Lecture 17: Blood 4 and Hemostasis 1 Flashcards
Anemia
A reduction below normal in the O2 carrying capacity of blood and is characterized by a low hematocrit
Hematocrit
The percentage of total blood volume occupied by erythrocytes
Hematocrit is often reported as the
volume of packed RBC
PCV (packed cell volume)
Hematocrit is lower in anemia because
of too few circulating erythrocytes
Three ways anemia can be brought about
- Decreased rate of erythropoiesis
- Excessive loss of erythrocytes
- Deficiency in the hemoglobin content of erythrocytes
6 Categories of anemia
- Nutritional
- Pernicious
- Aplastic
- Renal
- Hemorrhagic
- Hemolytic
Nutritional anemia
Caused by dietary deficiency of a factor needed for erythropoiesis
Nutritional anemia example: Iron deficiency
Occurs when not enough iron is available for hemoglobin synthesis due to an iron deficient diet or poor iron absorption from the digestive tract
The usual number of RBC are produces but they contain less hemoglobin than usual and transport less O2
Nutritional anemia example: folic-acid deficiency
Folic acid is critical for stem cell division and maturation of erythrocytes, so deficiency causes fewer RBC formed and they are very fragile
Anemia is due to the production of fewer RBC and the early demise due to fragility
Pernicious anemia
Caused by an inability to absorb adequate amounts of V B12 from digestive tract
B12 is essential for
Proliferation and development of RBC and only when it is combined with intrinsic factor can it be absorbed by the intestinal tract by special support mechanisms
Intrinsic factor
Secreted by lining of stomach or pancreatic cells
When it is deficient, B12 isn’t sufficiently absorbed from the intestinal tract resulting in impairment of RBC production, leading to anemia
Aplastic anemia
-Caused by failure of the bone marrow to produce adequate number of RBC, even though everything needed for erythropoiesis is available
Destructive process may selectively reduce the RBC output by the bone marrow.
Severity depends on extent of erythropoietic tissue damage and can be fatal
In aplastic anemia, reduced erythropoietic activity can be caused by destruction of red bone marrow by:
- Toxic chemicals
- Radiation exposure
- Invasion of marrow by cancer cells
Renal anemia
- May be a consequence of renal disease
- Since erythropoietin from the kidneys is the primary stimulus for promoting erythropoiesis, inadequate EPO as a result of kidney disease causes insufficient RBC production and anemia
Hemorrhagic anemia
Caused by loss of substantial quantities of blood
Anemia is present until the lost cells are replaced
Hemolytic anemia
Caused by rupture of excessive numbers of circulating erythrocites
Example of hemolytic anemia: Immunohemolytic Disease of the Newborn
- May occur in animals including horses and cats
- Similar to the Rh factor in humans
- Occurs when parents have different blood types and the offspring inherits father’s blood type
Immohemolytic disease of the newborn in horses
- Sensitization of mare to foal’s blood type occurs during parturition
- Mare produces antibodies against foal’s BT and transfers these antigens through her milk as foal nurses
- Her antibodies destroy offspring’s RBC
Two types of hemolytic anemia in dogs
- Primary - Autoimmune hemolytic anemia (immune mediated hemolytic anemia)
- Body attacks own RBC
- Cause is unknown - Secondary
- Caused by parasite or toxin
Viscosity of blood depends mostly on
concentration of RBC
In anemia, viscosity decreases, leading to
decreased resistance to blood flow in the peripheral vessels -> increased venous return -> increased work load on the heart -> cardiac hypertrophy due to volume overload -> heart failure
Polycythemia
excess of circulating RBC and an elevated hematocrit
Two types of polycythmia
Primary
Secondary
Primary polycythemia
- Caused by tumor-like condition of the bone marrow in which erythropoiesis proceeds at an excessive uncontrolled rate
- Extra O2 carrying capacity is not beneficial because O2 delivery is more adequate with normal RBC numbers
Primary Polycythemia adverse effects
- Excessive # of RBC increase the viscosity of blood up to 5-7x which reduces o2 delivery to tissues
- Increases total peripheral resistance, elevating blood pressure, and increase heart work load, and causes cardiac hypertrophy due to pressure overload
Secondary polycythemia is also called
physiological polycythemia
Secondary polycythemia
