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
Lymphocytes are
B & T cells
26
Lymphocytes shape
A large nucleus that fills the whole cytoplasm
27
Platelets are made from
Megakaryocyte cells
28
platelets have 2 zones
light peripheral hyalomere zone dark granulomere zone
29
Globulin types
alpha, beta, gamma
30
Alpha & beta Globulins are made in
liver
31
Gamma globulins are made by
Lymphocytes
32
Alpha & beta globulins are considered
clotting factors
33
what are Hemoproteins
Hemoglobin (Hb), Myoglobin | Cytochromes, Cytochrome P450 (CYP) monooxygenase system. catalase, NOS, Peroxidase
34
membranous | bones, such as:
1- the bodies of the vertebrae. 2- the breastbone (sternum). 3- the ribcage. 4- the pelvic bones.
35
The blood plasma volume
2.7-3.0 litres in an average human.
36
Hematocrit:
45 % for males,42 % for females
37
Acute hepatic porphyrias
``` ALA dehydratase–deficiency porphyria (AR) acute intermittent porphyria (hydroxymethylbilane synthase) hereditary coproporphyria (coproporphyrinogen III oxidase) variegate porphyria (protoporphyrinogen oxidase) ```
38
85% of heme destined for degradation comes from
senescent RBC.
39
Stages of differentiation of red blood cells:
Colony-forming-unit-erythrocytes → proerythroblasts →basophil erythroblasts→ polychromatophil erythroblasts→orthochromatic erythroblast →reticulocytes →erythrocytes.
40
The secretion of erythropoietin starts within
minutes to hours after stimulation
41
erythropoietin reaches maximum production within
24 | hours to 5 days.
42
The maturation of red blood cells requires
Vitamin B12 (Cyanocobalamin) and Folic acid
43
-The daily need for Vit.B12
about 1 to 3 micrograms,
44
How does hemin inhibit heme synthesis?
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.
45
Chronic hepatic porphyria clinical expression is influenced by various factors:
``` hepatic iron overload exposure to sunlight, alcohol ingestion estrogen therapy, the presence of hepatitis B or C or HIV infections. ```
46
what steps of heme synthesis takes place in mitochondria?
1st,6th,7th,8th
47
why does skin itch and burn when exposed to visible light in porphyria patients?
cuz of oxidation of colorless porphyrinogens to coloured porphyrins which are light sensitizing molecules
48
the most common type of porphyrias?
chronic hepatic porphyria (porphyria cutanea tarda)
49
The enzyme deficiency responsible for chronic hepatic porphyria:
(UROD) Uroporphyrinogen decarboxylase
50
Acute hepatic porphyrias symptoms:
acute attacks of gastrointestinal (GI), neuropsychiatric, and motor symptoms that may be accompanied by photosensitivity
51
which acute hepatic porphyria has no photosensitivity symptom?
Acute intermittent porphyria
52
if the protein that conjugates glucuronic acid to bilirubin is is deficient what diseases might occur?
Cigler-Najjar I&II or less severe gilbert syndrome
53
the major part of urobilinogen leaves as:
Stool as stercobilin and little goes to urine
54
If the protein that removes conjugated bilirubin from liver is deficient what rare disease might occur?
Dubin-Jhonson syndrome
55
How do bacteria in gut modify bilirubin?
it deconjugates it from glucuronic acid into Urobilinogen
56
normal bilirubin levels are:
<1mg/dl
57
jaundice is seen at what bilirubin levels?
2-3mg/dl
58
the normal production of bilirubin is about:
300mg/day
59
the liver can excrete about:
3000mg of bilirubin per day
60
If the liver is involved what type of jaundice might appear?
Hepatic Jaundice
61
what causes hepatic jaundice
Damage to liver cells
62
hepatic jaundice symptoms:
Dark urine, pale stool, conjugated hyperbilirubinemia
63
hemolytic jaundice shows:
Unconjugated hyperbilirubinemia
64
Obstructive jaundice shows:
conjugated hyperbilirubinemia
65
what might cause obstructive jaundice?
Tumours or bile stones may block the hepatic duct and CB cant get into gut
66
why is urobilinogen absent in obstructive jaundice?
because there is no conversion of CB into Urobilinogen
67
what causes newborn jaundice?
a rise in unconjugated bilirubin because of UGD deficiency
68
where does gene expression for alpha, beta, gamma , delta, epsilon happen?
chromosome #16 for alpha globins & #11 for beta globins
69
Mean Corpuscular Hemoglobin (MCH):
the normal value between 27-32 pictograms/cell.
70
Red Cell Distribution Width (RDW):
Its normal value is 10%-14.5%
71
Mean Corpuscular Hemoglobin Concentration (MCHC):
It’s normal value 32 to 36g/dL.
