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Anatomy II > Anatomy II - Exam I > Flashcards

Anatomy II - Exam I Flashcards

1
Q

What is blood?

A

fluid connective tissue

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2
Q

Blood Composition

A

fluid connective tissue
plasma
formed elements

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3
Q

Plasma

A

non living fluid matrix

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4
Q

Formed elements

A

living blood cells suspended in plasma

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5
Q

What are the formed elements?

A

erythrocytes
leukocytes
platelets

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6
Q

Erythrocytes

A

red blood cells

no nuclei or organelles

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7
Q

Leukocytes

A

white blood cells

complete cells

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8
Q

Platelets

A

thrombocytes

cell fragments

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9
Q

What is hematocrit?

A

percent of blood volume that is RBCs

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10
Q

Functions of blood

A

Transport= oxygen and nutrients, wastes, hormones

Regulation= temperature and pH

Protection = clot formation and immune system

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11
Q

Plasma Proteins

A

Albumins
Globulins
Fibrinogen
Transferrin

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12
Q

Source and function of Albumins

A

Liver

Colloid osmotic pressure of plasma
carriers for various substances

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13
Q

Source and function of Globulins

A

Liver and lymphoid tissue

Clotting factors, enzymes, antibodies, carriers for various substances

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14
Q

Source and function of Fribrinogen

A

Liver

Forms fibrin threads essential to blood clottting

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15
Q

Source and function of Transferrin

A

Lover and other tissues

Ion transport

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16
Q

Structure of Erythrocytes

A

Biconcave discs
lots of hemoglobin
flexible to fit through narrow capillaries

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17
Q

Function of Erythrocytes

A

respiratory gas transport

hemoglobin for gas transport

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18
Q

Hemoglobin Structure

A

Globin- 4 polypeptide chains

Heme- pigment bonded to each globin chain, central iron atom binds one O2,

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19
Q

Each Hb molecule can transport

A

four O2

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20
Q

Hb reversibly binds

A

O2 and CO2 to a lesser extent

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21
Q

Describe Hematopoietic stem cells

A

Give rise to all formed elements

Hormones and growth factors push cell toward specific pathway of blood cell development

Committed cells cannot change

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22
Q

New blood cells enter

A

blood sinusoids

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23
Q

What is Erythropoiesis
and
Describe the process

A

Red Blood Cell Production

HSC transforms into proerythroblast
Ribosomes synthesized
Hemoglobin synthesized; iron accumulates
Ejection of nucleus; formation of reticulocyte (young RBC)

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24
Q

HSC transforms into what?/

A

pro erythroblast

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25
Q

A young RBC

A

reticulocyte

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26
Q

Balance between RBC production and destruction depends on?

A
  • Hormonal controls

-Erythropoietin (EPO): Released by kidneys (some from liver) in response to hypoxia
Rapid maturation of committed marrow cells
Abused by endurance athletes; banned by WADA

-Adequate supplies of iron, amino acids, and B vitamins required

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27
Q

What are the causes of hypoxia?

A
  • Decreased RBC numbers due to hemorrhage or increased destruction
  • Insufficient hemoglobin per RBC (e.g., iron deficiency)
  • Reduced availability of O2 (e.g., high altitudes)
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28
Q

What is the life span of Erythrocytes?

A

100-120 days

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29
Q

Describe the destruction of erthrocytes?

A

Life Span
Macrophages engulf dying RBS in spleen
Heme and globin are separated

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30
Q

Described what happens when heme and globin are separated

A

Iron: - Stored in cells as ferritin and hemosiderin
Transported in blood bound to the protein transferrin

Heme: degraded to yellow pigment bilirubin
Liver secretes bilirubin (in bile) into intestines
Degraded to pigment urobilinogen
Excreted as stercobilin

Globin: metabolized into amino acids - Released into circulation

31
Q

What are the Erythrocyte Disorders?

A

Anemia

32
Q

Anemia

A

decreased RBCs or hemoglobin
Blood has abnormally low O2-carrying capacity

Blood O2 levels cannot support normal metabolism

33
Q

The three causes/types of Anemia

A

Blood loss
Low RBC production
High RBC destruction

34
Q

Blood Loss : Anemia Cause

A
  1. Hemorrhagic anemia
    Rapid blood loss (e.g., stab wound)
    Treated by blood transfusion
  2. Chronic hemorrhagic anemia
    Slight but persistent blood loss
    Hemorrhoids, bleeding ulcer
    Primary problem treated
35
Q

Low RBC Production

A
  1. Iron-deficiency anemia
    Caused by hemorrhagic anemia, low iron intake, or impaired absorption

