Physiology Exam 1: Blood

Front 1

What are the three most important functions of blood?

Back 1

Transport
Regulation
Protection

Front 2

List some things that blood transports?

Back 2

O2 and CO2 in RBC Hb
Nutrients
Hormones
Metabolic waste

Front 3

List some things that blood regulates?

Back 3

Body Temperature
pH
Fluid Volumes

Front 4

How does blood protect the body?

Back 4

Prevents blood loss via Coagulation
Prevents infections via WBCs and Antibodies

Front 5

What percent of Plasma is:
H2O
Protein

Back 5

H20 = 90% of plasma
Protein = 8% of plasma

Front 6

Of the Protein found in Plasma, what is the percent composition of:
Albumin
Globulins
Clotting Proteins

Back 6

Albumin = 60%
Globulins = 36%
Clotting Proteins = the rest?

Front 7

What is the remaining 2% of Plasma composition made up of?

Back 7

Nutrients
Gases (CO2, O2, N2)
Electrolytes (Na+, Cl-, K+, HCO3-)

Front 8

What are the 3 formed elements found in the blood?

Back 8

Erythrocytes (RBCs)
Leukocytes (WBCs)
Thrombocytes (Platelets)

Front 9

What is the difference in the binding of Oxygen vs. CO2 in hemoglobin?

Back 9

Oxygen is bound to the Heme
CO2 is bound to the Globin

Front 10

What % of CO2 is bound to Hb?

Back 10

20%

Front 11

Give the normal values of Hb for adults: Male and Female

Back 11

Male: 13-18 g/dL
Female: 12-16 g/dL

Front 12

What is the precursor for Hemoglobin and where are they found?

Back 12

Hemocytoblasts found in the Red Bone Marrow

Front 13

What is Polycythemia?
What are the two types?

Back 13

An increase in the number of RBCs.
Primary (vera)
Secondary (hypoxia of different origin)

Front 14

What is Anemia?
What are the three major subsets of Anemia?

Back 14

A decrease in the number of RBCs.

1. Insufficient # of RBCs
2. Insufficient # of Hemoglobin
3. Abnormal Hemoglobin

Front 15

If Anemia is caused by insufficient # of RBCs, what are the three types of Anemia?

Back 15

Hemorrhagic Anemia
Aplastic Anemia
Hemolytic Anemia

Front 16

If Anemia is caused by insufficient # of Hemoglobin, what are the three types of Anemia?

Back 16

Pernicious (B12 def.) Anemia
Fe2+ Deficiency Anemia
Folic Acid Deficiency Anemia

Front 17

If Anemia is caused by abnormal Hemoglobin, what are the two types of Anemia?

Back 17

Thalassemia's Anemia
Sickle-Cell Anemia

Front 18

How does high altitude relate to Secondary Polycythemia?

Back 18

Low oxygen levels makes the body increase the number of receptors/RBCs, and this is Secondary Polycythemia

Front 19

Which Granulocytes are phagocytic?

Back 19

All of them.
Neutrophils, Basophils, Eosinophils

Front 20

How are Monocytes found in tissues?

Back 20

As Macrophages

Front 21

Of all the Granulocytes and Agranulocytes, which ones have the highest percent composition of total Leukocytes?

Back 21

Granulocytes: Neutrophils (40-70%)
Agranulocytes: Lymphocytes (20-45%)

Front 22

What are the three types of agranulocytes?

Back 22

B + T Lymphocytes
Monocytes (macrophages in tissue)
Phagocytes

Front 23

Are Phagocytes found as granulocytes or agranulocytes?

Back 23

BOTH!
All Granulocytes are Phagocytes, but not all agranulocytes are phagocytes (just the monophages)

Front 24

What is the condition for a reduced number of Leukocytes?

Back 24

Leukopenia

Front 25

What is the nature of Leukopenia, and what can it do to bone marrow?

Back 25

It is generally of toxic nature (never beneficial) frequently seen in VIRAL infections.

Bone Marrow APLASIA

Front 26

What are the measurements of #WBC/mm3 in Leukopenia for: 1. Risk of Infection and 2. Risk for LIFE THREATENING infection?

Back 26

Less than 1000/mm3 = Risk of infection
Less than 500/mm3 = Risk for life-threatening infection

Front 27

What 4 factors can cause Leukopenia?

Back 27

Radiation
SLE (collagen autoimmune disease)
Anaphylactic Shock
Some Chemotherapeutical agents

Front 28

If Leukopenia is a disease to describe a reduced number of Leukocytes (WBCs), what is a disease that describes an abnormally high number of Leukocytes (WBCs)?

Back 28

Leukocytosis

Front 29

How are the two types of Leukocytosis divided?

