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PHARM 111 Midterm > Blood > Flashcards

Blood Flashcards

(56 cards)

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1
Q

What is blood made from?
What are the percentages?
What is Hematocrit?

A

Blood
- Plasma (platelets): 55%
- Erythrocytes: 45%
- Leukocytes and platelets: <1%

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2
Q

What are the role of the proteins contained in Plasma?
Albumin
Globulin (Alpha & beta, Gamma)

What type of nutrients do plasma have?

A

Albumin
- main contributor to osmotic pressure, and water balance

Alpha & Beta Globulins
- transport; binds to lipids and metals

Gamma Globulins
- Antibodies released by plasma cells (immune response)

Nutrients (organic)
- Carbs, AA, fats

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3
Q

Which type of blood has a nucleus/complete cell?

A

WBC

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4
Q

Does gene transcription occur in RBC’s

A

no, no nucleus or organelles

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5
Q

Why are Erythrocytes biconcave discs?
What are they filled with

A

-To increase the SA for O2 + CO2 to bind
- Filled with 97% hemoglobin (where it has the most O2)

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6
Q

What is the role of Spectrin?
What does it interact with?

A

Gives RBC’s the concave shape.
Interacts with Plasma

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7
Q

How is ATP generated in RBC’s

A

Anaerobically, glycolysis
- it does not use the O2 it carries

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8
Q

What is a heme group made of?
What does it bind?

A

Iron

  • binds O2
  • Can bind CO2 after O2 is absorbed
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9
Q

What are the phases of production of erythrocytes?

A

Yolk sac phase
- Major source of RBC

Hepatic/spleen phase
- liver & spleen makes blood

Bone marrow phase
- At around 5 months

Adult phase:
- pelvis, vertebra, skull, ribs, ends of long bones

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10
Q

What are the steps in Erythropoiesis?

A
  1. Hemocytoblast
    - Stem cell (precursor)
  2. Proerythroblast
    - committed cell
  3. erythroblast
    - ribosome synthesis (protein translation)
  4. Late erythroblast-normoblast
    - Hemoglobin accumulation
  5. Reticulocyte
    - Ejection of nucleus
  6. Erythrocyte
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11
Q

What does the regulation of Erythropoiesis require?

A
  • Proteins, lipids, and carbohydrates
  • Iron, Vitamin B12, Folic acid
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12
Q

Where is intracellular iron stored?
Where is circulating iron stored?

A

Intracellular iron
- ferritin, hemosiderin

Circulating iron
- loosely bound to the transport protein transferrin

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13
Q

What are the 6 steps of the regulation of erythropoiesis?

A
  1. Low O2 levels in blood stimulate kidneys to produce erythropoietin (EPO)
  2. EPO levels rise in blood
  3. EPO and necessary raw materials in blood promote erythropoiesis in red bone marrow
  4. New erythrocytes enter bloodstream; function= 120 days
  5. Aged and damaged RBC are engulfed by macrophages of liver, spleen, and bone marrow;
    the hemoglobin is broken down
  6. Raw materials are made available in blood for erythrocyte synthesis
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14
Q

Describe Anemia

A
  • symptom where the blood has low oxygen-carrying capacity (cannot support normal metabolism)
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15
Q

Describe the following anemia’s:
Hemorrhagic
Hemolytic
Aplastic

A

Hemorrhagic
- acute or chronic loss of blood

Hemolytic
- prematurely ruptured RBCs

Aplastic
- destruction or inhibition of red bone marrow

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16
Q

What type of anemia is iron-deficiency anemia a secondary result of?

A

Hemorrhagic anemia

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17
Q

What does pernicious anemia result from?

A
  • Deficiency of vitamin B12 (role in rapid DNA synthesis of RBC)
  • Lack of intrinsic factor needed for absorption of B12
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18
Q

What is sickle-cell anemia?

What does a sickle erythrocyte result from?

A

Sickle-cell anemia
- a defective gene coding for Hb
- does not maintain RBC shape after losing O2 (can block the flow of other RBCs and interrupt the delivery of O2)

Sickled erythrocyte
- single AA change in the BETA chain of Hb

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19
Q

What is polycythemia?

