Anemia etiological factor

Bethell (75) has found 54% of 158 pregnant women to have true macrocytic anemia which resembles that of pernicious anemia, being characterized by cell counts of less than 3.5 million and hemoglobin concentration of 10 g. %. In most instances, the etiological factors were lack of iron and insufficiency of animal protein. 

The first step in managing chronic HF is to determine the etiology or precipitating factors. Treatment of underlying disorders (e.g., anemia, hyperthyroidism) may obviate the need for treating HF. 

The first step in managing chronic HF is to determine the etiology or precipitating factors. Treatment of underlying disorders (e.g., anemia, hyperthyroidism) may obviate the need for treating HF. Nonpharmacologic interventions include cardiac rehabflitation and restriction of fluid intake (maximum 2 L/day from all sources) and dietary sodium (approximately 2 to 3 g of sodium per day). 

The first step in the management of chronic heart failure is to determine the etiology (see Table 14—1) and/or any precipitating factors. Treatment of underlying disorders such as anemia or hyperthyroidism may obviate the need for treatment of heart failure. Patients with valvular diseases may derive significant benefit from valve replacement or repair. Revascularization or anti-ischemic therapy in patients with coronary disease may reduce heart failure symptoms. Drugs that aggravate heart failure (see Table 14—3) should be discontinued, if possible. 

Patients with CKD are at increased risk of cardiovascular disease, independent of the etiology of their kidney disease. While a clearly unique pathogenesis of cardiovascular disease specific to CKD has not been identified, it is known that manifestations of kidney disease are contributory. Risk factors for cardiovascular disease in this population include hemodynamic and metabolic abnormalities, as well as hypertension, dyslipidemia, elevated homocysteine levels, anemia, hyperparathyroidism, malnutrition, and oxidative stress. Hypertension induced by volume expansion and increased systemic vascular resistance increases myocardial work and contributes to development of left ventricular hypertrophy (LVH). Hyperlipidemia may enhance atherogenesis, while some uremic toxins can decrease myocardial contractflity. In addition, uremic toxins can induce pericarditis, a potentially fatal complication. Currently, measures to screen this high-risk population for cardiovascular risk factors are not routine. ... 

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