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A&P 2 > Hematology > Flashcards

Hematology Flashcards

1
Q

3 parts of blood

A

Plasma: 55%, least dense
Buffy coat: <1% leukocytes& platelets
Erythrocytes: 45%, most dense

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2
Q

3 functions of blood + sub functions

A

Transport: O2, CO2, wastes, hormones
Regulation: body temp, pH, blood volume
Protection: Clotting, immune system

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3
Q

Characteristics of blood

A

Temp: 38 degrees C
pH: 7.35-7.45
Volume: 5-6 l (8% of body weight in kg)

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4
Q

Components of plasma

A 
90% water
ions (electrolytes)
organic molecules
trace elements & vitamins
gases (O2, CO2 not in RBC)
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5
Q

Organic molecules in plasma

A 
amino acids
proteins: albumin, globulin, fibirinogen
glucose
lipids
nitrogenous waste (uric acid, urea)
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6
Q

most common protein & where it’s made

A

albumin, liver

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7
Q

formed elements

A

erythrocytes, leukocytes, platelets

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8
Q

how many RBCs male/female

A

4.5 million/microliter (F), 5.5 mill (M)

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9
Q

What is Hematocrit & ranges for M/F

A

amount of RBCs per test tube volume. 42% (F), 47-48% (M)

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10
Q

shape & size of RBCs

A

biconcave, round, like donut w/o hole all the way through. 7.5 micrometer

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11
Q

hemoglobin, location and structure

A

RBCs are big bags full of haemoglobin molecules. haemoglobin binds O2 and is made up of 4 protein chains (globins, one alpha, one beta) and one heme which binds to iron with 2+ charge

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12
Q

what does oximeter measure

A

amount of O2 bound to haemoglobin

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13
Q

oxy vs deoxy hemoglobin

A

haemoglobin bound to 4 o2 is oxyhemoglobin. less than 4 is deoxyhemoglobin

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14
Q

how many haemoglobin fits into 1 micrometer

A

250 million

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15
Q

hematopoiesis

A

production of blood

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16
Q

production of RBCs is called

A

erythropoiesis

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17
Q

where do all formed blood elements derive from

A

hematopoietic stem cell/hemocytoblast

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18
Q

pathway of development for erythrocyte

A

stem cell
committed cell: proerythroblast
reticulocyte (baby RBC)
process involves committing to becoming RBC, filling up with haemoglobin, and kicking out organelles and nucleus.

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19
Q

hormone that regulates RBC production, where does it come from and what stimulates it’s activity

A

erythropoietin, kidneys, testosterone

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20
Q

dietary influences on RBC production

A

iron, B12 & folic acid, intrinsic factors

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21
Q

Iron storage and transport

A

iron is toxic in its free form. it has to be stored and transported within a storage/transport protein. Iron is mainly stored in the liver

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22
Q

iron storage proteins

A

ferritin and hemosiderin

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23
Q

iron transport protein

A

transferrin

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24
Q

B12 and folic acid role in RBC production

A

important for appropriate DNA replication

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25
Q

intrinsic factor role and what happens without it

A

lives in lining of stomach and allows absorption of B12 in GI tract. lack of intrinsic factor can lead to pernicious anaemia

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26
Q

how long do RBCs live

A

120 days

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27
Q

spleen role in destruction of RBCs

A

“cemetery” of RBCs, old ones get stuck in the narrow capillaries of the spleen where they are broken down by macrophages

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28
Q

what is recycled when RBCs are destroyed

A

iron and storage proteins, globins (proteins) are broken into amino acids and reused

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29
Q

bilirubin

A

pigment that comes from the breakdown of heme. called chief bile pigment, it makes bile green. it’s secreted into the intestine where it becomes stercobilin, which makes feces brown. liver failure pts sometimes have green or gray feces.

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30
Q

polycythemia

A

too many RBCs

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31
Q

anemia

A

too few RBCs/some component is missing

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32
Q

hemorrhagic anemia

A

loss of blood from bleeding

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33
Q

hemolytic anemia

A

something is destroying RBCs

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34
Q

aplastic anemia

A

destroys red marrow

35
Q

nutritional anemia

A

not eating well

36
Q

thalasemia

A

missing a globin–genetic. common in ashkenazi jews

37
Q

sickle cell anemia

A

a substituted amino acid changes the shape of haemoglobin causing RBCs to get stuck in capillaries

38
Q

number of WBCs in blood

A

much fewer than RBCs

4,800-10,800mm3

39
Q

primary function on WBCs

A

fight infections

40
Q

differences of WBC from RBC

A

i. Number of cells present in blood
ii. Diapedesis: WBC has the ability to exit out of the blood vessels to get to the tissue
iii. Ameboid action: WBCs ability to move and go where they need to go

41
Q

5 types of WBCs

A

granulocytes: neutrophils, eosinophils, basophils,
agranulocytes: lymphocytes, monocytes

(never eat bananas, let monkeys)

in order of abundance: never let monkeys eat bananas

42
Q

granulocytes vs agranulocytes

A

d. Granulocytes: contain lots of little “rocks”, which contain chemicals

43
Q

neutrophils: primary function, nucleus shape

A

can undergo phagocytosis. Primarily seen in presence of bacterial infection
Multilobed/segmented nucleus. Polymorpho nuclear cells (PMNs). If neutrophil has banded nucleus instead of segmented, it’s an immature neutrophil. This is referred to as “left shift”.

