Anemia Flashcards

1
Q

Physical signs of anemia include

A

pallor, tachycardia, systolic “flow”murmur heard at the apex and along the left sternal border, and a widened pulse pressure (increased systolic blood pressure with a decreased diastolic blood pressure).

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2
Q

asymptomatic until Hgb < 8 g/dL and may presented with F

A

Fatigue, pallor, dyspnea, dizziness, dyspnea on exertion, ischemic pain, cognitive abnormalities while Symptoms and signs of acute blood loss like (hemorrhage) are related to hypovolemia patient may came with shock state . Individuals with cardiorespiratory disease are more susceptible to symptoms of anemia early .while others may came with asymptomatic .

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3
Q

Laboratory Tests

A

Important laboratory tests include a CBC with erythrocyte indices, white cells count and leukocyte differential, and platelet count. Important chemistries include serum creatinine, calcium, liver profile including total and direct bilirubin, lactic dehydrogenase, total protein, and albumin. A reticulocyte count (corrected for anemia) . additional tests could include iron indices (serum ferritin or serum iron/transferrin/ saturation) , folic acid and cobalamin (vitamin B12) levels, hemoglobin electrophoresis, and direct antiglobulin (Coombs’) test.

A general approach to the laboratory diagnosis of the anemic patient is based largely on erythrocyte size (MCV). Naturally, the approach for each individual case will be modified by the history, physical examination, and other clinical and laboratory information for that specific patient.

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4
Q

Evaluation of a Microcytic Anemia (MCV < 80 fL)

Evaluation of a Macrocytic Anemia (MCV > 100 fL)

Evaluation of a Normocytic Anemia (MCV 80–100 fL)

A
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5
Q

The average diet contain 10-15 mg of iron per day .about 10%(1mg) of this amount is absorbed .Absorption occurs in

A

duodenum and upper jejunum.

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6
Q

Causes of Iron deficiency anemia:

A

Blood Loss: Malabsorption: Physiological demands:

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7
Q

Causes of Iron deficiency anemia:

A

Blood Loss: Menorrhagia is a common cause of anemia in pre-menopausal females, so women should

always be asked about their periods. The second common example is gastrointestinal blood loss This may result from occult gastric or colorectal malignancy, gastritis, peptic ulceration, inflammatory bowel disease, diverticulitis, polyps and angiodysplastic lesions. World-wide, hookworm and schistosomiasis are the most common causes of gut blood loss. Also the chronic use of aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) may be important causes of GIT blood loss. Very rarely, chronic hemoptysis or hematuria may cause iron deficiency.

Malabsorption: Iron is absorbed actively in the upper small intestine(duodenum and upper jejunum) and

hence can be affected by coeliac disease, Gastric acid is required to release iron from food and helps to keep iron in the soluble ferrous state. Hypochlorhydria in the elderly or that due to drugs such as proton pump inhibitors may contribute to the lack of iron availability from the diet, as may previous gastric surgery.

Physiological demands: dietary iron 7 mg/1000 kcalori. At times of rapid growth, such as infancy

and puberty, iron demands increase and may be more than absorption. In pregnancy, iron is diverted to the fetus, the placenta and the increased maternal red cell mass, and is lost with bleeding at delivery.

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8
Q

Symptoms and Signs of Ida

A

Tiredness, light headedness, breathlessness, development/worsening of

ischemic symptoms, e.g. angina . Dysphagia with solid foods from esophageal webbing (Plummer-Vinson syndrome) in long-term (chronic) iron deficiency anemia, eaten clay or chalk (pica) and craving ice.

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9
Q

Symptoms and Signs

A

Tiredness, light headedness, breathlessness, development/worsening of

ischemic symptoms, e.g. angina . Dysphagia with solid foods from esophageal webbing (Plummer-Vinson syndrome) in long-term (chronic) iron deficiency anemia, eaten clay or chalk (pica) and craving ice.

Nonspecific signs mucous membrane paller , glossy tongue with atrophy of papillae(smooth tongue), Fissures at the corners of the mouth (angular stomatitis) raised JVP, postural hypotension , tachycardia , , Spoon-shaped nails (koilonychia), legs edema and flow murmur.

