45 Anemia Resulting from other Nutritional Deficiencies Flashcards

1
Q

TRUE OR FALSE

Chronic deprivation of vitamin A results in anemia similar to that observed in iron deficiency.

A

TRUE

Chronic deprivation of vitamin A results in anemia similar to that observed in iron deficiency.

Unlike iron-deficiency anemia but similar to the anemia of chronic disease, the iron stores in the liver and marrow are increased, the serum transferrin concentration usually is normal or decreased, and administration of medicinal iron does not correct the anemia.

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2
Q

Patients receiving therapy with this antituberculosis agents interfere with vitamin B6 metabolism, develop a microcytic anemia

A

Isoniazid

Can be corrected with large doses of pyridoxine

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3
Q

B6

Pyridoxine deficiency has been reported in conjunction with folate deficiency in an infant fed with ________

A

Goat’s milk

Other acquired conditions that may influence pyridoxine metabolism:
* Drugs that react with pyridoxal phosphate or that affect its metabolism
* Malabsorptive states such as celiac disease, and
* Renal dialysis

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4
Q

Vitamin deficiency

_____________ results in a decrease in red cell glutathione reductase activity because this enzyme requires flavin adenine dinucleotide for activatio

A

Riboflavin Deficiency

B2

The glutathione reductase deficiency induced by riboflavin deficiency is not associated with a hemolytic anemia or increased susceptibility to oxidant-induced injury

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5
Q

TRUE OR FALSE

Poor riboflavin status may interfere with iron handling and contribute to the etiology of anemia when iron intakes are low.

A

TRUE

Poor riboflavin status may interfere with iron handling and contribute to the etiology of anemia when iron intakes are low.

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6
Q

TRUE OR FALSE

Pantothenic acid deficiency, when artificially induced in humans, is associated with anemia.

A

FALSE

Pantothenic acid deficiency, when artificially induced in humans, is not associated with anemia.

B5

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7
Q

Megaloblastic anemia, responsive to thiamine, occurs in a childhood syndrome in association with diabetes and sensorineural deafness

A

Rogers syndrome

B1

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8
Q

Mutation implicated in all cases of thiamine responsive megaloblastic anemia (Rogers syndrome)

A

SLC19A2 gene on chromosome 1q23.3

Result of a defect in the high-affinity thiamine transporter

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9
Q

This vitamin serves to facilitate intestinal iron absorption by maintaining iron in the more soluble reduced or ferrous (Fe2+) state

A

Vitamin C

Another potential intersection of ascorbate with iron deficiency has been noted in patients with the iron-refractory iron-deficiency anemia (IRIDA) phenotype caused by genetic defects in the TMPRSS6 gene

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10
Q

Anemia observed in subjects with scurvy is not simply the result of a deficiency of ascorbic acid but rather a result of

A

Bleeding or a deficiency of folic acid

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11
Q

Increase or Decrease

In patients with iron overload from repeated blood transfusions, the level of vitamin C in leukocytes is often _________________ because of rapid conversion of ascorbate to oxalate.

A

Decreased

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12
Q

Deficiency of this vitamin in humans are limited to the neonatal period and to pathologic states associated with chronic fat malabsorption.

A

Vitamin E

It is not an essential cofactor in any recognized reactions.

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13
Q

Vitamin E deficiency is common in patients with _________________ if the patients are not receiving daily supplements of the water-soluble form of the vitamin.

A

Cystic fibrosis

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14
Q

Vitamin E supplementation has been used in these conditions

A

Hereditary hemolytic anemias
Sickle cell anemia

in the absence of vitamin deficiency

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15
Q

Present in a number of metalloproteins

Namely cytochrome c oxidase, dopamine β-hydroxylase, urate oxidase, tyrosine and lysyl oxidase, ascorbic acid oxidase, and superoxide dismutase (erythrocuprein)

Required for the absorption and utilization of iron

A

Copper

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16
Q

More than 90% of the copper in the blood is carried bound to

A

Ceruloplasmin

17
Q

Form of copper that converts iron to the ferric (Fe3+) state for its transport by transferrin

A

Hephaestin

18
Q

Characterized by an anemia, often macrocytic, that is unresponsive to iron therapy, hypoferremia, neutropenia, and usually the presence of vacuolated erythroid and granulocytic precursors in the marrow

A

Copper deficiency

may microcytic din

Consequently, copper deficiency should enter the differential diagnosis in patients with features of myelodysplastic syndrome, particularly if there is a history of previous gastric surgery

19
Q

Copper deficiency with a resultant microcytic anemia can be produced by

A

Chronic ingestion of massive quantities of zinc

Dietary zinc in large doses leads to copper deficiency by impairing copper absorption

20
Q

The diagnosis of copper deficiency can be established by demonstrating

A

Low serum ceruloplasmin or serum or 24-hour urine copper level

The serum copper level is thought to be more reliable because ceruloplasmin behaves as an acute phase protein.