Back 29

Physiological
Pathological (called Leukemia)

Front 30

What are the causes for physiological Leukocytosis?

Back 30

Pathological Leukocytosis are a response to:
Infection
Strenuous Exercise
Emotional Stress
Temperature changes
Drugs
Anesthesia
Surgery
Pregnancy
Toxins
Hormones

Front 31

Leukemia is the term for what main condition?
What are the major 4 Subsets?

Back 31

Pathological Leukocytosis.
Subsets: Acute or Chronic, Myelocytic or Lymphocytic

How to match them (from wiki, for my own pleasure):
Acute lymphocytic leukemia (ALL)
Acute myeloid leukemia (AML)
Chronic lymphocytic leukemia (CLL)
Chronic myeloid leukemia (CML)

Front 32

For Pathological Leukocytosis, what are the two possible reasons?

Back 32

Malignancies
Hematological Disorders

Front 33

Thrombocytes (platelets) are not real cells, rather they are described as?

Back 33

Fragments of very large Megakaryocytes

Front 34

What are Thrombocytes essential for, and how is this done?

Back 34

Thrombocytes are essential for HEMOSTASIS by forming the temporary platelet PLUG which helps to seal the break, thus participating in the COAGULATION process.

Front 35

What is the term for a Platelet count lower than 100,000/mm3 of blood?

Back 35

Thrombocytopenia

Front 36

What happens in Thrombocytopenia when you have values lower than: 50,000/mm3, 10,000-15,000/mm3, 10,000/mm3?

Back 36

Less than 50,000/mm3 = Increased risk for hemorrhage with a minor trauma.
Between 10,000-15,000/mm3 = Spontaneous bleeding occurs.
Less than 10,000/mm3 = Severe bleeding (fatal if occurring in CNS, Respiratory System, or GI tract)

Front 37

When can it be fatal to have Thrombocytopenia?

Back 37

When platelet count is less than 10,000/mm3, severe bleeding occurs, and this is fatal when it occurs in the:
GI tract
Respiratory system
CNS

Front 38

What is the term for the fraction of blood composed of RBCs?

Back 38

Hematocrit

Front 39

How do you determine the Hematocrit level of someone's blood?
Why is this not entirely possible?

Back 39

Centrifugation of blood in a "hematocrit tube" until the cells become tightly packed in the bottom of the tube.

It cannot be done entirely because:
3-4% of plasma remains trapped among cells, so Hematocrit is +/-96% of what is actually measured.

Front 40

What is the normal Hematocrit volume fraction (Hematocrit:Blood) for Males and Females?

Back 40

Males = 0.4 (fraction, so = 40% of blood is RBC)
Females = 0.36

Front 41

What is the average blood volume of an adult in percent of total body weight and volume?

Back 41

+/- 8% of total body weight
5L of volume

Front 42

What antigens and antibodies are found on the surface of: Type A, Type B, Type AB, Type O

Back 42

Type A = (A) Antigens, (B) Antibodies
Type B = (B) Antigens, (A) Antibodies
Type AB = (A)+(B) Antigens, Neither (A) nor (B) Antibodies
Type O = No (A),(B),(O) Antigens, Both (A)+(B) Antibodies

Front 43

What types of blood can these blood types receive: Type A, Type B, Type AB, Type O

Back 43

Type A = A, O
Type B = B, O
Type AB = A, B, AB, O (Universal Recipient - no antibodies)
Type O = O (Universal Donor)

Front 44

If you have a (+) Rhesus Factor, will you have Rhesus Antibodies? Can you receive (+) or (-) Rh blood? When does a problem arise when finding a mate? What medication can we administer?

Back 44

(+) Rh = No Rhesus Antibodies
(+) Rh individuals can receive (+) and (-) Rh blood

If the mother is (-) and the father is (+), it is a big problem.
If mother is (-) and baby is (+), the baby will need a whole blood transfusion (Erythroblastosis Fatalis).
Must give expectant (-)Rh mothers Rhogam (immunosuppressant)

Front 45

Native Americans in the US are overwhelmingly which blood type?

Back 45

Type O

Front 46

What is the reason for needing to match blood types when blood is transfused?

Back 46

If it is non-matching, a bonding of serum antibodies to the cellular antigens triggers a Transfusion Reaction.
This causes clumping (agglutination) of the erythrocytes (due to the antibody matching up and binding) in the blood leading to massive hemolysis.

Front 47

What is the effect of agglutination in Erythrocytes during a Transfusion Reaction?

Back 47

Massive Hemolysis

Front 48

What are all the possible results in the patient having a Transfusion Reaction?

Back 48

Icterus
Thromboembolism
Hypoxemia
Increased inflammatory response
Intravascular coagulation

Front 49

What are the treatments for a patient undergoing a Transfusion Reaction?

