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PHA 222 > blood disorders 2/3 > Flashcards

blood disorders 2/3 Flashcards

1
Q

what is the haemoglobin molecude made up of?

A

Two pairs of polypetide chains (the globins)•Four complexes of iron plus protoporhyrins(the hemes)
oxygen carrying protein of erythrocytes

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2
Q

where is iron in the body bound to?

A

Total body iron is bound to heme or stored bound to ferritin or hemosiderin mononuclear phagocytes and hepatic parenchymal cells

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3
Q

how much iron is lost every day? and where from?

A

Less than 1 mg per day is lost in the urine, sweat, epithelial cells, or from the gut

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4
Q

what is transferrin? and where is it syntheised?

A

Transferrin: a glycoprotein
•primarily synthesized in the liver
also synthesized by tissue macrophages, submaxillary and mammary glands, ovaries and testes

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5
Q

what is an Apotransferrin?

A

Transferrin without attached iron

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6
Q

is heme/ ferrous iron better absorbed than non-heme/ferrous iron?

A

heme/ ferrous iron is better absorbed

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7
Q

what does Gastric acidity help?

A

helps to keep iron in the ferrous state and soluble in the upper gut

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8
Q

does Formation of insoluble complexes with phytate or phosphate increase/ decrease iron absorption?

A

decrease

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9
Q

how is iron absorption increased?

A

Iron absorption is increased with low iron stores and increased erythropoietic activity, e.g. bleeding, haemolysis, high altitude

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10
Q

how does high vs low iron plasma affect loss by shedding?

A

low- decreases loss by shedding

high- increases loss by shedding

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11
Q

what sort of anemia is iron deficiency anemia?

A

Hypochromic microcytic anaemia

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12
Q

what causes Hypochromic microcytic anaemia?

A

Inadequate iron intake in diet, as in infants during periods of rapid growth or with adolescents subsisting on an inadequate diet
–Inadequate reutilization of iron present in red cells due to chronic blood loss

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13
Q

whats the main lab test you would use to classify iron deficiency anaemia?

A

Low serum ferritin and serum iron

•Much higher than normal serum iron-binding protein with a much lower than normal percent iron saturation

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14
Q

how do you trest iron deficiency anaemia?

A

treat the cause rather than the symptoms

supplementary iron

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15
Q

what are examples of iron deficiency anaemia?

A

infant with a history of poor diet
• In adults: a common cause is chronic bloodloss from the gastrointestinal tract, as maybe caused by a bleeding ulcer or anulcerated carcinoma of the colon
• In women: excessive menstrual blood loss
• Too frequent blood donations

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16
Q

what are foods/ drugs that impair iron absorption?

A
  • Milk
  • Tea
  • Phytates
  • Antacids
  • Tetracyclines
  • Fluoroquinolones
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17
Q

what are foods/ drugs that aid iron absorption?

A
  • Vitamin C
  • Meat
  • Orange juice
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18
Q

what are the 3 different types of iron salts you can give?

A

Ferrous sulfate
Ferrous gluconate
Ferrous Fumarate

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19
Q

when is parental iron necessary?

A

Necessary in individual unable to absorb oral iron due to
–Malabsorption syndromes
–Due to surgical procedure
–Inflammatory condition involving GIT
•Patients who can not tolerate oral preparations
•Patients with chronic renal failure receiving treatment with erythropoietin

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20
Q

what are the 2 types of parental iron?

A

–Iron – dextran(deep intramuscular injection or slow intravenous infusion)
–Iron - sucrose(slow intravenous infusion)

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21
Q

what are the unwanted affects of iron?

A

Oral iron administration are dose-related and include nausea, abdominal cramps and diarrhoea
.•Parenteral iron can cause anaphylactoid reactions
•Acute iron toxicity, usually seen in young children who have swallowed attractively coloured iron tablets in mistake for sweets,occurs after ingestion of large quantities of iron salts.
•Chronic iron toxicity or iron overload is virtually always caused by conditions other than ingestion of iron salts

22
Q

where are vitb12 and folic acid found?

A

vit b12- found in meats/ livers/ animal proteins

folic acid- found in green veg

23
Q

what are folic acid and vit b12 needed for?

A

Both are required not only for normal hematopoiesis but also for normal maturation of many other types of cells

24
Q

what is the maturation of red blood cells know as?

A

megaloblastic erythropoiesis

25
Q

what are the 3 risk factors for folate deficiency?

A 
Decreased absorption caused by
•Coeliac disease
•Crohn’s disease
Inadequate intake caused by
•Alcoholism
•Advanced age
•Malnutrition/poverty
Hyperutilization caused by
•Pregnancy
•Growth spurts
26
Q

what is folic acid made up from?

A

pteridine +para-aminobenzoic acid+ glutamic acid)

27
Q

where does the absorption of folic acid occur?

A

in the upper small intestine

28
Q

how do anemia and folic acid deficiency symptoms differ

A

In folate deficiency anaemia similar symptoms to pernicious anaemia except neurologic manifestations are generally not seen

29
Q

what is Pernicious anaemia?

