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Hematolymphoid system > HLS > Flashcards

HLS Flashcards

1
Q

Blood consist of

A

Formed elements & Plasma

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2
Q

Blood tissue function is

A

a carrier

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3
Q

The lowest part of the tube after centrifugation consist of

A

RBC’s that make 45%

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4
Q

The middle part of the tube consist of

A

WBC’s and Platelets that make 1%

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5
Q

The upper part of the Tube consist of

A

The plasma that makes 55%

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6
Q

The buffy coat found in a centrifugation tube is made of

A

WBC’s and Platelets

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7
Q

The diameter of RBC’s is around

A

7-8 microns

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8
Q

Which protein maintains the RBC structure?

A

Spectrin mainly

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9
Q

If spectrin is abnormal, what disease do you suspect?

A

Spherocytosis

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10
Q

What is the precursor of RBC’s?

A

Reticulocytes

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11
Q

What is the percentage of Reticulocytes in normal hematocrit count?

A

1%

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12
Q

Leukocytes are classified according to?

A

The presence of granules in the cytoplasm

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13
Q

Granulocytes are:

A

Eosinophils, Basophils, Neutrophils.

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14
Q

Agranulocytes are:

A

Lymphocytes &Monocytes

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15
Q

The specific granules are considered to be:

A

Secondary granules

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16
Q

The non-specific granules are:

A

Primary granules

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17
Q

The non-specific granules are also called:

A

Azurophilic granules or Lysozymes

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18
Q

Neutrophils account for

A

60%-70% pf leukocytes

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19
Q

Neutrophils nucleus is

A

Multi-lobed and bi-lobed for newly made neutrophils

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20
Q

Increased number of neutrophils indicate

A

Bacterial infection

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21
Q

Eosinophils found mainly in

A

Parasitic infection

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22
Q

Eosinophils have

A

Abundant large, acidophilic granules

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23
Q

Basophils have a nucleus shaped as

A

bi-lobed nucleus

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24
Q

basophils are seen in

A

allergic reactions

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25
Q

Lymphocytes are

A

B & T cells

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26
Q

Lymphocytes shape

A

A large nucleus that fills the whole cytoplasm

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27
Q

Platelets are made from

A

Megakaryocyte cells

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28
Q

platelets have 2 zones

A

light peripheral hyalomere zone dark granulomere zone

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29
Q

Globulin types

A

alpha, beta, gamma

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30
Q

Alpha & beta Globulins are made in

A

liver

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31
Q

Gamma globulins are made by

A

Lymphocytes

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32
Q

Alpha & beta globulins are considered

A

clotting factors

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33
Q

what are Hemoproteins

A

Hemoglobin (Hb), Myoglobin

Cytochromes, Cytochrome P450 (CYP) monooxygenase system. catalase, NOS, Peroxidase

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34
Q

membranous

bones, such as:

A

1- the bodies of the vertebrae.
2- the breastbone (sternum).
3- the ribcage.
4- the pelvic bones.

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35
Q

The blood plasma volume

A

2.7-3.0 litres in an average human.

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36
Q

Hematocrit:

A

45 % for males,42 % for females

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37
Q

Acute hepatic porphyrias

A 
ALA dehydratase–deficiency porphyria (AR)
acute intermittent porphyria (hydroxymethylbilane synthase)
hereditary coproporphyria (coproporphyrinogen III oxidase)
variegate porphyria (protoporphyrinogen oxidase)
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38
Q

85% of heme destined for degradation comes from

A

senescent RBC.

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39
Q

Stages of differentiation of red blood cells:

A

Colony-forming-unit-erythrocytes →
proerythroblasts →basophil erythroblasts→
polychromatophil erythroblasts→orthochromatic
erythroblast →reticulocytes →erythrocytes.

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40
Q

The secretion of erythropoietin starts within

A

minutes to hours after stimulation

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41
Q

erythropoietin reaches maximum production within

A

24

hours to 5 days.

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42
Q

The maturation of red blood cells requires

A

Vitamin B12 (Cyanocobalamin) and Folic acid

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43
Q

-The daily need for Vit.B12

A

about 1 to 3 micrograms,

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44
Q

How does hemin inhibit heme synthesis?

A

Hemin decreases the amount (and, thus, the activity) of ALAS1 by :
1-Repressing transcription of its gene
2-increasing degradation of its messenger RNA
3-decreasing import of the enzyme into mitochondria.

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45
Q

Chronic hepatic porphyria clinical expression is influenced by various factors:

A 
hepatic iron overload
exposure to sunlight,
alcohol ingestion
estrogen therapy,
the presence of hepatitis B or C or HIV infections.
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46
Q

what steps of heme synthesis takes place in mitochondria?

A

1st,6th,7th,8th

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47
Q

why does skin itch and burn when exposed to visible light in porphyria patients?

A

cuz of oxidation of colorless porphyrinogens to coloured porphyrins which are light sensitizing molecules

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48
Q

the most common type of porphyrias?