2 .Pernicious anemia
Autoimmune disease - destroys stomach mucosa – unable to absorb Vitamin B12
Vegetarians – low B12 in diet

  1. Renal anemia
    Lack of EPO – kidney disease
  2. Aplastic anemia
    Destruction or inhibition of red marrow by drugs, chemicals, radiation, viruses
36
Q

High RBC Destruction

A
  1. Hemolytic anemias
    Premature RBC lysis due to: Hb abnormalities, incompatible transfusions or infections
  2. Thalassemias
    One globin chain absent or faulty
    Found in people of Mediterranean ancestry
  3. Sickle-cell anemia
    Genetic disease resulting in one amino acid wrong in a globin beta chain
37
Q

Describe Sickle Cell Anemia

A

Emerged in people of Sub-Saharan Africa and their descendants

  1. Malaria kills 1 million each year
  2. Sickle-cell gene
    One copy  Sickle-cell trait; milder disease; better chance to survive malaria
    Two copies  Sickle-cell anemia
    Many RBCs are crescent shaped (and spikey, as you will see in the lab), rupture easily
    Poor O2 delivery; pain
38
Q

Function of Leukocytes

A

Function in defense against disease

Can leave capillaries via diapedesis

Move through tissue spaces by ameboid motion and positive chemotaxis

39
Q

Types of Leukocytes

A

Granulocytes and Agranulocytes

40
Q

Granulocytes

A

Visible cytoplasmic granules

Neutrophils, eosinophils, basophils

41
Q

Agranulocytes

A

No visible cytoplasmic granules
Lymphocytes, monocytes
Decreasing abundance in blood
Never let monkeys eat bananas

42
Q

Types of Granulocytes

A

Neutrophils
Eosinophils
Basophils

43
Q

Neutrophils

A

Most common WBCs
contain hydrolytic enzymes or defensins
3-6 lobes in nucleus; twice size of RBCs
Phagocytize bacteria

44
Q

Eosinophils

A

Red/Orange-staining granules
Bilobed nucleus
Digest parasitic worms
Role in allergies, asthma and immune response

45
Q

Basophils

A

Rarest WBCs with large purple granules

Granules contain histamine - inflammatory chemical that acts as vasodilator

46
Q

Types of Agranulocytes

A

Lymphocytes and Monocytes

47
Q

Lymphocytes

A

2nd most common WBC
Large, dark-purple, circular nuclei with thin rim of blue cytoplasm
Mostly found in lymph nodes and spleen
Two types
T lymphocytes (T cells) act against virus-infected cells and tumor cells
B lymphocytes (B cells) give rise to plasma cells, which produce antibodies

48
Q

Monocytes

A

Largest WBC
U- or kidney-shaped nuclei
Leave circulation, enter tissues, and differentiate into macrophages
Activate lymphocytes to mount an immune response

49
Q

Leukopoiesis

A

Production of WBCs
Stimulated by 2 types of chemical messengers: Interleukins and
Colony-stimulating factors (CSFs)

50
Q

Name the Leukocyte Disorders

A

Leukopenia
Leukemia – Cancer
Infectious Mononucleosis (Mono)

51
Q

Infectious Mononucleosis (Mono)

A

Highly contagious viral disease caused by transmission of Epstein-Barr virus in saliva

52
Q

overproduction of abnormal WBCs

A

Leukemia – Cancer

53
Q

Abnormally low WBC count—drug induced

A

Leukopenia

54
Q

Thrombocytes

A

Cytoplasmic fragments of megakaryocytes
Form temporary platelet plug that helps seal breaks in blood vessels
Formation regulated by thrombopoietin
Granules contain substances like platelet-derived growth factor (PDGF)

55
Q

Hemostasis

A

Fast series of reactions for stoppage of bleeding

Requires clotting factors, and substances released by platelets and injured tissues

Three steps
Vascular spasm
Platelet plug formation
Coagulation (blood clotting)

56
Q

What are the three phases of coagulation?

A

Prothrombin activator formed in both intrinsic and extrinsic pathways

Prothrombin converted to enzyme thrombin

Thrombin catalyzes fibrinogen  fibrin

57
Q

Describe Clot Retraction

A

Stabilizes clot

Actin and myosin in platelets contract

Contraction pulls on fibrin strands, squeezing serum from clot

Draws ruptured blood vessel edges together

58
Q

Vessel Repair

A

Vessel is healing as clot retraction occurs

Platelet-derived growth factor (PDGF) stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall

Vascular endothelial growth factor (VEGF) stimulates endothelial cells to multiply and restore endothelial lining

Fibrinolysis
Removes unneeded clots after healing

59
Q

What are the disorders of Hemostasis ?

