Anemia of chronic disease pathophysiology case study essay

Case Study #1
Mr. X is a 34y/o Hispanic male who presented to the emergency room for a fatigue, dyspnea and chest pain which started yesterday morning. He has been experiencing some nausea, vomiting, and reports that he is needs dialysis. He was diagnosed with chronic kidney disease 4 years ago and HIV 5 years ago. He is currently taking antiretroviral therapy for his HIV infection and reports compliance. He was last seen at a free clinic for his HIV care 2 weeks ago and does not know his current CD4 count or viral load. He has been receiving hemodialysis for 8 months and no longer produces urine. He was last dialyzed 5 days ago. His past medical history is significant for HIV, Chronic Kidney disease stage 5, Anemia, hypertension, pneumonia, hyperlipidemia
Past surgical history is positive for only a permacath (central venous access for dialysis access) placement 8 months ago.
Physical exam:

Vitals: 38.1-97-18-183/139
Normocephalic.
Alert & Oriented x3. Well developed.
Eyes: PERL. No nystagmus
Neck: Supple, no cervical lymphadenopathy
Cardiovascular: Normal Rate and rhythm. No murmur, gallops. 2+/4+ radial, brachial, dorsalis pedis pulses bilaterally. 2+ pitting edema of bilateral lower extremities.
Pulmonary: Dyspneic. Lungs are clear anemia of chronic disease pathophysiology case study essay.
Abdomen: Soft and nontender, active bowel sounds. No peritoneal signs.
Skin: warm, dry and pale.
Rectal exam: stool is brown, no rectal masses

Lab Result
Sodium 133 mEq/L
Potassium 6.0 mEq/L
Creatinine 19.95 mg/dL
BUN 114 mg/dL
CO2 14 mEq/L
Anion gap 26 mEq/L
WBC 10,000
Hematocrit 25.4%
Hemoglobin 8.4 g/dL
MCV 85 fL
Platelets 154,000
Serum Iron 70 mcg/dL
Total Iron Binding Capacity 150 mcg/dL
Ferritin 450 ng/ml
Glucose 124 mg/dL

Questions
1. The clinical scenario is most consistent with which type of anemia? You may simply list your answer below using a bullet point format. This does not have to be in a complete sentence anemia of chronic disease pathophysiology case study essay. A citation is not required.

2. What specific data in the clinical scenario supports your diagnosis? You may simply list your answers below using bullet point format. This does not have to be in a complete sentence. A citation is not required.

3. What is the most likely cause of this patient’s anemia? You may simply list your answer below using a bullet point format. This does not have to be in a complete sentence. A citation is not required.

4. Describe the key pathophysiologic concepts of the diagnosis in question 1. To answer this question completely, you must answer all of the sub-questions below using complete sentences. Each sub-question may be answered in 1-6 sentences. ***Citations are required for each answer to each question using APA format.

a. What is the electron transport chain and how is it altered by anemia?

b. Why is the ferritin level 450 ng/ml?

c. What effects does anemia/low blood volume have on the cardiovascular system?

d. What are the effects of tissue hypoxia on the cardiovascular system, pulmonary system and CNS?

e. How does chronic kidney disease cause anemia? anemia of chronic disease pathophysiology case study essay

5. For what actual or potential complications related to the diagnosis in question 1 does he need to be monitored? You may simply list your answer below using a bullet point format. This does not have to be in a complete sentence. A citation is not required.

References:
McCance 2018

Advanced Pathophysiology: Anemia of Chronic Disease

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Date

Question 1

The clinical scenario described is most consistent with Anemia of chronic disease secondary to infection with HIV and Chronic Kidney Disease (CKD). Since this type of anemia is multifactorial, diagnosis is only based on the presence of a condition that causes chronic inflammation such as cancer, an infection, kidney disease or an autoimmune condition anemia of chronic disease pathophysiology case study essay.