A

chronic hepatic porphyria (porphyria cutanea tarda)

49
Q

The enzyme deficiency responsible for chronic hepatic porphyria:

A

(UROD) Uroporphyrinogen decarboxylase

50
Q

Acute hepatic porphyrias symptoms:

A

acute attacks of gastrointestinal (GI), neuropsychiatric, and motor symptoms
that may be accompanied by photosensitivity

51
Q

which acute hepatic porphyria has no photosensitivity symptom?

A

Acute intermittent porphyria

52
Q

if the protein that conjugates glucuronic acid to bilirubin is is deficient what diseases might occur?

A

Cigler-Najjar I&II or less severe gilbert syndrome

53
Q

the major part of urobilinogen leaves as:

A

Stool as stercobilin and little goes to urine

54
Q

If the protein that removes conjugated bilirubin from liver is deficient what rare disease might occur?

A

Dubin-Jhonson syndrome

55
Q

How do bacteria in gut modify bilirubin?

A

it deconjugates it from glucuronic acid into Urobilinogen

56
Q

normal bilirubin levels are:

A

<1mg/dl

57
Q

jaundice is seen at what bilirubin levels?

A

2-3mg/dl

58
Q

the normal production of bilirubin is about:

A

300mg/day

59
Q

the liver can excrete about:

A

3000mg of bilirubin per day

60
Q

If the liver is involved what type of jaundice might appear?

A

Hepatic Jaundice

61
Q

what causes hepatic jaundice

A

Damage to liver cells

62
Q

hepatic jaundice symptoms:

A

Dark urine, pale stool, conjugated hyperbilirubinemia

63
Q

hemolytic jaundice shows:

A

Unconjugated hyperbilirubinemia

64
Q

Obstructive jaundice shows:

A

conjugated hyperbilirubinemia

65
Q

what might cause obstructive jaundice?

A

Tumours or bile stones may block the hepatic duct and CB cant get into gut

66
Q

why is urobilinogen absent in obstructive jaundice?

A

because there is no conversion of CB into Urobilinogen

67
Q

what causes newborn jaundice?

A

a rise in unconjugated bilirubin because of UGD deficiency

68
Q

where does gene expression for alpha, beta, gamma , delta, epsilon happen?

A

chromosome #16 for alpha globins & #11 for beta globins

69
Q

Mean Corpuscular Hemoglobin (MCH):

A

the normal value between 27-32 pictograms/cell.

70
Q

Red Cell Distribution Width (RDW):

A

Its normal value is 10%-14.5%

71
Q

Mean Corpuscular Hemoglobin Concentration (MCHC):

A

It’s normal value 32 to 36g/dL.

72
Q

Which stain to use in Peripheral blood smear?

A

use Gimesa-Wright’s stain

73
Q

Normal reticulocyte count is

A

less than 1.5%.

74
Q

The total quantity of iron in the body is about

A

4-5 grams.65 % of which is in the form of

hemoglobin. 0.4 % of which is in the form of myoglobin

75
Q

Daily Loss of Iron

A 
In men, 0.6 mg of iron is
excreted into the faeces each day.
• In women, 1.3 mg of iron
is excreted into the faeces and
in menses.
76
Q

Myelophthisic anemia:

A

(Myelophthisis refers to the displacement of hemopoietic bone-marrow
tissue by fibrosis, tumors, or granulomas.)

77
Q

shift the Hb-dissociation curve to the left

A

CO

78
Q

Fetal blood has a higher affinity for oxygen than does adult

blood

A

because Hb F has a decreased affinity for 2,3-BPG.

79
Q

carbon dioxide that must be
carried to lungs by
three ways

A

Blood plasma
Binding to hemoglobin
Bicarbonate ion (the best one)

80
Q

why fetal hemoglobin doesn’t have 2,3-BPG?

A

2,3-BPG binds with
positively charged amino acids on beta chains .fortunately, fetal
hemoglobin has no beta chains(alpha and gamma only)

81
Q

white blood cells enter the tissue spaces by

A

diapedesis

82
Q

chemical factors which cause the activation of chemotaxis, these factors are:

A

bacterial or viral toxins
products of the inflamed tissues
products of the complement complex
products caused by plasma clotting in the inflamed area

83
Q

Reticuloendothelial system.

A

the total combination of monocytes, mobile macrophages, fixed tissue macrophages, and
a few specialized endothelial cells in the bone marrow, spleen, and lymph nodes

84
Q

Variables that increase sickling:

A

low
pO2, high pCO2,low pH, dehydration,
and an increased [2,3-BPG] in RBC.

85
Q

β-Thalassemia

CAUSES:

A

Point mutations in the promoter.
Mutations in the translational initiation
codon.
A point mutation in the polyadenylation
signal.
An array of mutations leading to splicing
abnormalities.

86
Q

a normal adult hemoglobin is approximately

A

97.5% HbA1,
2% HbA2
0.5% HbF

87
Q

Elemental iron is

A

amount of iron in the supplement available for absorption.

88
Q

Parenteral iron formulations may be used in those who

A

cannot tolerate or inadequately
absorb oral iron, as well as those receiving erythropoietin with hemodialysis or
chemotherapy.

89
Q

Fatal hypersensitivity and anaphylactoid reactions can occur in

A

parenteral iron (mainly iron dextran formulations).