A

Vitamin B12 deficiency macrocytic anaemia

Often associated with autoantibodies directed against gastric mucosal cells and intrinsic factor

30
Q

what are the causes of vitb12 deficiency?

A

Following gastric resection to treat ulcer disease or to treat gastric cancer
•Following gastric bypass procedures to treat obesity
•Due to distal small bowel resection or disease(because Vitamin B12is absorbed in the ileum)
•Nutritional deficiency in strict vegetarians after many years without meat, eggs and dairy products

31
Q

what is the treatment of vit b12 deficiency?

A

intramuscular administration of Vitamin B12available as cyanocobalamin(C) or hydroxocobalamin
h-1000μg i.m.in five doses 2or3days apart followed by maintenance therapy 1000μgevery three months

32
Q

what is retained in the body longer H/C?

A

h

33
Q

what is the treatment of folate deficiency?

A

Oral folic acid 5mg daily for 3 weeks (acute deficiency)

•Maintenance therapy 5mg once weekly

34
Q

what are Pregnant women given and before conception?

A

folic acid

35
Q

what causes depression of bone marrow?

A

anaemia- mild supression
marrow injured by radiation, anticancer drugsor toxic chemicals; aplastic anaemia, which ismuch more serious, can cause severe bone marrow damage
A manifestation of an autoimmune disease in which the body’s own cytotoxic T lymphocytes attack and destroy the marrow stem cells

36
Q

what does treatment of Bone Marrow Suppression, Damage, or Infiltration depend on?

A

on cause:
–Blood and platelet transfusions–Immunosuppressive drugs–Bone marrow transplant in highly selected cases of aplastic anaemia

37
Q

what are the 4 types of genetically determined abnormalities of red blood cells?

A

Abnormally shaped cells
Abnormal hemoglobins:–Hemoglobin S (sickle hemoglobin)–Hemoglobin C–both predominantly - persons of African descent
Defective hemoglobin synthesis:–in thalassemia, the globulin chains are normal but their synthesis defective- normally greek/italian
Red cell enzyme deficiencies:–very common one is deficiency of an enzymecalledglucose-6-phosphatasedehydrogenase, where the enzyme is unstable and does not function normally

38
Q

what is Acquired Hemolytic Anaemia?

A

The red cells are normally formed but are unable to survive normally because they are released into a “hostile environment”
•Red cells unable to survive when antibodies attack and destroy
•Red cells destroyed by mechanical trauma

39
Q

what is Polycythemia?primary

A

manifestation of a diffuse hyperplasia of bone marrow of unknown etiology
–Characterized by overproduction of red cells, white cells, and platelets

40
Q

what is secondary polycythemia?

A

Compensatory increase in red blood cells(increased erythropoietin production) as a response to low arterial O2that may accompany underlying disease

41
Q

what is the treatment of polycythemia?

A

Many patients develop thromboses due to the increased blood viscosity and elevated platelet count
•Primary Polycythemia: drugs that suppress bone marrow over - activity
•Secondary Polycythemia: periodic removal of excess blood

42
Q

what is Hemochromatosis?

A

Genetic disease: autosomal recessive trait
•Body becomes overloaded with iron
•Iron is absorbed and excreted with difficulty

43
Q

what are the manifestations of hemochromatosis?

A

The manifestations of the disease take years to develop :tan to brown skin, diabetes, cirrhosis, heart failure
can lead to organ damage

44
Q

what is the treatment for hemochromatosis?

A

Repeated phlebotomies(withdrawal of blood)until iron stores are depleted and then periodic for life

45
Q

what is secondary Thrombocytopenia Purpura

A

–Drugs, chemicals damage the bone marrow–Bone marrow infiltrated by leukemic cells ormetastatic carcinoma

46
Q

what is primary thrombocytopenia purpura?

A

–Associated with antiplatelet autoantibodies
–The bone marrow produces platelets but are rapidly destroyed
–Often encountered in children and subsides spontaneously after a short time–Tends to be chronic in adults

47
Q

what are the factors involved in controlling the balance?

A

Haemopoeitic Growth Factors ( Erythropoietin& Granulocyte colony – stimulating factor)

48
Q

what is Erythropoietin? and where is it produced?

A

Produced in juxtatubular cells in the kidney and also macrophages
•Regulate red cell production

49
Q

Recombinant human erythropoietin can be admisitered IP? TRUE OR FALSE?

A

FALSE- only IV AND SC

50
Q

What is erytheropoietin used for?

A

Anaemia of chronic renal failure
–Chemotherapy of cancer
–Preventing anaemia in premature infants
–anaemia of AIDS ( exacerbated byZidivudine)
–Anaemia of chronic inflammatoryconditions such as rheumatoid arthritis

51
Q

what is a granulocyte colony?

A
  • Stimulate neutrophil progenitors
  • Produced mainly by monocytes, fibroblasts and endothelial cells
  • Control development of neutrophils

PHA 222 (41 decks)

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