A
  • increased proportion of blood volume (increase in RBC or decrease in plasma)
  • increases blood viscosity
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20
Q

What are the 2 types of WBCs and their subcategories?

What is the order of % in WBC?

A

Granulocytes
- Neutrophils
- Eosinophils
- Basophils

Agranulocytes
- Lymphocytes
- Monocytes

NLMEB

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21
Q

Describe granulocytes in general.
(4)

A
  • contain cytoplasmic granules that stain specifically with WRIGHT’s stain
  • larger and shorter-lived than RBCs
  • have lobed nuclei
  • All phagocytic cells
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22
Q

Describe neutrophils

A
  • multilobed nucleus
  • 2 types of granules that can take up ACIDIC + BASIC dyes
  • contain antibiotic-like proteins (peroxidases, hydrolytic enzymes and defensins)
  • SPECIALIZED IN KILLING BACTERIA
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23
Q

Why do neutrophils have multilobed nuclei?

Study These Flashcards
A

to help with extravasation from the blood vessel to the tissue

24
Q

Describe Eosinophils (4)

Study These Flashcards
A
  • bilobed nucleus
  • red (acidophilic) large coarse granules
  • help fight parasites
  • with mast cells, they help control mechanisms with allergy & asthma
25
Describe Basophils (4)
- purplish granules - bilobed nucleus - low density - has histamine: (inflammatory chemical that acts as a vasodilator and attracts other WBC) - also deals with infections
26
Describe Lymphocytes What are the 2 types and their function?
- Dark purple nuclei - no granules - Found in lymph tissue - Large spherical nucleus 2 types: - T cells: function in immune response - B cells: give rise to plasma cells, which produce antibodies
27
Describe Monocytes
- kidney shaped nucleus - they leave the circulation (diapedesis) and differentiate into MACROPHAGES to phagocytize - can activate lymphocytes
28
Describe platelets and megakaryocyte. Describe the 2 types of granules they have Function?
Megakaryocyte: produces platelets in bone marrow sinus (DOES NOT LEAVE BONE MARROW) - no nucleus - cell fragments that have mitochondria, glycogen, and cytoskeleton 2 granules 1. ALPHA (clotting factors) - contain serotonin, CA2+, and platelet-derived growth factor (PDGF) 2. DENSE CORE (histamine) Function - clot formation - effective method for homeostasis (stop bleeding)
29
How are platelets kept inactive?
By NO and prostacyclin (PGI2)
30
Describe the developmental pathway of platelets (5)
1. Hemocytoblast - stem cell 2. Megakaryoblast 3. Promegakaryocyte 4. megakaryocyte - stays in bone marrow - can have membrane fragmentationn 5. platelets
31
What are the most important sources of cytokines (2)
Macrophages and T cells
32
What is leukopoiesis stimulated by? (2)
Interleukins and colony-stimulating factors (CSFs)
33
What are 2 things a hemocytoblast make in the formation of leukocytes?
- lymphoid stem cell - myeloid stem cell
34
What are 2 things granulocute-macrophage CFUs make?
1. monoblast --> macrophage 2. Myeloblast --> neutrophil
35
What are the 3 steps in hemostasis?
1. Vascular Spasm 2. Platelet plug formation 3. Coagulation
36
Explain the Vascular Spasm step in hemostasis
- smooth muscle contractions - reduces blood flow - local response
37
What are the 3 stimuli to cause vasospasm?
1. direct injury to vascular smooth muscle 2. chemicals released by endothelial cells & platelets 3. Reflexes initiated by local pain receptors Spasm becomes more efficient with increasing tissue damage
38
Explain the platelet plug formation step in hemostasis
- usually platelets are inactive due to prostacyclin (PGI2) and NO - von Willebrand factor (vWF) increases bond by binding to collagen and platelets to activate the platelets - this will work once the endothelial cell is broken down - CD39 reduces ATP -> ADP which prevents abnormal platelet aggregation - after binding to collagen platelets release ADP, serotonin and thromboxane A2 (activator of platelets, eicosonoid) - Serotonin and TxA2 stimulate vasoconstriction, reducing blood flow to wound - ADP & TxA2 cause other platelets to become sticky and attach