Question 2

The diagnosis of anemia of chronic disease is supported by the following clinical data:

Iron levels below the borderline
A low hematocrit and hemoglobin level
High levels of ferritin- ferritin is only released when there’s the need to make RBCs and is stored in the liver. However, when the erythropoietin to make RBCs is produced in small amounts, the amount of ferritin used is also less thus, its levels automatically increase. anemia of chronic disease pathophysiology case study essay.
The total binding capacity of iron is low-Total binding capacity is an indirect way of measuring transferrin. In this patient case scenario, although iron is present, it is not readily available for use hence the low levels.
A normal mean corpuscular volume which indicates that the Red Blood cells are of average size and normal

Question 3

The most likely cause for this patient’s anemia is a reduction in erythropoietin due to Chronic Kidney Disease. Diminished renal function influences a reduction in erythropoietin secretion which is vital for the production of erythrocytes. Besides, it is indicated that the patient no longer produces urine and this can result in the gradual accumulation of uremic toxins which shorten the lifespan of RBCs.

Question 4

What is the electron transport chain and how is it altered by anemia?

The electron transport chain is the step by step process of oxidation and reduction that facilitates the ATP process within a mitochondrion. It occurs in three major steps namely: glycolysis, Krebs cycle and electron transport. The process aims at promoting a concentration gradient through a surplus buildup of hydrogen ions between the membrane interspaces and the mitochondria matrix (McCance, 2019). In the process, FADH and NADH transfer electrons to molecular oxygen influencing the release of hydrogen ions. Oxygen is a key requirement for this process to take place. Therefore, if not present, ATP cannot be formed. When anemia exists, low hemoglobin levels reduce the oxygen-carrying capacity and this generally reduces the electron transport chain anemia of chronic disease pathophysiology case study essay.

b. Why is the ferritin level 450 ng/ml?

Ferritin is a blood cell protein which contains and stores iron inside cells. Ferritin is used in the formation of red blood cells. However, when the kidneys produce limited amounts of erythropoietin as it is in this patient case scenario, fewer amounts of ferritin are utilized. This leads to gradual accumulation within plasma hence the high levels (McCance, 2019).

What effects does anemia/low blood volume have on the cardiovascular system?

Low blood volume creates a concentration gradient between intravascular space and the interstitial compartment. Blood becomes less viscous and fluid moves from the interstitial spaces to intravascular space. As a result, the heart rate and stroke volume increase leading to dilatation of the cardiac muscles, insufficiency of valves and heart murmurs (Zadrazil & Horak, 2015). The most likely outcome is that of high-output heart failure/anemic heart failure.

What are the effects of tissue hypoxia on the cardiovascular system, pulmonary system, and CNS?

When tissue hypoxia sets in, blood vessels dilate causing a reduction in vascular resistance. This can lead to cardiac failure since both the heart rate and stroke volume increase in response. To ensure adequate oxygen supply to vital organs and tissues, the respiratory rate increases leading to dyspnea (Zadrazil & Horak, 2015). When there is diminished oxygen supply to the brain, lethargy and dizziness sets in.
e. How does chronic kidney disease cause anemia?

The major cause of anemia among patients with CKD (Chronic Kidney Disease) is limited erythropoietin production. Erythropoietin is a hormone that facilitates how red blood cells mature and differentiate. When there’s reduced erythropoietin production, the production of red blood cells also reduces which influences low hemoglobin levels and subsequent anemia (Zadrazil & Horak, 2015). Other factors that have proven to cause anemia in CKD include reduced iron levels available for erythropoiesis, inflammation and high levels of hepcidin which accounts for impaired absorption of dietary iron. Lastly, the gradual accumulation of uremic toxins due to impaired renal function shortens the half-life of red blood cells which ultimately causes anemia.
Question 5

CNS complications-delirium, dizziness and syncope

Cardiovascular complications- Anemic heart failure, Anasarca, Hypertension, Heart murmurs, and angina

Musculoskeletal complications- paresthesia as a result of poor perfusion to muscles and tissues

References

McCance, K.L. (2019). Cellular biology. In K.L. McCance & S.E. Huether (Eds). Pathophysiology: The biologic basis for disease in adults and children (pp 28). St. Louis, MO: Mosby Elsevier.

Zadrazil, J., & Horak, P. (2015). Pathophysiology of anemia in chronic kidney diseases: A review. Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub, 159(2), 197-202 anemia of chronic disease pathophysiology case study essay.