44
Q

eosinophils: function, nucleus shape

A

known to fight worms and allergic reactions and weird diseases. Bilobal nucleus

45
Q

basophils: function, nucleus shape

A

work the same way as mast cells. Filled with histamine which trigger an inflammatory reaction. Nucleus shaped like a swan or S.

46
Q

lymphocytes function & where they hang out, structure, 2 types

A
  1. Hang out in lymphatic tissue (spleen, nodes)
  2. Tiny cell, mostly made up of its nucleus
  3. 2 types: B lymphocytes and T lymphocytes
47
Q

monocytes function, nucleus shape, size

A
  1. Largest of all WBC
  2. U-shaped nucleus
  3. Macrophage (eat a lot)
  4. Viruses, Tb, parasites
48
Q

production of WBCs is called

A

leukopoiesis

49
Q

chemical that drives leukopoiesis

A

interlukins

50
Q

Colony stimulating factors

A

Each type of WBC has a stimulating factor, so that production can be tailored to what infections are present.

51
Q

leukocytosis

A

too many WBCs

52
Q

leukopenia

A

too few WBCs

53
Q

platelets aka

A

thrombocytes

54
Q

what are platelets

A

Fragments of cells filled with chemicals that help stop bleeding through clotting

55
Q

where do platelets derive from

A

Comes from a type of cell called megakaryocytes, which comes from hematopoietic stem cells just like RBCs and WBCs

56
Q

how many platelets in microliter of blood

A

150,000-300,000

57
Q

thrombocytopenia

A

too few platelets

58
Q

thrombocytosis

A

too many platelets

59
Q

meaning of hemostasis and 3 steps

A

stop bleeding.

vascular spasm, platelet plug formation, coagulation

60
Q

vascular spasm

A

decrease in the diameter of the blood vessel (vasoconstriction) so that less blood can leak out.

a. Usually seen in smaller blood vessels b/c larger vessels cannot decrease in size due to importance of circulation
b. Spasm response increased with increased damage

61
Q

activation of platelets

A

activated by chemicals or interaction with other platelets. Inactive platelets are smooth, when activated they get spiky and release their contents

62
Q

chemicals released from platelets and what they do

A

i. Seratonin: increases vascular spasm
ii. ADP: causes aggregation (platelets coming together)
iii. Thromboxane A2: increases both of above

63
Q

Von Willebrand factor

A

protein in the plasma. When platelets become activated this protein helps them stick together.

64
Q

prostaglandin

A

released by endothelial cells lining the blood vessels. Inhibitory for the formation of platelets

65
Q

how many clotting factors (coagulants are there)

A

13, Designated by roman numerals. In the order they were discovered, not sequence they’re used

66
Q

intrinsic pathway

A

activated by trauma inside the blood vessel. slow process because many steps

67
Q

extrinsic pathway

A

requires tissue trauma to occur. fast process because it has fewer steps

68
Q

common pathway

A

intrinsic and extrinsic pathways leads to common pathway. Common pathway begins with factor 10. Factor 10 activates prothrombin activator, this takes prothrombin to thrombin. Thrombin makes fibrinogen which makes fibrin. Fibrin is the clot, which is tied together by factor 13.

69
Q

fibrinolysis & plasminogen

A

a. Fibrinolysis: the process of breaking down fibrin (the clot) as a part of healing
i. Plasminogen is wrapped up inside the clot and is an inactive bomb. Endothelial cells in vessels release tissue plasminogen activator (TPA) which activates plasmin, breaking down the fibrin mesh of the clot

70
Q

intrinsic ways to inhibit clot formation

A

large vessels inhibit clots due to velocity

Antithrombin III: protein that inactivates thrombin so clotting rcess can’t be initiated.

71
Q

medications that inhibit clot formation and examples

A

fibrinolytics
heparin: increases activity of antithrombin III
aspirin
coumadin

72
Q

thromboembolytic

A

too many clots

73
Q

Disseminated intravascular coagulopathy

A

Causes clotting that uses up too many clotting factors which causes bleeding.

74
Q

thrombocytopenia

A

too few platelets, can be caused by impaired liver function and not enough vitamin K

75
Q

hemophilia + 3 types

A

missing particular clotting factors

  1. A—classic—missing factor VIII
  2. B—factor IX
  3. C—Factor XI—not genetic
76
Q

blood classifications

A
  1. A 42%
  2. B 10%
  3. AB 3%
  4. O 45%
77
Q

antigens

A

substance that causes generation of antibodies

78
Q

antibodies

A

attack and neutralize antigens and are specific to an antigen

79
Q

universal recipient

A

type AB

80
Q

universal donor

A

type O

81
Q

Rh factor

A
  1. D antigen (+), 85% of population

2. Without antigen you are Rh -

82
Q
  1. Erythroblastosis fetalis / hemolytic disease of the newborn
A

a. If someone who is Rh negative gets pregnant with an Rh+ baby, they start developing Rh antibodies
b. If they get pregnant a second time with an Rh+ baby, these antibodies start attacking the antigens on the RBCs of the baby
c. Drug called Rhogam which prevents the formation of Rh antibodies.
d. If pregnant person has received a blood transfusion with Rh antibodies in the past it may also affect the first baby.
e. This is the reason O- is most often given in transfusions

83
Q

4 types of leukaemia

A

Acute/chronic myelocytic

Acute/chronic lymphocytic

84
Q

Developmental paths of different types of leukemia

A

Chronic comes from fully developed leukocytes; myelocytic from granular and lymphocytic from agranular

Acute comes from promyelocyte or lymphocyte precursor cells (earlier in developmental pathway)

A&P 2 (8 decks)

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