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pathophysiology > blood disorders > Flashcards

blood disorders Flashcards

1
Q

Mean corpuscular volume

A

the average volume of a single red blood cell

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2
Q

fL

A

units for MCV - fentolitres

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3
Q

mean corpuscular haemoblobin concenration

A

the average haemoglobin concentration in a single red blood cell in g/L

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4
Q

Colour index (CI)

A

the ratio of the % of haemoglobin to the RBC count.

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5
Q

the ‘normal’ haemoglobin % count

A

150g/L

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6
Q

the ‘normal’ RBC count

A

5 T/L

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7
Q

if CI < 1

A

hypochromia

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8
Q

if CI = 1

A

Normochromia

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9
Q

if CI > 1

A

Hyperchromia

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10
Q

MCV < 80fL

A

microcytic anaemia

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11
Q

MCV = 80-100fL

A

normocytic anaemia

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12
Q

MCV > 100 fL

A

macrocytic anaemia

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13
Q

poikilocytosis

A

nonuniformity of cell shapes

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14
Q

anisocytosis

A

nonuniformity of cell sizes

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15
Q

most common causes of anaemia

A
  1. blood loss
  2. inadequate RBC production
  3. Excessive RBC destrucstion (haemolysis)
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16
Q

nutritional deficiencies causing anaemia can lead to

A
  • impaired DNA synthesis
  • impaired haemoglobin synthesis
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17
Q

iron deficiency anaemia

A

caused by the loss of iron through blood loss from the genitourinary tract

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18
Q

iron homeostasis

A

regulated through controlling absorption of iron. whereas iron loss/excretion is NOT under control

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19
Q

functional iron

A
  • 80% haemoglobin.
  • 20% myoglobin and iron containing enzymes
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20
Q

site of iron absorption

A

duodenum in the forms of heme and nonheme iron molecules

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21
Q

iron molecules bind to a protein called..

A

ferritin, as iron in its free form is toxic.

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22
Q

hepcidin

A

inhibits iron transfer from the enterocyte to plasma by binding to the ferroportin and causing it to be degraded

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23
Q

transferrin

A

a binding protein hat transports iron to the plasma

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24
Q

apo-transferrin

A

the protein without a binded iron

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25
Q

ferritin content in the blood

A

can help identify the iron supply in the body

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26
Q

haemosiderin

A

granules formed as a result of the degradation of ferritin protein shells

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27
Q

heme synthesis

A

ferrous iron + protoprphyrin IX (with presence of ferrochelatase)

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28
Q

pernicious anaemia

A

stems from a vitaminb12 deficiency, impairs cell division, does not affect haemoglobin synthesis

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29
Q

stores for vitaminb12

A

there are significant intrahepatic stores which last for several years

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30
Q

which food groups contain little vitaminb12

A

plants &vegetables

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31
Q

intrinsic factor

A

required for the absorption of vitaminb12.nintrinsic factor is produced by the parietal oxyntic cells of the stomach

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31
Q
A
32
Q

transcobalamin II

A

associates with vitaminb1 and delivers it to the liver and other cells of the body

33
Q

haptocorrin

A

a salivary protein that binds to vitaminb12 for transportation

34
Q

achlorhydria and loss of pepsin secretion

A

vitaminb12 is not readily released by proteins in food

34
Q

gastrectomy

A

intrinsic factor is not available for uptake in the ileum

35
Q

loss of exocrine pancreatic function

A

vitaminb12 cannot be released from haptocorrin-vitaminb12 complexes

36
Q

ileal resection or diffuse ileal disease

A

can remove or damage the site of intrinsic factor-vitaminb12 complex absorption

37
Q

tapeworms

A

compete with the host for b12 and can induce a deficiency state

38
Q

pregnancy, hyperthyroidism, disseminated cancer, and chronic infection

A

an increased demand for vitaminb12 can produce a relative deficiency even with normal absorption

39
Q

which 2 biochemical processes is vitaminb12 required for

A

physiological lipid metabolism and DNA synthesis

40
Q

macro-ovalocyes

A

larger than normal RBCs and contain ample haemoglobin. they lack the central pallor of normal RBCs and even appear hyperchromic

41
Q

cell characteristics of pernicious anaemia

A

-significant anisocytosis and poikilocytosis
- nucleated precursors in peripheral blood
- macro-ovalocytes
- hypersegmented neutrophils

