin and diffuse into the cells. However, carbon monoxide has a 250 fold greater affinity than oxygen. So, when CO enters the blood from the lungs, CO would bind with hemoglobin instead of oxygen, and block the blood’s ability to carry oxygen to the cells throughout the body. In a normal healthy individual, the total carboxyhemoglobin (COHb) complex is 1% or less, whereas, smoking increases COHb to 3-8% and further to 15% for chain smokers. When smoking a cigarette, CO binds to hemoglobin and displaces to

Pernicious anemia due to decreased B12 affects the hematopoietic,gastrointestinal and nervous systems of the body. The hematopoietic system is affected in that, B12 is essential for the formation of red blood cells, therefore without adequate B12, there is a reduction in the production of red blood cells causing abnormally large shaped red blood cells to be produced. Red blood cells carry oxygen , therefore the NP will anticipate patients with anemia to have symptoms like dizziness, fatigue, pallor, tinnitus, cardiomegaly with murmur, tachycardia, and chest pain. Additionally, symptoms of the affected gastrointestinal system include anorexia, weight loss, abdominal cramping, weight loss, and glossitis. Moreover, symptoms of the affected

However, it was difficult to achieve a remission, standard haemoglobin without haemolysis, despite following the steroid therapy. At her three months check-up, she complained of mild shortness of breath and fatigue of ten days duration. She was receiving prednisolone 10 mg daily along with folic acid. Examination revealed mild pallor and a palpable spleen. Laboratory workup showed low Hb (11.8 g/l); Reticulocyte count had slightly risen (2.7%) and PBF showed polychromatic and few spherocytes. Her direct Coomb's test was still strongly positive. Serum biochemistry revealed normal indirect bilirubin and a raised LDH (295 u/l). B12 and folate levels were normal. Consequently, due to signs of some improvement, the steroids were initially maintained but gradually reduced to 5mg every other day. After about six months of steroid therapy and folate, the haemoglobin became standard. Currently, she is in remission with no

In 1747 Dr Vincezo Menghini wrote he had blunt blood to obtain a red powder substance and discover this substance was attracted to magnets, quickly confirming that this substance contained iron. Friedrich Ludwig Hunefeld many years later confirm these findings and chemically split the blood pigments into two components. A protein structure known as globulin and a red compound with iron oxide known as haem. This was the beginning of iron therapy for anaemia. It was Hopp Seyler that called the term haemoglobin in 1862 and determine its structure for further studies. In this research paper, it will discuss the importance roles haemoglobin play in the physical structure. It will explore the importance of gas exchange how carbon dioxide enters and exit from the body during breathing and their structure and function.

My topic for this paper is aplastic anemia. I intend to discuss the definition of aplastic anemia, pathophysiology of the disease, statistics, signs and symptoms, diagnoses, treatment, and prognosis.

The symptoms of anaemia are: Lethargy, an interesting change of stool colour due to low amount of bilirubin, weak muscles, lack of appetite, malaise (Somehow uncomfortable) and in serious cases: fainting, heart attack (Not enough red blood cells to carry oxygen) and angina. So why does this happen anyway? Simple. Not at

is attributable to administration of a drug that interferes with DNA synthesis or, rarely, to a congenital metabolic defect. Some patients with acute myeloid leukaemia (AML) or MDS also have megaloblastic erythropoiesis. The bone marrow aspirate is often markedly hypercellular. Erythropoiesis is hyperplastic and is characterized by the presence of megaloblasts. These are large cells with a chromatin pattern more primitive than is appropriate for the degree of maturation of the cytoplasm. Late megaloblasts may be fully haemoglobinized and lack any cytoplasmic basophilia and may therefore be described as orthochromatic. Erythropoiesis is ineffective so that early erythroid cells are over-represented in comparison with

Investigating haemoglobin (Hb) concentration in blood samples using the haemoglobincyanide method and in foetal haemoglobin samples

Laboratory findings revealed a hemoglobin (Hgb) of 6.6 g/dL (normal 12–16) with a mean corpuscular volume (MCV) of 89.3 fL (normal 80–100); white cell count (WBC) 1,900/mm3 (normal 3,500–11,000); platelet 79,000/mm3 (normal 140,000–450,000), prothrombin time (PT) 16.4 s (normal 11.8–14.6); international normalized ratio (INR) 1.3 (normal 0.8–1.2); partial thromboplastin time (PTT) 35.9 s (normal 23.4–36.2); D-dimer 15.09 μg/mL (normal 0–0.5); fibrin split products (FSP) < 40 μg/mL (normal < 10). However, reticulocyte count was not available. Thyroid studies revealed a thyroid-stimulating hormone (TSH) of 4.43 mlU/L (normal 0.4 –4.42). A thyroxin (free T4) level was not available due to nearly normal value of TSH. Iron studies revealed an iron level of 132 μg/dL (normal 37–170); transferrin 158 mg/dL (normal 200–360); ferritin 137.2 ng/mL (normal 5–148); TIBC 261 μg/dL (normal 265–497); and iron saturation 51% (normal 15–50). Liver function tests (LFT) revealed AST of 240 U/L (normal 3–34); ALT 38 U/L (normal 15–41); total bilirubin 2.4 mg/dL (normal 0.5–1.3); and indirect bilirubin 1.9 mg/dL (normal 0–3). Metabolic panel was significant for potassium 2.8 mmol/L (normal 3.5–5.1) with normal kidney

A hematocrit and hemoglobin value can provide with an indirect measurement for levels of RBC’s in the blood and how much hemoglobin there is in the blood. My patients Hct was 29.3L on 10/25 which is higher than a few days prior which was 24.5L but lower than admit day 10/17 32.3L. A low level of RBC’s can indicate anemia or hemorrhage but not immediately after, not until the blood volume is replaced with fluids (Pagana et. al. 2014). However, in her case low levels of H&H are also a consequence of hemodialysis. The patients Hgb was 9.1L on 10/25 but 10.5L on admit 10/17 her lowest being 10/21 at 7.9L. This value can also indicate anemia due to decrease of RBC’s which is also an indicator of the rapid blood loss through hemodialysis or through

The first is whether or not the patient has polycythemia. This can be determined by a complete blood count to evaluate the hemoglobin, hematocrit, and red blood cell concentration. Diagnosis of Polycythemia Vera includes a hemoglobin level greater than 18.5 g/dl (16.5 g/dl in women) and genetic testing for JAK2 mutations (The Editors of Encyclopædia Britannica, 2014). Erythropoietin levels are a secondary determinate (The Editors of Encyclopædia Britannica, 2014) and in Primary polycythemias tend to be normal or low, as the issue pertains more to precursor over-sensitivity to erythropoietin as opposed to an overabundance of erythropoietin. In secondary polycythemias, this level would be expected to be elevated.

The haemoglobinopathy, SCD is a severe blood disorder that is accountable for 33.5% per 100,000 hospital admissions in the UK (Aljuburi et al, 2012). The number of admissions has seen a steady increase over the last few years. In 1910, James Herrick was first to record that a Bajan male suffered from anaemia due to sickled red blood cells however in 1949 Linus Pauling identified that there was a molecular difference in the haemoglobin of a sickled and wild-type individual (Gabriel, A. and Przybylski, J., 2010). Ingram V. made the further observation that a single nucleotide polymorphism (SNP) resulting in valine instead of glutamic acid led to the conformational change in haemoglobin (Gabriel, A. and Przybylski, J., 2010).