Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue

Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue
Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue. He also complains of frequent dyspepsia with nausea and occasional epigastric pain. He states that at night he has trouble breathing especially while lying on his back. This is relieved by him sitting up. His vitals are 180/110, P = 88, T = 98.0 F, R = 20. After a thorough work-up, he is diagnosed with congestive heart failure.
What is the etiology of congestive heart failure?
Describe in detail the pathophysiological process of congestive heart failure.
Identify hallmark signs identified from the physical exam, diagnostic lab work and symptoms.
Describe the pathophysiology of complications of congestive heart failure
What teaching would you provide this patient to avoid heart failure symptoms?
In addition to the textbook, utilize at least one peer-reviewed, evidence-based resource to develop your post.
Describe in detail the pathophysiological process of congestive heart failure.
In general, the pathophysiologic mechanisms of CHF in infants and children are very similar to those in adults. The same compensatory mechanisms are activated in the face of inadequate cardiac output. An acute decrease in blood pressure stimulates
Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue
stretch receptors and baroreceptors in the aorta and carotid arteries, which in turn stimulate the sympathetic nervous system. With the release of catecholamines and the stimulation of ? receptors, heart rate and the force of myocardial contraction increase (McCance et al., 2013). Venous smooth muscle tone also increases, which increases the return of venous blood to the heart. Sympathetic stimulation also decreases blood flow to the kidneys, skin, spleen, and extremities so that maximum flow to the brain, heart, and lungs can be maintained. Decreased blood flow to the kidneys causes the release of renin, angiotensin, and aldosterone. If chronic, this cycle results in retention of sodium and fluid by the kidneys, which in turn increases volume in the circulatory system (McCance et al., 2013). These neurohumoral and hemodynamic changes create abnormal ventricular wall stress and cause the myocardium to hypertrophy. The myocardial fibers also stretch to accommodate the increased volume. Hypertrophy and fiber stretch temporarily increase contractility and hence the force of ventricular contraction. These mechanisms eventually fail to maintain cardiac output as CHF progresses.
The fact that this patient has had gastric bypass surgery is a big risk factor for iron deficiency anemia.
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However, iron deficiency is normally diagnosed by a microcytosis in the laboratory, however macrocytes predominated on our patient’s peripheral smear, suggesting iron deficiency an improbable cause of her anemia.
The formation of IgG or IgM antibodies that react with protein antigens on the red blood cell surface causes autoimmune hemolytic anemia.
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In autoimmune hemolytic anemia, the peripheral smear exhibits typical spherocytes, which were not present in our case.
In the case of hypothyroidism, macrocytic anemia might develop.
Weight gain, constipation, cold intolerance, dry skin, or myxedema were not present in our patient, despite the fact that he exhibited all of the clinical signs of severe hypothyroidism.
Hemolytic uremic syndrome is a microangiopathic hemolytic anemia accompanied by impaired renal function and thrombocytopenia, which is most typically linked to Shiga toxin-producing Escherichia coli (particularly type O157:H7).
It’s also linked to the usage of certain drugs, such as chemotherapeutics, over-the-counter quinine formulations, and clopidogrel.
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Because our patient’s platelet count and renal function were normal, and he had none of the risk factors listed, hemolytic uremic syndrome was ruled out.
It’s difficult to tell the difference between vitamin B12 and folate deficiency in a clinical setting.
Megaloblastic anemia is the most likely diagnosis for this patient at this time due to their deficits.
1
The patient was admitted to the hospital for blood transfusions and other testing.
A evaluation of her systems found that she had become “clumsy” over the previous two years.
Her legs were easily falling asleep, she was unsteady, and she couldn’t walk in the dark or on rough terrain.
She also reported tingling and numbness in both her upper and lower extremities, as well as shooting pains in both.
The patient’s legs had lost sensitivity to gentle touch and she lacked proprioception up to her ankles.
Both of her feet developed hyperesthesia on the plantar surface.
Her reflexes were quick, and she had flexor plantar reflexes.