Back 49

Administration of Steroids (reduce inflammation)
Heparin (anticoagulant)
Diuretics
Administration of O2 to support ventilation function

Front 50

What are the 4 major events in Hemostasis?

Back 50

Vascular Spasm
Formation of the Platelet Plug
Blood Coagulation (first step of hemostasis)
Growth of fibrous tissue into the blood clot

Front 51

During a Vascular Spasm, when a blood vessel is smashed or damaged, this triggers constriction of the vessel's wall due to three factors:

Back 51

Constriction occurs because of:
1. Nervous reflexes
2. Local Humoral Factors
3. Local Myogenic Spasm (drastic reduction of blood loss)

Front 52

The formation of the Platelet Plug mechanism:

Back 52

When in contact with a damaged vascular surface, the Platelets:
Begin to swell
Adopt irregular shapes
Become sticky
Secrete large amounts of ADP and Thromboxane to make them stickier and stickier

Front 53

What two substances are secreted during the formation of the Platelet Plug? What is their main function in this process?

Back 53

ADP and Thromboxane.
Make the Platelets stickier.

Front 54

During Blood Coagulation, how soon after the trauma does the clot begin to form?

Back 54

Almost immediately, 15 seconds -> 2 minutes

Front 55

What initiates the clot formation during blood coagulation?

Back 55

Activator Substance from the vascularized traumatized vessel wall initiates clot formation.
Platelets and Blood Protein adhere to it.

Front 56

How soon after the trauma to the vessel is the entire opening filled with a clot?

Back 56

3-6 minutes

Front 57

How long does it take for the clot to retract, closing the vessel further?

Back 57

20 minutes -> 1 hour

Front 58

What is the limiting factor in causing blood coagulation?

Back 58

The formation of the Pro-thrombin Activator.
(Because from this point on, events occur very quickly)

Front 59

Where is Pro-thrombin synthesized, and what is required for it's synthesis?

Back 59

Pro-thrombin is a plasma protein, continually synthesized by the Liver.
Vitamin K is required for it's synthesis.

Front 60

Where is Fibrinogen synthesized?

Back 60

Fibrinogen is a plasma protein synthesized by the Liver
(same as Pro-thrombin)

Front 61

What is the organ most responsible for the production of plasma protein clotting factors?

Back 61

The Liver

Front 62

Fibrinogen and Prothrombin both ultimately get converted to what?

Back 62

Fibrin

Front 63

Name the Blood Coagulation Factor:
A Plasma Protein, synthesized by the liver.

Common pathway = converted to fibrin, weblike substance of a clot.

Back 63

(I) Fibrinogen

Front 64

Name the Blood Coagulation Factor:
A Plasma Protein, synthesized by the liver, formation requires Vitamin K.

Common pathway = converted to thrombin, enzymatically converting to fibrinogen then to fibrin.

Back 64

(II) Prothrombin

Front 65

Name the Blood Coagulation Factor:
Lipoprotein complex, released from damaged tissues.

Activates Extrinsic Pathway.

Back 65

(III) Tissue Factor (TF) or tissue thromboplastin

Front 66

Name the Blood Coagulation Factor:
Inorganic ion present in the plasma, acquired from diet or released from bone.

Needed for essentially all stages of the coagulation process.

Back 66

(IV) Calcium Ions

Front 67

Name the Blood Coagulation Factor:
A Plasma Protein, synthesized by the liver, also released by platelets.

Both Extrinsic and Intrinsic Mechanisms.

Back 67

(V) Proaccelerin, Labile Factor, or Platelet Accelerator

Front 68

Name the Blood Coagulation Factor: Substance now believed to be the same as Factor V

Back 68

(VI)

Front 69

Name the Blood Coagulation Factor:
A Plasma Protein, synthesized in the Liver in a process that requires Vitamin K.

Both Extrinsic and Intrinsic Mechanisms.

Back 69

(VII) Serum Prothrombin Conversion Accelerator (SPCA), or Stable Factor.
(X) Stuart Factor, Stuart Prower Factor, or Thrombokinase.

Front 70

Name the Blood Coagulation Factor:
Globulin synthesized by the liver, a deficiency causes Hemophilia A.

Intrinsic Mechanism.

Back 70

(VIII) Antihemophilic Factor (AHF)

Front 71

Name the Blood Coagulation Factor:
A Plasma Protein, synthesized in the liver, deficiency results in Hemophilia C.

Intrinsic Mechanism.

Back 71

(XI) Plasma Thromboplastin Antecedent (PTA)

Front 72

Name the Blood Coagulation Factor:
A Plasma Protein, synthesized by the liver, requires Vitamin K, deficiency results in Hemophilia B.