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10
Q

A high TIBC or transferrin usually indicates ……. low TIBC or transferrin may also occur if……..

A

A high TIBC or transferrin usually indicates iron deficiency, but they are also increased in pregnancy and with the use of oral contraceptives. A low TIBC or transferrin may also occur if someone has malnutrition, inflammation, liver disease, or nephrotic syndrome.

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11
Q

Investigation of the cause of IDA

A

This will depend upon the age and sex of the patient, as well as the

history and clinical findings:

the upper and lower gastrointestinal tract endoscopy or barium studies , Serum anti-endomysial antibodies and possibly a duodenal biopsy) to detect coeliac disease, stool and urine examined for parasites

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12
Q

Unless the patient has………. transfusion is not necessary and oral iron supplementation is appropriate.

A

angina, heart failure or evidence of cerebral hypoxia

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13
Q

oral iron supplementation is

A
  • Ferrous sulphate 200 mg 8-hourly for 3-6 months to replete iron stores
  • Ferrous gluconate 300 mg 12-hourly

-Ferrous fumarate 200 mg 12-hourly

The hemoglobin should rise by 1 g/dl every 7-10 days and a reticulocyte response will be evident within a week. A

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14
Q

failure to respond adequately may be due

Adverse effects

A

non-compliance, continued blood loss, malabsorption or an incorrect diagnosis.

nausea, metallic taste, vomiting, dyspepsia, epigastric pain , constipation, and noncompliance.

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15
Q

Anemia of Chronic Disease (ACD)
Cusses
Indexes
Pathophys

A

This is a common type of anemia in hospital populations, It occurs in chronic renal disease, inflammatory bowel disease ,chronic infection, chronic inflammation or neoplasia. The anemia is mild, with Hb in the range of 8.5-11.5 g/dL, and is usually associated with a normal MCV (normocytic, normochromic), The serum iron is low but iron stores are normal or increased, as indicated by the ferritin or stainable marrow iron.

Anemia of chronic disease is characterized by :

Decreased availability of iron Relatively decreased levels of erythropoietin Mild decrease in the lifespan of RBCs to 70-80 days (normally 120 days) It has recently become clear that hepcidin, which is produced by the liver encouraged by pro-inflammatory cytokines, especially IL-6. Hepcidin binds to ferroportin on the membrane of iron exporting cells, such as small intestinal enterocytes and macrophages which eventually lead to anemia of chronic disease

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16
Q

difficult to distinguish ACD associated with a low MCV from iron deficiency

A

trial of oral iron can be given in difficult situations. A positive response occurs in true iron deficiency but not in ACD.

17
Q

deficiency of vitamin B12 or folic acid, the ineffective erythropoiesis results in

A

expanded hyper cellular marrow., and hemolysis within the marrow results in a raised bilirubin and lactate dehydrogenase (LDH), but without the reticulocytosis , Iron stores are usually raised.

18
Q

Symptoms B12 deficiency

Signs

A

Malaise, breathlessness ,paraesthesiae Sore mouth, Weight loss

altered skin pigmentation ,grey hair, impotence, poor memory, depression ,personality change, personality change ,hallucinations and visual disturbance .

Smooth tongue ,angular cheilosis, vitiligo Skin pigmentation ,heart failure and pyrexia.

19
Q

B12 deficiency occurs in

A

Dietary deficiency: The average daily diet contains 5–30 μg of vitamin B12 mainly in meat, fish, eggs

and milk. The liver stores enough vitamin B12 for 3 years means that vitamin B12 deficiency takes years to become manifest. B12 deficiency occurs in elderly and strict vegans but the onset of clinical features can occur at any age.

Gastric factors: Release of vitamin B12 from the food requires normal gastric acid and enzyme secretion,

and this is impaired by hypochlorhydria in elderly patients or following gastric surgery. Total gastrectomy invariably results in vitamin B12 deficiency within 5 years, often combined with iron deficiency; these patients need life-long 3-monthly vitamin B12 injections. After partial gastrectomy vitamin B12 deficiency only develops in 10-20% of patients by 5 years; an annual injection of vitamin B12 should prevent deficiency in this group.