39
What are the 3 steps of Coagulation in hemostasis?
Follow an intrinsic and extrinsic pathways 3 steps 1. Prothrombin activator is formed 2. Prothrombin is converted into thrombin 3. Thrombin catalyzes the joining of fibrinogen into a fibrin mesh
40
Explain phase 1 of coagulation
A series of procoagulants that goes towards factor X - Once factor X has been activated, it complexes with Ca2+, PF3 (platelet factor), and factor V to form PROTHROMBIN ACTIVATOR 4 things to make prothrombin activator - Factor X - Ca2+ - PF3 - Factor V
41
Explain phase 2 of coagulation
Prothrombin is converted to THROMBIN through the catalysis of prothrombin activator
42
Explain phase 3 of coagulation
Thrombin catalyzes the joining of fibrinogen into a FIBRIN - causes plasma to become a gel-like trap (traps RBC, proteins) - Thrombin in the presence of Ca2+ activates Factor XIII that - cross-links fibrin - strengthens and stabilizes the clot
43
How does clot retraction and skin repair happen?
Clot retraction - stabilization of the clot by squeezing serum from the fibrin strands Repair - Fibroblasts form a connective tissue - Platelet-derived growth factor (PDGF) stimulates rebuilding of blood vessel wall - Endothelial cells multiply and restore endothelial lining, Stimulated by vascular endothelial growth factor (VEGF)
44
How can fibrin act as an anticoagulant? What does this action prevent? (3)
by binding Fibrin with thrombin This prevents: - positive feedback effects of coagulation - prevents ability to speed up the production of prothrombin activator via Factor V - prevents acceleration of the intrinsic pathway by activating platelets
45
what happens if thrombin is not absorbed to fibrin?
Inactivated by antithrombin III - heparin can also inhibit thrombin activity
46
How can we prevent platelet adhesion/coagulation? (3)
By: - the smooth endothelial lining of blood vessels - Heparin, NO and PGI2 secreted by endothelial cells - Vitamin E quinone, potent anticoagulant
47
Why do we want to prevent abnormal clotting? Explain Thrombus and Embolus
Thrombus - a clot that develops and persists in an unbroken blood vessel - can block circulation, resulting in tissue death Embolus - a thrombus freely floating in the blood stream - pulmonary emboli: impair the ability of body to get O2 - Cerebral emboli: cause strokes
48
Describe hemophilias Which factors affect hemophilia A, B, C? Which pathway is affected?
Hemophilias: bleeding disorder caused by lack of clotting factors A: lack of Factor 8 B: Lack of factor 9 C: lack of factor 11 - Intrinsic pathway is affected (micro bleeds) (long acting) - extrinsic pathway NOT affected (large bleeds) (quick acting)
49
What does Warfarin inhibit? Which factors are affected?
Inhibits vitamin K synthesis Affects factors: 2, 7, 9, 10
50
How do we tell blood types of humans?
By the presence or absence of glycoprotein antigens on the RBC surface
51
Antigens of which blood group cause vigorous transfusion when they are improperly transfused?
ABO and Rh blood groups
52
Which blood group is universal donor and which is the universal recipient?
Donor - O Recipient - AB
53
What blood type can you give for emergency cases? What blood type do you give for non-emergency cases?
Emergency - O or the same type (if file is present) Non-emergency - Give same type
54
What does Rh- and Rh+ mean?
Rh+ : presence of Rh agglutinogens (no anti-Rh) Rh-: no anti-Rh antibodies formed spontaneously (has anti-Rh)
55
What happens if an Rh- person receives blood from an Rh+ person?
Anti-Rh antibodies will form Rh+ antibodies of a sensitized Rh- mother crosses the placenta and attack and destroy the RBC's of a Rh+ baby
56
What does RhoGAM do?
prevents an Rh- mother from becoming sensitized at birth

PHARM 111 Midterm (5 decks)

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