90
Q

Iron is stored in

A

intestinal mucosal cells, liver, spleen, and bone marrow as ferritin

91
Q

The amount of iron absorbed depends on

A

current body stores of iron. If iron stores are

adequate, less iron is absorbed. If stores are low, more iron is absorbed.

92
Q

Folate deficiency may be caused by

A

1) increased demand (for example, pregnancy and lactation),
2) poor absorption caused by pathology of the small intestine,
3) alcoholism,
4) treatment with some drugs:

93
Q

Folic acid is rapidly absorbed in the

A

jejunum unless abnormal pathology is

present.

94
Q

Deficiencies of vitamin B12 can result from either

A

low dietary levels or,

2) more commonly, poor absorption of the vitamin due to

the failure of gastric parietal cells to produce intrinsic factor

95
Q

what’s the difference between epoetin alfa and darbepoetin?

A

Darbepoetin has a half-life about three

times that of epoetin alfa due to the addition of two carbohydrate chains.

96
Q

Agents Used to Treat Neutropenia

A

Filgrastim (G-CSF) and (GM-CSF) sargramostim can be dosed either
subcutaneously or intravenously, whereas tbo-filgrastim (G-CSF) and
pegfilgrastim (G-CSF) are dosed subcutaneously only.

97
Q

The main difference between the available agents for neutropenia

A

is in the frequency of dosing.

98
Q

Pegfilgrastim is a pegylated form of G-CSF,

A

resulting in a longer half-life when
compared to the other agents, and is administered 24 hours after chemotherapy, as
a single dose, rather than once daily. Monitoring of ANC is typically not necessary
with pegfilgrastim.

99
Q

Filgrastim, tbo-filgrastim, and sargramostim are

A

dosed once a day beginning 24 to
72 hours after chemotherapy, until the absolute neutrophil count (ANC) reaches
5000 to 10,000/μL.

100
Q

hydroxyurea treats only

A

15% of cases

101
Q

Recently approved drugs for Sickle cell disease

A

L-glutamine oral powder (Endari)
Crizanlizumab (Adakveo)
Voxelotor (Oxbryta)

102
Q

Main drug for sickle cell anemia:

A

Hydroxyurea

103
Q

Hemostasis is achieved by several mechanisms:

A
  1. Vascular constriction
  2. Formation of a platelet plug
  3. Formation of a blood clot as a result of
    blood coagulation
  4. Eventual growth of fibrous tissue into
    the blood clot to close the hole
104
Q

Causes of smooth muscle contraction

A
  1. Local myogenic spasm
  2. Local autacoid factors released from the
    traumatized tissues and blood
    platelets(thromboxane A 2 ).
  3. nervous reflexes which are initiated by
    pain nerve impulses.
105
Q

Physical and chemical characteristics of

platelets:

A 
They are minute discs 1 to 4 micrometers
in diameter
2. They are formed in the bone marrow
from megakaryocytes
3. The normal concentration is between
200,000-300,000 mm 3
4. They do not have nuclei and cannot
reproduce
106
Q

The platelet has a half-life of

A

8-12 days

107
Q

The blood clot begins to develop in

A

15 to 20
seconds if the trauma is severe, and in 1 to 2
minutes if the trauma is minor.

108
Q

if the opening is not too large,

the entire opening is filled with clot Within

A

3 to 6 minutes after rupture of a

blood vessel,

109
Q

the clot retracts after:

A

After 20 min to an hour,

110
Q

-Once a blood clot has formed, it can follow

one of two courses:

A

It can become invaded by fibroblasts, Or, it can dissolve.

111
Q

complete organization of

the clot into fibrous tissue happen within

A

about 1 to 2

weeks

112
Q

Clotting takes place in three essential

steps:

A

1- Formation of prothrombin activator
2- which catalyzes conversion of prothrombin
into thrombin
3- Thrombin converts fibrinogen into fibrin
fibres that enmesh platelets, blood cells, and
plasma to form the

113
Q

Conversion of prothrombin to thrombin;

A 
Prothrombin activator is formed as a
result of rupture of a blood vessel
2. Prothrombin activator, in the presence
of sufficient amount of ionic calcium,
causes conversion of prothrombin to
thrombin
3. The thrombin causes polymerization of
fibrinogen molecules into fibrin fibres
within another 10 to 15 seconds
114
Q

Bleeding time ;

- Normal time is about

A

1-6 minutes depends

on the depth of the wound

115
Q

Clotting time:

- The normal clotting time

A

about 6-10

minutes

116
Q

Prothrombin time:

17

  • Gives an indication of the
A 
concentration of
prothrombin in the blood
- The time required for coagulation to take
place
- Normal time is about 12 seconds
117
Q

microcytic anaemias

A

Iron deficiency
anaemia of chronic disease
sideroblastic anaemia
thalassemia

118
Q

Agglutinins in the plasma originates from

A

Gamma Globulins

119
Q

frequencies of the different blood types:

A

Type O = 47%
• Type A = 41%
• Type B = 9%
• Type AB = 3%

Hematolymphoid system (2 decks)

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