Blood Flashcards

(60 cards)

1
Q

Blood Functions

A

Transport
Acid-Base Balance
Protective

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2
Q

Plasma composition

A

Ions, nutrients, waste, respiratory gases, proteins

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3
Q

Separating Plasma Proteins

A
  1. Differential precipitation by salts
  2. Sedimentation in ultracentrifuge
  3. Electrophoretic mobility
  4. Immunological characteristics
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4
Q

Electrophoresis

A

Fractional method where particles move through gel on voltage gradient
a. molecular weight
b. charges of particles

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5
Q

Plasma Proteins

A

Made in liver
- Albumin
- Fibrinogen
- Golublins a, b
Lymphoid tissue
- Globulin y

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6
Q

Role of Plasma Proteins

A

Determines distribution of fluid between plasma + ISF compartments by controlling transcapillary movement

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7
Q

Colloidal Osmotic Pressure

A

Plasma proteins are not diffusible through the capillary wall so exert pressure to move fluid in
COP increases = water –> plasma
COP decreases = water –> ISF

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8
Q

Bulk flow

A

Change in hydrostatic pressure moving molecules

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9
Q

Starling Forces

A

Filtration
Osmotic Flow

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10
Q

Filtration

A

Pushes fluid out of capillaries

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11
Q

Colloidal Osmotic Pressure

A

Plasma proteins pull fluid into capillaries

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12
Q

Influences on COP

A

Albumin is the most common plasma protein = small and oval size makes COP rise
- Concentration in the plasma
- Molecular weight of protein

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13
Q

Factors in Transcapillary Dynamics

A
  1. Hydrostatic pressure
  2. COP
  3. Capillary permeability
  4. Lymphatic drainage
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14
Q

Edema

A

Accumulation of fluid in Interstitial spaces

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15
Q

Causes of Edema

A

Increased hydrostatic pressure
Lowered COP
Increased capillary permeability
Obstruction of lymphatic drainage

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16
Q

Role of Plasma Proteins

A
  1. Distribution between ISF and plasma
  2. Viscosity of plasma
  3. Buffering power of plasma (pH = 7.4)
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17
Q

Hematopoiesis

A

Production of blood cells

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18
Q

Erythropoiesis

A

Production of RBCs

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19
Q

Thrombopoiesis

A

Production of platelets

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20
Q

Leukopoiesis

A

Production of WBCs

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21
Q

Sites of Hematopoiesis

A

Prenatal
Flat bones of skull
Shoulder blades
Pelvis
Vertebrae
Sternum
Ribs
Epiphyseal site in long bones

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22
Q

Hematopoiesis Steps

A

Multipotential Stem Cells –> Committed Stem Cells –> Blood Cells
Cytokines promote growth
HGFs = proliferation + differentiation of blood cell precursors

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23
Q

Erythrocytes

A

Facilitate transport of respiratory gases between lungs

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24
Q

Erythrocyte Properties

A

Shape: Biconcave disk
No organelles
Lots of hemoglobin

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25
Advantage of Biconcave Disk
1. Maximal surface area (efficient diffusion) 2. Lots of flexibility (squeeze through narrow capillaries)
26
Hemoglobin
Found in erythrocytes Can bind to 4 O2 molecules Oxygen links to polypeptide chains of heme and iron
27
Hb functions
1. Transport O2 and CO2 2. Act as buffer
28
Why is Hb inside RBCs and not in plasma?
i) Plasma viscosity ii) Plasma COP iii) Less loss via kidney
29
Factors influencing ability of Hb to bind to O2
1. Temperature 2. Ionic composition 3. pH 4. Intracellular enzyme concentration
30
RBC Precursors Differentiation
Start with Stem Cells --> Reticulocytes --> RBCs 1. Decrease in size 2. Lose nucleus 3. Accumulation of Hb
31
Erythropoietin
Glycoprotein hormone/ cytokine produced by kidney Stimulus is Hypoxia
32
Erythropoiesis Cycle
1. O2 supply decreases 2. Increased release of erythropoietin 3. Erythropoietin goes in plasma 4. Bone marrow stimulated 5. RBCs produced 6. Oxygen levels increase
33
Testosterone
Increases release of erythropoietin Increases sensitivity of RBC precursors Estrogen has opposite effect
34
Destruction of RBCs
Life span: 120 days Macrophages recognize old RBCs and engulf them
35
Jaundice
1. Excessive Hemolysis 2. Hepatic Damage 3. Bile Duct Obstruction
36
Polycythemia
Relative: due to decreased plasma volume Absolute: Physiological or Pathological Increases blood viscosity = prone to blood clots
37
Physiological Causes of Polycythemia
- High altitudes - Increased exercise - Lung diseases (emphysema) - Heavy smoking (high CO in blood)
38
Pathological Causes of Polycythemia
Tumours cause unregulated production of RBCs in bone marrow Due to genetic mutation
39
Anemia
Decrease in oxygen carrying capacity of blood
40
Morphologic Description of cells - Microcytic - Normocytic - Macrocytic - Normochromic - Hypochromic
Smaller cells (< 80) Normal size cells (80 - 94) Larger cells (> 94) Normal amount of Hb Decreased levels of Hb in RBCs
41
Etiological Classifications of Anemia
Diminished production Ineffective Maturation Survival Disorders
42
Diminished production Anemia
Aplastic anemia: caused by outside factor (radiation) Stimulation failure: renal disease Iron deficiency: not enough iron = less O2 carried
43
Ineffective Maturation
Deficiency in B12 or Folic Acid - Intrinsic factor deficiency = pernicious anemia
44
Survival Disorders
Congenital: abnormal membrane structure, missing enzymes, abnormal Hb structure Acquired: toxins, drugs, antibodies
45
Why do women have less RBCs
Lower muscle mass = don't need as much oxygen Menstrual loses
46
Hemostasis
Arrest of bleeding following vascular injury a) Vasoconstriction b) Platelet Plug c) Clotting
47
Vasoconstriction
i) Nervous reflex ii) Myogenic response, smooth muscle in vessel wall contracts iii) Chemical vasoconstrictors
48
Platelet Response
1. Adhesion 2. Activation + release of cytokines 3. Aggregation 4. Consolidation
49
Platelet functions
Release vasoconstriction agents Form platelet plug Release clotting factors Clot retraction Stabilize endothelial integrity
50
Platelets
Bind to damaged area by collagen Adhesion to cell membrane Aggregation = change shape once connected to collagen Thrombin promotes platelet plug
51
Prolonged Bleeding
Failure of blood vessel to constrict Could be due to platelet deficiencies a) Numerical: have less than normal b) Functional: can't perform their role
52
Aspirin
Inhibits the synthesis and release of TXA2 - No constriction
53
Clotting
Initiated by injury to blood vessel wall Interaction of plasma proteins and clotting factors (enzymes or co-factors) Presence of Ca2+ and phospholipid agents
54
Required Factors of Coagulation
Ca2+ Phospholipids Protein plasma proteins
55
Clotting Factor Deficiencies
Congenital Acquired: liver disease or vitamin K deficiency (involved in synthesis of prothrombin)
56
Control of coagulation
inhibitors and coagulants block reactions in pathway scheme
57
Clot Lysis (Fibrinolysis)
Plasminogen --> plasmin --> breaks fibrin into fibrin fragments
58
Inhibitors of platelet adhesion
Aspirin
59
Anticoagulant drugs
Coumadin: blocks synthesis of functional prothrombin Heparin: promotes inhibition of thrombin activation and action
60
Thrombolytic drugs
Promote clot lysis