42
Q

megaloblasts

A

large nucleated RBCs found in bone marrow following pernicious anaemia

43
Q

stores of folate

A

are modest

44
Q

sickle cell anaemia

A

common hereditary haemoglobinopathy caused by a point mutation in beta-globin that promotes the polymerisation of deoxygenated haemoglobin, leading to red cell distortion, hemolytic anaemia, microvascular obstruction, and ischaemic tissue damage

45
Q

HbA1 abundancy

A

> 95%

46
Q

HbA2

A

<3.5%

47
Q

HbF

A

1-2%

48
Q

HbS containing RBC characteristics

A

rigid and tend to adhere to each other, they form plugs in small blood vessels and easily fall apart. However, RBCs in heterozygous individuals do not sickle except under conditions of profound hypoxia

48
Q

aplastic anaemia

A

chronic primary haematopoietic failure and attendant pancytopenia

49
Q

haemolytic anaemias key features

A
  • shortened RBC lifespan
  • elevated erythropoietin levels and a compensatory increase in erythropoiesis
  • accumulation of haemoglobin degradation products
49
Q

erythropoietin (EPO)

A

a glycoprotein hormone, naturally produced by the peritubular cells of the kidney, that stimulates RBC production

50
Q

erythropoiesis

A

the process of making RBC

51
Q

extravascular haemolysis

A
  • slenomegaly
  • anaemia
  • jaundice
52
Q

intravascular haemolysis

A
  • haemosiderinuria
  • anaemia
  • haemoglobinaemia
  • haemoglobinuria
  • jaundice
  • no splenomegaly
53
Q

reticulocytosis

A

an increase in circulating reticulocytes

54
Q

reticulocytes

A

immune RBCs produced in the bone marrow and released into the peripheral blood

55
Q

extramedullary haematopoiesis

A

refers to deposits of erythroid precursors in sites other than the bone marrow and peripheral blood

56
Q

platelets

A

platelet membranes are sources of phospholipids and contain receptors that are needed for platelet aggregation

57
Q

platelet activation

A

inititated by exposure to thrombin, collagen and platelet-activating factor (PAF)

58
Q

main phases of haemostasis

A
  1. Vascular phase
  2. Platelet phase
  3. Coagulation phase (thrombus formation)
59
Q

coagulation factors

A

most are produced by the liver but some derive from endotheleal cells and platelets.

60
Q

stages in secondary haemostasis

A
  1. initiation
  2. amplification
  3. propagation
61
Q

thromboplastin

A

released by damages cells during coagulation, this activates factor VII

62
Q

fibrinolysis

A

fibrin is degraded by plasmin

63
Q

excessive bleeding

A
  • increased fragility of BV
  • platelet deficiency or dysfunction
  • derangement of coagulation
64
Q

megakaryocytes

A

large progenitor cells in the bone marrow, are the source of platelets

65
Q

haemarthrosis

A

bleeding due to coagulation factor deficiencies often occurs into the gastrointestinal and urinary tracts and into weight-bearing joints

66
Q

inherited clotting factor deficiencies

A
  • haemophilia A
  • Von Willeband disease
  • haemophilia B
67
Q

Aquired clotting factor deficiencies

A
  • decreased protein sythesis
  • shortened half life
68
Q

multiple clotting factors affected

A

aquired clotting factor deficiencies

69
Q

a single clotting factor is affected

A

inherited clotting factor deficiencies

70
Q

Von Willebrand disease

A

An autosomal dominant disorder, spontaneous bleeding from mucous membranes, wounds or menorrhagia, often goes unnoticed until some haemostatic stress occurs.

71
Q

haemophillia A

A

X-linked recessive hereditary disease resulting in life-threatening bleedings.

72
Q

haemophilia B

A

X-linked recessive inheritance

73
Q

prothrombin time (PT)

A

measurement in seconds of the clotting of plasma after addition of an exogenous source of tissue thromboplastin and calcium ions.

assesses the extrinsic and common coagulation pathways

74
Q

partial thromboplastin time (PTT)

A

the clotting of plasma after the activation of contact factor XII.

assesses the intrinsic and common coagulation pathways

75
Q

Disseminated intravascular coagulation (DIC)

A
  • triggered by overwhelming infection, specific leukemias or lymphomas, or massive haemorrhage
  • aberrant activation of the clotting system results in microthrombi at various location
  • because all clotting factors have been consumes, no blood clotting can occur where it would be needed.

pathophysiology (9 decks)

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