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A&PII > Blood Ch. 18 > Flashcards

Blood Ch. 18 Flashcards

1
Q

Generalized function of blood (1)

A

Transportation: blood flows to transport cells, molecules, & ions throughout the body

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2
Q

Generalized function of blood (2)

A

Regulation: body temperature (by generating friction), body pH (contains bicarbonate ions, in the plasma), fluid balance

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3
Q

Generalized function of blood (3)

A

Protection: Immunity, clotting

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4
Q

Characteristics of whole blood

A

Volume: between 4-6L

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5
Q

Characteristics of whole blood

A

Viscosity: 5X thicker than water. % of RBCs is the reason its higher, higher hematocrit.

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6
Q

Characteristics of whole blood

A

Temperature: 2 degrees warmer than body temp.

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7
Q

Characteristics of whole blood

A

Blood pH: 7.35-7.45; we need buffers to help regulate

anything lower than 7.35= acidosis
anything higher than 7.45= alkalosis

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8
Q

Components of whole blood

A

Plasma (55% of whole blood, liquid component of blood)

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9
Q

Components of whole blood

A

inorganic substances
a. electrolytes- Na+, K+, Ca+2
b. respiratory gases- O2, CO2
c. nitrogenous wastes- urea and uric acid

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10
Q

Components of whole blood

A

Organic substances
a. nutrients- like glucose (monosaccharides), amino acids, and lipids

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11
Q

Components of whole blood

A

Organic substances
b. plasma proteins-
i. albumins (most abundant) solutes, exerts osmotic pressure to keep fluids in, transports ions, hormones, some lipids

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12
Q

Components of whole blood

A

Organic substances
b. plasma proteins
ii. globulins
1. Alpha- and beta- globulins: transport ions, metals, hormones, some lipids.
2. Gamma-globulins: immunoglobulins- antibodies for defense to protect against pathogens

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13
Q

Components of whole blood

A

Organic substances
b. plasma proteins
iii. Fibrinogen: fiber fibers *clotting protein

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14
Q

Components of whole blood

A

Organic substances
c. regulatory proteins
i. Hormones- chemical messengers produced by glands
ii. enzymes- biological catalyst

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15
Q

Erythrocytes (RBCs, 44% of whole blood)

A

Are transport cells.
i. structure: small, flexible, anucleated discs full of hemoglobin

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16
Q

Erythrocytes (RBCs, 44% of whole blood)

A

ii. function of hemoglobin: respiratory gas transport. in order to be produced we need protein, iron and vitamin B12 in our diet.

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17
Q

Erythrocytes (RBCs, 44% of whole blood)

A

Hemoglobin:

heme: the iron containing red pigment.
oxygen binds to iron

globin: is composed of amino acids.
carbon dioxide binds globin

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18
Q

5 types of Leukocytes (WBCs, <1% of whole blood)

A

3 granulocytes: cytoplasmic granes, your “phils”

2 agranulocytes: without granes, your “cytes”

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19
Q

Neutrophils

A

multi-lobed, segmented nuclei

phagocytosis, they engulf things that don’t belong.

*Most abundant WBC

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20
Q

Eosinophils

A

red-pink granules, bi-lobed nucleus

phagocytic to small allergens, kills parasites

*Rare WBC
*Inflammatory reaction

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21
Q

Basophils

A

deep-blue-violet granules, lobed nucleus

release heparin and histamine

heparin= natural blood thinner
histamine= inflammatory chemicals

*Rare WBC
*Inflammatory reactions

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22
Q

Monocytes

A

larges WBC, dark staining, “U”/kidney shaped nuclei

develop into macrophages, phagocytose foreign bodies and particles

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23
Q

Lymphocytes

A

smallest WBC, round nucleus, thin, lighter staining rim of cytoplasm

activate immune response, attack pathogens, secrete antibodies

*Do not phagocyte

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24
Q

Thrombocytes (platelets, <1% of whole blood)

A

small fragments of megakaryocytes, which is the precursor cell

functions are to form platelet plugs to stop bleeding to prevent hemorrhage

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25
Q

Erythrocyte disorders

A

anemias: lower O2 carrying capacity

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26
Q

Erythrocyte disorders

A

anemias due to low hematocrit (%RBCs)

a. hemorrhagic anemia
b. hemolytic anemia: immune attack on RBC
c. aplastic anemia: exposure to harsh chemicals like chemo and radiation, results from defective red bone marrow which causes decrease in the formation of RBCs and hemoglobin

27
Q

Erythrocyte disorders

A

anemias due to low Hemoglobin

a. iron deficiency anemia (IDA): low iron intake, fix with diet
b. pernicious anemia: not able to absorb enough vitamin B12 which is needed to build up hemoglobin proteins. your guts cannot absorb but now can be fixed with B12 shots. (used to be deadly)

28
Q

Erythrocyte disorders

A

anemias due to genetic mutations

a. Thalassemia: fragile hemoglobin. this anemia affects the production of hemoglobin resulting in abnormal erythrocyte development.
b. sickle-cell disease: an autosomal recessive anemia that occurs when a person inherits 2 copies of the sickle cell gene. effects the shape and have lower O2 concentrations.

29
Q

Erythrocyte disorders

A

polycythemia: abnormal excess RBCs, viscosity is higher causing thickness, sludgy blood, can obstruct and cause organ damage and issues.