The movement was shaky, and tandem gait was challenging.
The Romberg sign was visible.
With some previous pointing, she slowly and methodically executed the finger-to-nose test.
It was tough to achieve a heel-to-shin motion.
Due to a failure in myelin synthesis, vitamin B12 deficiency causes subacute combined degeneration of the dorsal and lateral spinal columns.
The neuropathy is symmetrical, and the legs are frequently more affected than the arms.
Because to a loss of vibration and location perception, it starts with paresthesias and sensory ataxia.
This can lead to serious frailty.
Our patient also showed macrocytic anemia, indicating that B12 insufficiency is the underlying cause.
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Although folate insufficiency may be a cause of her hematologic problems, it does not explain her neurologic symptoms.
Multiple sclerosis (MS) is a central nervous system autoimmune inflammatory demyelinating disease that primarily affects young white women, such as our patient.
Multifocal regions of demyelination characterize it pathologically.
Tingling numbness, loss of sensation to mild touch, and gait instability are all common MS symptoms (present in this patient).
She didn’t have the relapsing-remitting nature of MS, nor did she have vision abnormalities, bladder or bowel involvement, or severe symptoms.
MS also does not produce the blood dyscrasias that our patient had.
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Dysmetria, which shows as overshooting in point-to-point motions, is a symptom of cerebellar ataxia.
The finger-to-nose test and the heel-to-shin movement were both tough for this patient.
Furthermore, her walk was shaky.
In cerebellar ataxia, however, the normal gait is wide-based with a short step length, referred to as “drunken” or “stumbling” in the literature.
Scanning speech is common in patients with cerebellar impairment.
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Our patient didn’t exhibit any of the symptoms associated with this illness.
When vision and proprioceptive cues are diminished, bilateral vestibular dysfunction is an uncommon cause of ataxia that results in a markedly altered gait.
When walking in the dark or on uneven ground, this causes trouble.
A positive Romberg sign is common in patients with bilateral vestibular impairment.
They generally experience oscillopsia and/or vertigo as well, which our patient did not have.
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The patient’s medical records revealed that she had been suffering from anemia for quite some time.
She stated that she had no previous history of chemotherapy, radiation therapy, or unusual chemical exposure.
She had, in particular, been getting outpatient oral iron replacement therapy for some months.
Since the onset of her neurologic problems, she had been receiving B12 supplements intramuscularly once a week, but her symptoms had worsened.
Her iron, transferrin, ferritin, B12, and folate levels were all within acceptable limits in her blood.
Her levels of thyroid-stimulating hormone were within normal limits.
The levels of haptoglobin, lactate dehydrogenase, urine hemosiderin, and bilirubin were all normal, indicating that there was no evidence of hemolysis.
The Coombs tests for the presence of antibody-related illness, both direct and indirect, came back negative.
Fanconi anemia and paroxysmal nocturnal hemoglobinuria were both ruled out by the tests.
Virus serologies were acquired and found to be negative for the human immunodeficiency virus, Epstein-Barr virus, cytomegalovirus, parvovirus, and hepatitis virus.
Peripheral blood flow cytometry with immunophenotyping was used to look for malignancy because the patient was leukopenic with a lymphocytic predominance.
There was no monotypic B-cell population or increase in blasts as a result of this.
There were no morphologic indications of acute leukemia or lymphoma on a Wright-Giemsa–stained slide made from peripheral blood.
Lymphoma was not detected on computed tomography scans of her chest, abdomen, or pelvis.
A bone marrow biopsy was eventually performed to discover the cause of her anemia and leukopenia.
A bone marrow biopsy revealed trilineage hematopoiesis and a normocellular bone marrow.
The erythroid precursors had been vacuolated, and 10% of them had ringed sideroblasts.
There were no clear morphologic signs of myelodysplastic syndrome (MDS) or lymphoproliferative disease.
A slight increase in the number of cytotoxic T-cells was observed.
Her iron store in the marrow was normal.

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