72
Which stain to use in Peripheral blood smear?
use Gimesa-Wright's stain
73
Normal reticulocyte count is
less than 1.5%.
74
The total quantity of iron in the body is about
4-5 grams.65 % of which is in the form of | hemoglobin. 0.4 % of which is in the form of myoglobin
75
Daily Loss of Iron
``` 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
Myelophthisic anemia:
(Myelophthisis refers to the displacement of hemopoietic bone-marrow tissue by fibrosis, tumors, or granulomas.)
77
shift the Hb-dissociation curve to the left
CO
78
Fetal blood has a higher affinity for oxygen than does adult | blood
because Hb F has a decreased affinity for 2,3-BPG.
79
carbon dioxide that must be carried to lungs by three ways
Blood plasma Binding to hemoglobin Bicarbonate ion (the best one)
80
why fetal hemoglobin doesn’t have 2,3-BPG?
2,3-BPG binds with positively charged amino acids on beta chains .fortunately, fetal hemoglobin has no beta chains(alpha and gamma only)
81
white blood cells enter the tissue spaces by
diapedesis
82
chemical factors which cause the activation of chemotaxis, these factors are:
bacterial or viral toxins products of the inflamed tissues products of the complement complex products caused by plasma clotting in the inflamed area
83
Reticuloendothelial system.
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
Variables that increase sickling:
low pO2, high pCO2,low pH, dehydration, and an increased [2,3-BPG] in RBC.
85
β-Thalassemia CAUSES:
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
a normal adult hemoglobin is approximately
97.5% HbA1, 2% HbA2 0.5% HbF
87
Elemental iron is
amount of iron in the supplement available for absorption.
88
Parenteral iron formulations may be used in those who
cannot tolerate or inadequately absorb oral iron, as well as those receiving erythropoietin with hemodialysis or chemotherapy.
89
Fatal hypersensitivity and anaphylactoid reactions can occur in
parenteral iron (mainly iron dextran formulations).
90
Iron is stored in
intestinal mucosal cells, liver, spleen, and bone marrow as ferritin
91
The amount of iron absorbed depends on
current body stores of iron. If iron stores are | adequate, less iron is absorbed. If stores are low, more iron is absorbed.
92
Folate deficiency may be caused by
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
Folic acid is rapidly absorbed in the
jejunum unless abnormal pathology is | present.
94
Deficiencies of vitamin B12 can result from either
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
what's the difference between epoetin alfa and darbepoetin?
Darbepoetin has a half-life about three | times that of epoetin alfa due to the addition of two carbohydrate chains.
96
Agents Used to Treat Neutropenia
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
The main difference between the available agents for neutropenia
is in the frequency of dosing.
98
Pegfilgrastim is a pegylated form of G-CSF,
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
Filgrastim, tbo-filgrastim, and sargramostim are
dosed once a day beginning 24 to 72 hours after chemotherapy, until the absolute neutrophil count (ANC) reaches 5000 to 10,000/μL.
100
hydroxyurea treats only
15% of cases
101
Recently approved drugs for Sickle cell disease
L-glutamine oral powder (Endari) Crizanlizumab (Adakveo) Voxelotor (Oxbryta)
102
Main drug for sickle cell anemia:
Hydroxyurea
103
Hemostasis is achieved by several mechanisms:
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
Causes of smooth muscle contraction
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
Physical and chemical characteristics of | platelets:
``` 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
The platelet has a half-life of
8-12 days
107
The blood clot begins to develop in
15 to 20 seconds if the trauma is severe, and in 1 to 2 minutes if the trauma is minor.
108
if the opening is not too large, | the entire opening is filled with clot Within
3 to 6 minutes after rupture of a | blood vessel,
109
the clot retracts after:
After 20 min to an hour,
110
-Once a blood clot has formed, it can follow | one of two courses:
It can become invaded by fibroblasts, Or, it can dissolve.
111
complete organization of | the clot into fibrous tissue happen within
about 1 to 2 | weeks
112
Clotting takes place in three essential | steps:
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
Conversion of prothrombin to thrombin;
``` 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
Bleeding time ; | - Normal time is about
1-6 minutes depends | on the depth of the wound
115
Clotting time: | - The normal clotting time
about 6-10 | minutes
116
Prothrombin time: 17 - Gives an indication of the
``` concentration of prothrombin in the blood - The time required for coagulation to take place - Normal time is about 12 seconds ```
117
microcytic anaemias
Iron deficiency anaemia of chronic disease sideroblastic anaemia thalassemia
118
Agglutinins in the plasma originates from
Gamma Globulins
119
frequencies of the different blood types:
Type O = 47% • Type A = 41% • Type B = 9% • Type AB = 3%