30
Q

Leukocyte disorders

A

leukocytosis:

  1. -philia: a lot of it or elevated
  2. -penia: low levels, too little
31
Q

Leukocyte disorders

A

leukemia: cancer, malignancy in the leukocyte forming cells. abnormal development and proliferation of leukocytes

*You will find stem cells in blood smear which they should have stayed int he bone marrow

32
Q

thrombocyte disorders

A

bleeding disorders: hypo coagulation (excessive bleeding)

  1. hemophilia: genetic condition, missing 1 or more clotting factors causing excessive bleeding, unable to clot (these pts rely on platelet donations)
  2. thrombocytopenia: low platelet count. person will continue to bleed if injured.
33
Q

thrombocyte disorders

A

clotting disorders: hypercoagulation- forming too many clots causing obstructions

  1. embolism: a dislodged clot (thrombus) can be a result to trauma or child birth
  2. Leiden mutation: hypercoagulation disorder. genetic caused. inability to inactive a clotting factor, loss of control of “on and off” switch. were supposed to have a feedback mechanism, when we clot out blood. these people continue to clot.
34
Q

Hematopoiesis

A

production of formed elements from the hemocytoblast (stem cell)

i. erythropoiesis
ii. leukopoiesis
iii. thrombopoiesis

35
Q

Erythropoiesis and the life cycle of the RBC

STEP 1

A

step 1: stimulus/ trigger- what makes you create more blood
possible causes: hypoxia which means low blood O2 by higher elevation, respiratory condition, anemia, blood loss

36
Q

Erythropoiesis and the life cycle of the RBC

STEP 2

A

step 2: (receptor) your kidneys detect the hypoxia

37
Q

Erythropoiesis and the life cycle of the RBC

STEP 3

A

step 3: (control center) kidneys secrete the hormone EPO

38
Q

Erythropoiesis and the life cycle of the RBC

STEP 4

A

step 4: (effector) EPO then stimulates the bone marrow to perform erythropoiesis. this is is in the red bone marrow.

39
Q

Erythropoiesis and the life cycle of the RBC

STEP 5

RESULT

A

step 5: (net effect) RESULT
new erythrocytes were created and then released into the bloodstream which are rich in O2 thus increasing O2 levels.

40
Q

Erythropoiesis and the life cycle of the RBC

STEP 6

A

step 6: kidneys then detect the increased O2 levels that will inhibit EPO release.

41
Q

Erythropoiesis and the life cycle of the RBC

STEP 7

A

step 7: after about 120 days, macrophages in the liver and spleen phagocytose dead and damaged RBCs.

42
Q

Erythropoiesis and the life cycle of the RBC

STEP 7

  1. step 7a
A

step 7a: what happens to the globin?
it’s an amino acid o they are useful and recycled. the globin portion is returned to the bloodstream.

43
Q

Erythropoiesis and the life cycle of the RBC

STEP 7

  1. step 7b
A

step 7b: what happens to the iron from heme?
iron is stored in ferritin and hemosiderin and carefully transported by the protein transferrin.

44
Q

Erythropoiesis and the life cycle of the RBC

STEP 7

  1. step 7c
A

step 7c: what happens to the heme pigment?
heme is a pigment, so we get rid of it by breaking down the green pigment biliverdin, then the yellow pigment bilirubin is converted into urobilin which is peed out and stercobilin which is pooped out

45
Q

hemostasis

A

the stoppage of bleeding

46
Q

how we get to hemostasis

step 1

A

step 1: vascular spasm- vasoconstriction to limit blood loss. this happens immediately after blood vessel damage and bleeding.

47
Q

how we get to hemostasis

step 2

A

step 2: platelet plug formation-
positive-feedback mechanism that recruits platelets to site of injury. chemical events happen, this won’t stop until the formation of a platelet plug.

48
Q

how we get to hemostasis

step 3

A

step 3: coagulation-
this is when the actual clotting happens. the enzyme thrombin converts dissolved plasma protein FibroGen into insoluble fibrin threads to create fibrin mesh

49
Q

how we get to hemostasis

step 4

A

step 4: blood vessel repair-
injured epithelia (regenerates fast) and smooth muscle tissue undergo mitosis. the clot eventually retracts, and the enzyme plasmin dissolves the clot via fibrinolysis (desolation process to break down gradually)

50
Q

throbin

A

an enzyme

51
Q

fibrinogen

A

a salt in your plasma

52
Q

fibrin

A

insoluble and it’s in a form of threads which is to act as a mesh.

53
Q

blood typing

A

antibodies-RBC antigens-agglutination

54
Q

antibodies

A

are small plasma proteins (immunoglobulins) that recognize antigens

55
Q

RBC antigens

A

proteins on RBC cell surfaces that can be recognized by antibodies

56
Q

agglutination

A

clumping of erythrocytes as a result of antibodies recognizing RBC antigens

57
Q

AB+

A

universal acceptor

58
Q

O-

A

universal donor

59
Q

AB-

A
  • only receives -
60
Q

O+

A

only gets O+

61
Q

Rh incompatibility

A

erythroblastosis fetalis, a hemolytic disease of the newborn- moms antibodies cross over the placenta and attacks the baby’s blood cells causing the baby’s blood to lyse or burst.

62
Q

Rh incompatibility

first pregnancy:

A

mothers’ immune system is naive to Rh antigen

1st pregnancy usually successful why? because surface antigen D (Rh) is introduced to mothers’ blood

problem: exposes the Rh antigen stimulates immune response

mother creates anti- Rh antibodies

63
Q

Rh incompatibility

subsequent pregnancies:

A
  1. mother has already been exposed to Rh antigen
  2. mothers’ anti-Rh antibodies can cross placenta and attach Rh+ fetus’s blood
  3. hemolysis occurs and can kill the fetus
  4. solution: RhoGAM shots to suppress mothers’ immune system

A&PII (4 decks)

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