21
Q

In later infancy, childhood, and adulthood, serum copper values should normally exceed

A

70 mcg/ dL

Despite these limitations, a serum copper level less than 70 mcg/dL (11 μmol/L) or a ceruloplasmin level less than 15 mg/dL after age 1 or 2 months can be regarded as evidence of copper deficiency.

22
Q

Low serum copper values may be observed in hypoproteinemic states, such as exudative enteropathies and nephrosis, and in Wilson disease.

In these circumstances, a diagnosis of copper deficiency cannot be established by serum measurements alone but requires analysis of

A

Liver copper content or clinical response after a therapeutic trial of copper supplementation

  • Dose in infants: 2.5 mg of copper (~80 mcg/kg per day) oral supplementation
  • IV bolus injection of copper chloride also has been used
  • Hematologic manifestations of copper deficiency are fully reversible over a 4- to 12-week period after copper supplementation.
23
Q

TRUE OR FALSE

Although human zinc deficiency may produce growth retardation, impaired wound healing, impaired taste perception, immunologic abnormalities, and acrodermatitis enteropathica, at present, there is no evidence that isolated zinc deficiency produces anemia.

A

TRUE

Although human zinc deficiency may produce growth retardation, impaired wound healing, impaired taste perception, immunologic abnormalities, and acrodermatitis enteropathica, at present, there is no evidence that isolated zinc deficiency produces anemia.

Deficiency of this micronutrient is seen in conjunction with deficiencies of iron, folate, and vitamin B12

24
Q

TRUE OR FALSE

Selenium deficiency results in a striking decrease in the level of red cell glutathione peroxidase, there do not appear to be any adverse hematologic consequences.

A

TRUE

Selenium deficiency results in a striking decrease in the level of red cell glutathione peroxidase, there do not appear to be any adverse hematologic consequences.

25
Q

A major factor responsible for the reduction in hemoglobin concentration in anemia of starvation

A

Dilution

26
Q

In persons subjected to complete starvation either for experimental purposes or as treatment of severe obesity, anemia was not observed during the first_____ weeks of fasting.

A

2–9 weeks

Starvation for 9–17 weeks produced a decrease in hemoglobin and marrow hypocellularity.

27
Q

In malnourished communities, anemia with erythroblastopenia resulting from _________ should be distinguished from the similar picture that can arise as a result of protein-calorie malnutrition.

A

Parvovirus B-19 infections

28
Q

TRUE OR FALSE

An abrupt fall in hemoglobin after protein feeding may be an ominous harbinger of adverse and even fatal outcome and prompt transfusion to restore hemoglobin may be lifesaving.

A

TRUE

An abrupt fall in hemoglobin after protein feeding may be an ominous harbinger of adverse and even fatal outcome and prompt transfusion to restore hemoglobin may be lifesaving.

It may respond to either riboflavin or prednisone.

  • During the third or fourth week, when the child has clinically improved and serum protein levels are approaching normal, another episode of erythroid marrow aplasia may develop.
  • The relapse is not associated with infection, does not respond to antibiotics, and does not remit spontaneously.
29
Q

Deficiencies that are common in people with alcoholism

A

Pyridoxal phosphate and folate deficiency

In addition to folate deficiency, people with chronic alcoholism frequently demonstrate multiple other micronutrient deficiencies, including thiamine, pyridoxine, and vitamin A, which aggravate the risk of anemia.

30
Q

Morphology seen on PBS of people with alcoholism:

A

“dimorphic,” with macrocytes, hypersegmented neutrophils, and hypochromic microcytes

IDA+Folate deficiency

31
Q

TRUE OR FALSE

Megaloblastic anemia occurs almost exclusively in people with alcoholism who have been eating poorly.

A

TRUE

Megaloblastic anemia occurs almost exclusively in people with alcoholism who have been eating poorly.

It is seen more commonly in heavy drinkers of wine and whiskey, which contain little or no folate, than in drinkers of beer, which is a rich source of the vitamin.

32
Q

Condition where macrocytosis usually is mild, with mean cell volume in the range of 100–110 fl, and anemia is usually absent.

In the blood film, the macrocytes are typically round rather than oval, and neutrophil hypersegmentation is not present.

The macrocytosis persists until the patient abstains from this agent

A

Macrocytosis of alcoholism

33
Q

Alcohol ingestion for____ days produces vacuolization of early red cell precursors, and formation of vacuoles can be observed in in vitro marrow cell cultures.

A

5–7 days

34
Q

Condition characterized by alcohol-induced liver disease, often hyperlipidemia, jaundice, and transient spherocytic hemolytic anemia, and spur cell hemolytic anemia, associated with severe alcohol-induced liver disease

A

Zieve syndrome

35
Q

Treatment for Zieve syndrome

A

Hepatic transplantation

36
Q

The association of myelodysplasia with chronic alcohol consumption may result from polymorphisms in______________, which lead to accumulation of reactive aldehydes from ethanol, resulting in genetic damage to hematopoietic stem cells.

A

Alcohol dehydrogenase