A

Thromboembolic disorders: undesirable clot formation

Bleeding disorders: abnormalities that prevent normal clot formation

Disseminated intravascular coagulation (DIC)
Involves both types of disorders

60
Q

What are the Thromboembolic Conditions?

A

Thrombus: clot that develops and persists in unbroken blood vessel
May block circulation leading to tissue death

Embolus: thrombus freely floating in bloodstream

Embolism: embolus obstructing a vessel
E.g., pulmonary and cerebral emboli
Risk factors – atherosclerosis*, inflammation, slowly flowing blood or blood stasis from immobility

61
Q

What are the Anticoagulant Drugs?

A

Aspirin
Antiprostaglandin that inhibits thromboxane A2

Heparin
Anticoagulant used clinically for pre- and postoperative cardiac care

Warfarin
Used for those prone to atrial fibrillation
Interferes with action of vitamin K

Dabigatran directly inhibits thrombin

62
Q

Hemophilia

A 
Includes several similar hereditary bleeding disorders affecting different clotting factors
Hemophilia A(most common), B and C

Symptoms include prolonged bleeding, especially into joint cavities

Treated with plasma transfusions and injection of missing factors
Increased hepatitis and HIV risk

63
Q

Disseminated Intravascular Coagulation

A

Clotting causes bleeding
Widespread clotting blocks intact blood vessels
Severe bleeding occurs because residual blood unable to clot

Occurs as pregnancy complication; in septicemia, or incompatible blood transfusions

64
Q

Transfusions

A

Whole-blood transfusions used when blood loss rapid and substantial

Packed red cells (plasma and WBCs removed) transfused to restore oxygen-carrying capacity

Transfusion of incompatible blood can be fatal

65
Q

Human Blood Groups Important Terms

A

Agglutination – clumping together of RBC

Agglutinogens – Antigens or surface markers on RBC cell membrane that are bound by antibodies

Agglutinins – Antibodies that recognize and bind the antigens and cause agglutination

66
Q

Human Blood Groups

A

RBC membranes possess surface glycoprotein antigens
Anything perceived as foreign; generates an immune response
agglutinogens

Mismatched transfused blood (e.g. type A blood given to person with type B) perceived as foreign
May be agglutinated and destroyed; can be fatal

Presence or absence of each antigen is used to classify blood cells into different groups

Antigens of ABO and Rhesus blood groups cause vigorous transfusion reactions

67
Q

Type A Group

A

has only A agglutinogens

and Anti-B agglutinins – will agglutinate B or AB blood cells

68
Q

Type B Group

A

Has only B agglutinogens

and Anti-A agglutinins – will agglutinate A or AB blood cells

69
Q

Type AB Group

A

Universal Recipient

Has A and B agglutinogens

70
Q

Type O

A

Universal Donor
Has no A or B agglutinogens – won’t be agglutinated by recipient
and A and B agglutinins
Universal Donor
Has no A or B agglutinogens – won’t be agglutinated by recipient
and A and B agglutinins

71
Q

Rh Blood Groups

A

Rh+ indicates presence of D antigen
85% Americans Rh+

Anti-Rh antibodies(agglutinins) are not spontaneously formed in Rh– individuals
Anti-Rh antibodies form if Rh– individual receives Rh+ blood, or Rh– mother carries a Rh+ fetus
Second exposure to Rh+ blood will result in typical transfusion reaction

72
Q

Homeostatic Imbalance: Hemolytic Disease of the Newborn

A

Also called erythroblastosis fetalis
Only occurs in Rh– mom with Rh+ fetus

Rh– mom exposed to Rh+ blood of fetus during delivery of first baby – baby healthy
Mother synthesizes anti-Rh antibodies

Second pregnancy
Mom’s anti-Rh antibodies cross placenta and destroy RBCs of Rh+ baby

Baby treated with prebirth transfusions and exchange transfusions after birth

RhoGAM serum containing anti-Rh can prevent Rh– mother from becoming sensitized

73
Q

Transfusion Reactions

A

Occur if mismatched blood infused

Donor’s cells
Attacked by recipient’s plasma agglutinins
Agglutinate and clog small vessels
Rupture and release hemoglobin into bloodstream

Result in
Diminished oxygen-carrying capacity
Diminished blood flow beyond blocked vessels
Hemoglobin in kidney tubules  renal failure

74
Q

Before Transfusion

A

Blood typing
Mixing RBCs with antibodies against its agglutinogen(s) causes clumping of RBCs
Done for ABO and for Rh factor

Cross matching
Mix recipient’s serum with donor RBCs
Mix recipient’s RBCs with donor serum
To see if agglutination occur in both cases

Anatomy II (7 decks)

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