Pernicious anemia: This is an autoimmune disorder of elderly patient in which the gastric mucosa is

atrophic, with loss of parietal cells causing intrinsic factor deficiency. It is more common in individuals with other autoimmune disease (Hashimoto’s thyroiditis, Graves’ disease, vitiligo, hypoparathyroidism or Addison’s disease, or a family history of these or pernicious anemia. The finding of anti-intrinsic factor antibodies in the context of B12 deficiency is diagnostic of pernicious anemia without further investigation. Antiparietal cell antibodies are present in over 90% of cases but are also present in 20% of normal females over the age of 60 years, a negative result makes pernicious anemia less likely but a positive result is not diagnostic. Patients with low B12 levels and negative anti-intrinsic factor antibodies should have a Schilling test performed to determine whether there is B12 malabsorption, and if so, where it is occurring. distinguishes pernicious anemia from the other causes of vitamin B12 deficiency.

Small bowel factors

One-third of patients with pancreatic exocrine insufficiency fail to transfer dietary vitamin B12 from R protein (B12 carrier protein)to intrinsic factor. This usually results in slightly low vitamin B12 values but no tissue evidence of vitamin B12 deficiency.

Motility disorders or hypogammaglobulinaemia can result in bacterial overgrowth and the ensuing competition for free vitamin B12 can lead to deficiency. This is corrected to some extent by appropriate antibiotics.

A small number of people heavily infected with the fish tapeworm develop vitamin B12 deficiency. Inflammatory disease of the terminal ileum, such as Crohn’s disease, may impair the interaction of the vitamin B12-intrinsic factor complex with its receptor, as will surgery on part of the bowel. Both may result in vitamin B12 malabsorption.

common cause of vitamin B12 deficiency, malabsorption, is affected by many factors including prolonged use of proton pump inhibitors or metformin.

20
Q

Schilling test:

A
21
Q

Folate deficiency. Causes

A

The edentulous elderly or psychiatric patient. gut disease or malignancy. Pregnancy-( twin pregnancies, multiparity and hyperemesis gravidarum).Diet Poor intake of vegetables

Malabsorption: e.g. Coeliac disease

Increased Demand: e.g. increase cell proliferation, e.g. hemolysis, Pregnancy

Drugs: Certain anticonvulsants (e.g. phenytoin),Contraceptive pill, Certain cytotoxic drugs (e.g.

methotrexate).

22
Q

Management of Megaloblastic Anemia

A

Vitamin B12 deficiency is treated with hydroxycobalamin 1000 μg i.m. in five doses 2 or 3 days apart, followed by maintenance therapy of 1000 μg every 3 months for life. The reticulocyte count will peak by the 5th-10th day after therapy and may be as high as 50%. The haemoglobin will rise by 10 g/L every week

• Oral folic acid 5 mg daily for 3 weeks will treat acute deficiency and 5 mg once weekly is adequate maintenance therapy. Prophylactic folic acid in pregnancy prevents megaloblastosis in women at risk, and reduces the risk of fetal neural tube defects.

23
Q

Sideroblastic Anemias

A

The sideroblastic anemias are a group of inherited and acquired bone marrow disorders , a rare disease. Characterized by pathological iron accumulation in the mitochondria of red blood cell precursors (nucleated erythroblasts). morphological feature of sideroblastic anemias, the ring sideroblast in the bone marrow.

24
Q

Causes of sideroblastic anemia

A

Congenital sideroblastic anemia is X-linked or autosomal

• Nutritional deficiencies (copper, vitamin B-6)

• Lead poisoning

• Zinc overdose

• Alcohol

• Drugs (eg, antituberculous agents, antibiotics(chloramphenicol), progesterone, busulfan)

25
Q

Treatment of sideroblastic anemia may include the following:

A

Removal of toxic agents

• Administration of pyridoxine, thiamine, or folic acid

• Blood transfusion (together with antidotes if an iron excess occurs as a result of the transfusion)