- EPO induced adaptive mechanism to improve O2 carrying capacity of blood in response to a prolonged reduction in O2 delivery to tissues
- Occurs in high altitudes where there is less O2
- Occurs with chronic lung disease and heart disease
Hematocrit in secondary polycythemia is usually _____ than that of primary polycythemia
lower
The rbc count usually rises about 30% above normal, causing increased viscosity -> pressure overloading of the heart -> cardiac hypertrophy
An elevated hematocrit can occur when body loses fluid but not _______, such as in diarrhea
erythrocytes
dehydration
Relative polycythemia
- Dehydration
- Normal number of erythrocytes but in a higher concentration due to less plasma
- Blood viscosity increases, leading to sluggish blood flow
The life span of erythrocytes is dependent on
- species
- It has no nucleus so it is not able to replace the enzymes it needs for metabolism
Erythrocytes are able to use some _____ as a source of energy
glucose
Erythrocyte aging and degradation
- Proteins go through a process of degradation and cannot be replaced
- This causes leaky cell membranes
- Aged cells pass through capillaries of spleen, liver, and bone marrow, and their leaky membranes rupture
- Cellular remnants are engulfed by resident phagocytic macrophages
Are platelets whole cells?
Nope
Thrombocytopoiesis means
platelet production
Platelet production occurs where?
In the bone marrow
Normal bone marrow contains giant cells called _____ that give rise to platelets
megakaryocytes
Upon maturing, megakaryotcytes
- Shed cytoplasm in small membrane-enclosed packets which enter the circulation as platelets
- It will gradually lose all cytoplasm, shedding about 4000 platelets before nucleus is engulfed by macrophages
What hormone influences megakaryocyte maturation and platelet formation?
Thrombopoietin
Thrombopoietin (TPO) is also called
Thrombocyte-stimulating factor
Where is thrombopoietin produced?
The kidneys
Thrombopoietin
A peptide hormone that accelerates platelet formation and stimulates the production of megakaryocytes resulting in a rapid increase in platelets
Platelets remain functional for an average of ____ days
10
Do platelets leave the blood?
Nope
At any given time, about 1/3 of total platelets are
In storage in the spleen
These can be released into circulation by sympathetically induced splenic contraction in times of need (ex. bleeding from a vessel occurs)
The vascular clotting system includes (3)
- Plasma proteins
- Tissues of circulatory network
- Platelets
Three functions of platelets
- Transport chemicals important to clotting process
- Formation of a temporary platelet plug that can slow the rate of blood loss while clotting occurs at the walls of damaged blood vessels
- Active contraction after clot formation has occured
How/why do platelets actively contract after clot formation has occurred?
- Contain filaments of actin and myosin
- Contraction of platelets shrinks the clot and reduces the size of the break in the vessel wall
Hemostasis
The arrest of bleeding from a broken blood vessel and establishes a framework for tissue repair
Although hemostasis is a series of steps, it is more like a
chain reaction
Three major steps are involved in hemostasis
- Vascular spasm
- Platelet plug formation
- Clotting (coagulation) phase
Vascular spasm stage of hemostasis
- Cutting the wall of a blood vessel triggers contraction in the smooth muscle fibers in the vessel wall
- Contraction produces a local vascular spasm that decreases the diameter of the vessel at the site of the injury
- Constriction slows blood flow through the defect and thus minimizes blood loss
During vascular spasm phase, what changes occur in the endothelium at the injury?
- Endothelial cells contract and expose underlying basement membrane to the bloodstream
- Endothelial cells begin releasing chemical factors
- Endothelial cell membranes become sticky and in small blood vessels, endothelial cells on the opposite sides of the blood vessels may stick together which further seals off the damaged vessel
Endothelin
- Example of chemical factor released by endothelial cells during vascular phase
- Stimulates smooth muscle contraction
- Stimulates the division of endothelial cells, smooth muscle cells, and fibroblasts to accelerate the repair process
Are physical measures alone enough to completely prevent blood loss during vascular stage?
Nope, but important in minimizing blood flow until other hemostatic measures are able to plug up defect