Intrinsic Mechanism.

Back 72

(IX) Plasma Thromboplastin Component (PTC) or Christmas Factor

Front 73

Name the Blood Coagulation Factor:
A Plasma Protein, Proteolytic enzyme, synthesized in the liver.

Intrinsic Mechanism = Activates plasmin, known to be activated by contact with glass and may initiate clotting in-vitro.

Back 73

(XII) Hageman Factor, Glass Factor

Front 74

Name the Blood Coagulation Factor:
A Plasma Protein, synthesized in the liver, present in platelets.

Cross-links fibrin and renders it insoluble.

Back 74

(XIII) Fibrin Stabilizing Factor (FSF)

Front 75

What are the 3 steps of the Extrinsic Pathway?

Back 75

Following trauma to the vascular structure and/or surrounding tissues:
1. Release of Tissue Thromboplastin
2. Activation of Factor X to form Factor X
3. Effect of Activated Factor X forming the Pro-thrombin Activator

Front 76

What are the 5 steps of the Intrinsic Pathway?

Back 76

Begins with trauma to the blood itself or it's exposure to collagen in a traumatized vascular wall.
1. Activation of Factor XII and the release of platelet phospholipids.
2. Activation of Factor XI.
3. Activation of Factor IX by the Activated Factor XI.
4. Activation of Factor X.
5. Formation of Pro-thrombin Activator

Front 77

What is the difference between the triggers for the Extrinsic vs. the Intrinsic Pathways?

Back 77

Extrinsic: Begins with trauma to the vascular structure and/or surrounding tissues.

Intrinsic: Beings with trauma to the blood itself, or it's exposure to collagen in a traumatized vascular wall.

Front 78

What is a common cofactor in the intrinsic and extrinsic pathway?

Back 78

Ca2+

Front 79

When is Ca2+ not required?

Back 79

The first two steps of the Intrinsic Pathway.

Aside from that, it is required in ALL the reactions.

Front 80

What is required in the activation of Factor X?
What would make it deficit?

Back 80

Activated (IX) acting in concert with (VIII), with platelets and phospholipids and (III).

If VIII or Platelets are in short supply, this step is Deficit.

Front 81

In a person with "classic hemophilia" which factor is missing?

Back 81

Factor VIII
(Antihemophilic Factor)

Front 82

In a person with Thrombocytopenia, what factor of clotting is missing?

Back 82

Platelets

Front 83

How are Factor VIII and Platelets imperative?

Back 83

With both in short supply = Activation of Factor X is deficit.

With Factor VIII missing = "classic hemophilia"
With Platelets missing = Thrombocytopenia

Front 84

After blood vessels are damaged, how is blood clotting initiated?

Back 84

Both the Extrinsic and Intrinsic mechanisms initiate clotting SIMULTANEOUSLY.

Front 85

Explain how tissue Thromboplastin uses both pathways to form a clot?

Back 85

Tissue Thromboplastin begins with the Extrinsic pathway, while contact of Factor XII and Platelets with Collagen in the Vascular Wall initiates the Intrinsic Pathway.

Front 86

Which clotting pathway is explosive in nature?

Back 86

Extrinsic

Front 87

How soon after SEVERE tissue trauma can clotting begin?
How is this compared to the Intrinsic pathway?

Back 87

15 seconds.
The Intrinsic Pathway is slower, about 1-6 minutes to cause clotting.

Front 88

What prevents the excessive spreading of a clot throughout the blood?

Back 88

When a clot is forming, 85-90% of the Thrombin formed from the Prothrombin is absorbed into the Fibrin as the clot develops.

Front 89

What happens to the remaining Thrombin that is not absorbed by the Fibrin?

Back 89

The Thrombin that is not absorbed into the Fibrin fibers soon combines with Antithrombin (III), which BLOCKS the effect of the Thrombin on the Fibrinogen, inactivating the bound Thrombin.

Front 90

What is Plasminogen doing at the time of clot formation?
What about after a day after the bleeding stops?

Back 90

It is trapped in the clot together with some other proteins.
After a day, the vascular endothelium and injured tissues slowly release Tissue Plasminogen Activator, converting Plasminogen into Plasmin.

Front 91

What is the proteolytic enzyme present about a day after bleeding stops, that causes LYSIS of the clot, allowing slow clearing, and sometimes reopening of clotted vessels?

Back 91

Plasmin

Front 92

What are digested by Plasmin?

Back 92

Fibrin Fibers
Fibrinogen
Factors (V), (VII), (XII)
Pro-thrombin

Front 93

Minute clots from the millions of tiny peripheral vessels that eventually would become occluded from no way to clean them, are removed by what?

Back 93

Plasmin