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PHGY 209 > Blood > Flashcards

Blood Flashcards

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
Q

Advantage of Biconcave Disk

A
  1. Maximal surface area (efficient diffusion)
  2. Lots of flexibility (squeeze through narrow capillaries)
26
Q

Hemoglobin

A

Found in erythrocytes
Can bind to 4 O2 molecules
Oxygen links to polypeptide chains of heme and iron

27
Q

Hb functions

A
  1. Transport O2 and CO2
  2. Act as buffer
28
Q

Why is Hb inside RBCs and not in plasma?

A

i) Plasma viscosity
ii) Plasma COP
iii) Less loss via kidney

29
Q

Factors influencing ability of Hb to bind to O2

A
  1. Temperature
  2. Ionic composition
  3. pH
  4. Intracellular enzyme concentration
30
Q

RBC Precursors Differentiation

A

Start with Stem Cells –> Reticulocytes –> RBCs
1. Decrease in size
2. Lose nucleus
3. Accumulation of Hb

31
Q

Erythropoietin

A

Glycoprotein hormone/ cytokine produced by kidney
Stimulus is Hypoxia

32
Q

Erythropoiesis Cycle

A
  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
Q

Testosterone

A

Increases release of erythropoietin
Increases sensitivity of RBC precursors
Estrogen has opposite effect

34
Q

Destruction of RBCs

A

Life span: 120 days
Macrophages recognize old RBCs and engulf them

35
Q

Jaundice

A
  1. Excessive Hemolysis
  2. Hepatic Damage
  3. Bile Duct Obstruction
36
Q

Polycythemia

A

Relative: due to decreased plasma volume
Absolute: Physiological or Pathological
Increases blood viscosity = prone to blood clots

37
Q

Physiological Causes of Polycythemia

A
  • High altitudes
  • Increased exercise
  • Lung diseases (emphysema)
  • Heavy smoking (high CO in blood)
38
Q

Pathological Causes of Polycythemia

A

Tumours cause unregulated production of RBCs in bone marrow
Due to genetic mutation

39
Q

Anemia

A

Decrease in oxygen carrying capacity of blood

40
Q

Morphologic Description of cells
- Microcytic
- Normocytic
- Macrocytic

  • Normochromic
  • Hypochromic
A

Smaller cells (< 80)
Normal size cells (80 - 94)
Larger cells (> 94)

Normal amount of Hb
Decreased levels of Hb in RBCs

41
Q

Etiological Classifications of Anemia

A

Diminished production
Ineffective Maturation
Survival Disorders

42
Q

Diminished production Anemia

A

Aplastic anemia: caused by outside factor (radiation)
Stimulation failure: renal disease
Iron deficiency: not enough iron = less O2 carried

43
Q

Ineffective Maturation

A

Deficiency in B12 or Folic Acid
- Intrinsic factor deficiency = pernicious anemia

44
Q

Survival Disorders

A

Congenital: abnormal membrane structure, missing enzymes, abnormal Hb structure
Acquired: toxins, drugs, antibodies

45
Q

Why do women have less RBCs

A

Lower muscle mass = don’t need as much oxygen
Menstrual loses

46
Q

Hemostasis

A

Arrest of bleeding following vascular injury
a) Vasoconstriction
b) Platelet Plug
c) Clotting

47
Q

Vasoconstriction

A

i) Nervous reflex
ii) Myogenic response, smooth muscle in vessel wall contracts
iii) Chemical vasoconstrictors

48
Q

Platelet Response

A
  1. Adhesion
  2. Activation + release of cytokines
  3. Aggregation
  4. Consolidation
49
Q

Platelet functions

A

Release vasoconstriction agents
Form platelet plug
Release clotting factors
Clot retraction
Stabilize endothelial integrity

50
Q

Platelets

A

Bind to damaged area by collagen
Adhesion to cell membrane
Aggregation = change shape once connected to collagen
Thrombin promotes platelet plug

51
Q

Prolonged Bleeding

A

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
Q

Aspirin

A

Inhibits the synthesis and release of TXA2
- No constriction

53
Q

Clotting

A

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
Q

Required Factors of Coagulation

A

Ca2+
Phospholipids
Protein plasma proteins

55
Q

Clotting Factor Deficiencies

A

Congenital
Acquired: liver disease or vitamin K deficiency (involved in synthesis of prothrombin)

56
Q

Control of coagulation

A

inhibitors and coagulants block reactions in pathway scheme

57
Q

Clot Lysis (Fibrinolysis)

A

Plasminogen –> plasmin –> breaks fibrin into fibrin fragments

58
Q

Inhibitors of platelet adhesion

A

Aspirin

59
Q

Anticoagulant drugs

A

Coumadin: blocks synthesis of functional prothrombin
Heparin: promotes inhibition of thrombin activation and action

60
Q

Thrombolytic drugs

A

Promote clot lysis

PHGY 209 (4 decks)

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